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Fundamentals of Molecular Virology, 2nd Edition By Nicholas H. Acheson
Email: richard@qwconsultancy.com
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 01
Question type: Multiple Choice
1) Which of the following terms describes the protein shell that surrounds the viral genome? a) capsid b) envelope c) matrix d) virion e) capsomere Answer: a
2) Which of the following would not be a nucleic acid form found in a viral genome? a) dsDNA b) ssDNA c) dsRNA d) ssRNA e) an RNA:DNA hybrid Answer: e
3) Which of the following is an enzyme that most RNA viruses encode in their genome? a) DNA-dependent-RNA-polymerase b) RNA-dependent-RNA-polymerase c) DNA-dependent-DNA-polymerase d) DNA-dependent-RNA-polymerase e) RNA-dependent-protein-synthetase Answer: b
4) Viruses play a major role in the ecology of the ocean by doing which of the following? a) By infecting photosynthetic bacteria and increasing their growth. b) By infecting harmful bacteria found in the ocean and limiting their growth. c) By killing off fish and preventing them from becoming too plentiful. d) By lysing unicellular organisms and releasing carbon and oxygen back into the ocean. e) All of the above statements are correct.
Answer: d 5) If you wanted to show that an infectious agent is a virus, what experiment could you do? a) Show that the agent can be seen under a light microscope. b) Show that agent contains a lipid membrane. c) Show that the agent can form single colonies on an agar plate. d) Show that the agent can be diluted and can still cause disease in an animal. e) Show that the agent can pass through a porcelain filter and is still infectious. Answer: e 6) What does the word “virus” mean in Latin? a) infectious agent b) liquid c) poison d) death e) disease Answer: c 7) The word “phage” is a shortened version of the name of a virus that can infect which type of organism? a) bacterial cell b) human cell c) eukaryotic cell d) plant cell e) inset cell Answer: a
8) The study of which group of viruses led to the discovery of cellular genes that can promoter cancer in animal cells? a) papillomaviruses b) retroviruses c) adneoviruses d) polyomaviruses e) picornaviruses Answer: b
9) When doing a plaque assay with human or animal cells, a layer of nutrient media mixed with agar is put on top of the cells after they have been infected with the diluted virus. What is the major purpose of this agar layer? a) It helps to feed the cells as they grow. b) It promotes the replication of the virus. c) It makes the infected cells easier to visualize. d) It limits the movement of virus particles. e) All of the above are correct. Answer: d
10) To start an experiment, you do an infection by putting 0.5 ml of a virus stock that has a titer of 6 x 107 pfu/ml onto a plate of animal cells that contains 5 x 106 cells. What is the multiplicity of infection for this experiment? a) 12 b) 6 c) 5 d) 3 e) 1 Answer: b
11) During a single growth cycle experiment, the titer of extracellular and intracellular virus drops in the first hour. What explains this observation? a) The virus is inactivated by antibodies in the medium. b) The virus is inactivated by cellular enzymes. c) The virus enters the cell and is uncoated. d) The virus binds to the cells in the dish and can’t be released. e) The cell’s antiviral defenses prevent replication of the virus Answer: c
12) What is another term for an RNA-dependent-DNA-polymerase? a) DNA polymerase b) RNA polymerase II c) RNA replicase d) RNA transcriptase e) Reverse transcriptase
Answer: e 13) Plant viruses use which cellular structures to spread between host cells? a) endosomes b) plasmodesmata c) plasma membranes d) vesicles e) receptors Answer: b
14) All viruses that use a negative-sense RNA genome must package which of the following proteins in their virion? a) RNA-dependent-RNA-polymerase b) matrix protein c) RNA helicase d) RNA methylase e) scaffolding protein Answer: a
15) Which of the following is a description of a plaque? a) A viral particle as seen by electron microscopy. b) A region of dead cells in a monolayer of infected cells. c) A skin lesion caused by a virus infection in an animal. d) A button of red blood cells seen in a hemagglutination assay. e) A region of crystallized virus particles in an infected cell. Answer: b
16) Which of the following processes in cells was NOT discovered by studying a virus? a) the sequence of the genetic code. b) DNA replication in both prokaryotic and eukaryotic cells c) DNA is the genetic material d) regulation of gene expression in eukaryotic cells. e) mRNA splicing in eukaryotic cells Answer: a
17) You are given a solution of virus and asked to determine the titer. You carry out a plaque assay with 0.5mls of a 105 dilution of the virus solution and obtain an average of 150 plaques. What is the titer of the solution? a) 1.5 x 105 pfu/ml b) 3 x 105 pfu/ml c) 1.5 x 107 pfu/ml d) 3 x 107 pfu/ml e) 1.5 x 108 pfu/ml Answer: d
18) The Baltimore classification system describes the relationship between a viral genome and the: a) the complementary genome sequence. b) early viral proteins. c) early mRNAs. d) cellular polymerases. e) Latin classification system. Answer: c
19) If the genome of a positive-strand RNA virus, which has been purified away from all of the virion proteins, was injected into the cytoplasm of an appropriate host cell, what would happen first? a) The genome would be copied into complementary negative RNA. b) The genome would be translated by cellular ribosome’s. c) The genome would be transcribed by a cellular RNA-dependent-RNA-polymerase. d) The genome would be transcribed by a viral RNA-dependent-RNA-polymerase. e) None of the above. Answer: b
20) If the genome of a negative-strand RNA virus, which has been purified away from all of the virion proteins, was injected into the cytoplasm of an appropriate host cell, what would happen first? a) The genome would be copied into complementary negative RNA. b) The genome would be translated by cellular ribosome’s. c) The genome would be transcribed by a cellular RNA-dependent-RNA-polymerase. d) The genome would be transcribed by a viral RNA-dependent-RNA-polymerase. e) None of the above.
Answer: e 21) Most DNA viruses that replicate in the nucleus of the host cell use which of the following to transcribe their genes into mRNA? a) cellular DNA-dependent-RNA polymerase b) viral DNA-dependent-RNA polymerase c) viral DNA-dependent-DNA polymerase d) cellular DNA-dependent-DNA polymerase e) viral RNA-dependent-DNA polymerase Answer: a 22) The development of which of the following instruments or techniques in the 1930’s allowed scientists to visualize viral particles for the first time? a) polymerase chain reaction b) electron microscope c) confocal microscope d) thermal cycler e) plaque assay Answer: b
Question Type: True/False
24) The common cold can be caused by viruses from three different families, some of which have RNA genomes and some of which have DNA genomes. Answer: True
25) The major advantage of a hemagglutination assay to measure the amount of virus particles in a solution is that it is very accurate. Answer: False
26) Phages, viruses that can infect bacterial cells, may someday be used to treat bacterial infections. Answer: True
Question type: Essay
27) The particle to plaque ratio for most animal viruses is much greater than one. What are the reasons why not 100% of animal virus particles, as seen under the electron microscope, can productively infect cells? Answer: Not all virus particles as seen under the electron microscope are intact virions capable of binding and entering a host cell. Some virus particles contain defective genomes that lack one or more critical genes necessary for viral replication. Some viral particles contain empty capsids, which means that there is not genome inside the virion. Finally, cells have many antiviral defense mechanisms that can shut down a virus infection before it can be completed.
28) Viruses are not the only obligatory intracellular parasites. Describe how the replication of viruses is different than cellular organisms that replicate inside of cells, like chlamydiae and rickettsiae. Answer: Unicellular parasitic cells that need to replicate inside of other cells do not replicate in the same way that viruses do. First of all, unicellular parasites have their own ribosomes to translate their mRNAs and do not use the host cell ribosomes, like viruses do. In addition they are intact cells that contain their genome entirely within their own cellular membranes and do not release their genome into the host cell, the way that viruses do. These cellular parasites undergo binary fission in the same way that independently living cells do. Viruses do not have their own ribosomes and actually disintegrate their virion, releasing the genome out of the capsid and into the cytoplasm before they begin their replication. They do not undergo binary fission.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 02
Question type: Multiple Choice
1) The lipid membrane that surrounds the nucleocapsid of some virus particles is called the: a) matrix b) tegument c) capsid d) envelope e) glycoprotein Answer: d
2) The nucleocapsid describes the structure that includes the: a) capsid and the genome b) capsid and the envelope c) envelope and the glycoproteins d) helical capsid and an envelope e) icosahedral capsid and an envelope Answer: a
3) Depending on the type of virus, which of the following is a function of the virus capsid? a) To attach to the correct type of host cell. b) To protect the viral genome from nucleases. c) To ensure delivery of the genome into the host cell. d) To protect the viral genome from damage by UV light. e) All of the above functions are correct. Answer: e
4) Virus particles can be visualized with which of the following? a) negative staining of virions with electron microscopy b) negative staining of virions with x-ray diffraction c) negative staining of thin sections of infected cells with electron microscopy d) positive staining in cryoelectron microscopy e) positive staining of infected cells with x-ray diffraction
Answer: a 5) Most viruses that use a spherical shaped capsid arrange their capsid proteins with which of the following symmetries? a) cubic b) tetrahedral c) icosahedral d) dodecagon e) helical Answer: c
6) Which of the following is NOT a characteristic of a regular icosahedron? a) It has 12 vertices of 5-fold symmetry. b) It has 20 triangular faces. c) It has 20 sides with 3-fold symmetry. d) It has 30 edges with 2-fold symmetry e) It has 6 square faces. Answer: e
7) How many copies of the capsid protein would there be in an icosahedral capsid with a Triangulation number of 7? a) 70 b) 210 c) 280 d) 420 e) 490 Answer: d
8) Which of the following h and k values will produce a triangulation number of 13? a) 1 and 1 b) 1 and 2 c) 1 and 3 d) 2 and 3 e) 2 and 4 Answer: c
9) The capsid of SV40 contains 360 protein copies. Why is this unusual? a) There is only 1 kind of protein in this capsid. b) 360 is not the correct number of protein capsids for a T = 6 capsid. c) Six is not a mathematically allowed triangulation number. d) The proteins have equivalent interactions. e) The capsid is not large enough to hold the entire genome. Answer: c 10) The Jelly Roll barrel is: a) a structure found in many viral envelope glycoproteins. b) a structure found in many viral capsid proteins. c) the structure the viral genome takes inside of a helical capsid. d) the structure the viral genome takes inside an icosahedral capsid. e) the structure of many helical capsids as the wrap around the genome. Answer: e
11) Which of the following describes the number of subunits per turn in a helical capsid? a) P (pitch) b) (mu) c) (rho) d) Triangulation number e) symmetry Answer: b
12) A very common structure for bacteriophage particles is which of the following? a) an icosahedral head and an envelope b) a naked icosahedral head c) a naked helical tail d) an icosahedral head with a helical tail e) a cubic head with a helical tail Answer: d
13) A Type I membrane protein has which of the following structures?
a) Both the C-terminus and the N-terminus face the inside of the virion. b) It passes through the viral envelope multiple times. c) The N-terminus faces outside the virion and the C-terminus faces inside the virion. d) The N-terminus faces inside the virion and the C-terminus faces outside the virion. e) The protein lacks a transmembrane domain and is secreted from the infected cell. Answer: c 14) What does the term “quasi-equivalent” mean with respect to the proteins in an icosahedral capsid? a) If the identical protein is used, it has both 5-fold and 6-fold interactions with the other proteins in the capsid. b) There are different proteins in the capsid with similiar shapes. c) They all use the “jelly-roll” protein structure. d) There can be more than one type of glycoprotein in the envelope. e) All of the proteins interact in a 5-fold arrangement. Answer: a
15) Which of the following is a description of a scaffolding protein? a) A cellular protein that acts as a chaperone during assembly of a helical capsid. b) A viral protein that is used on the outside of an icosahedral capsid during assembly. c) A viral protein used on the inside of an icosahedral capsid during assembly and then removed. d) A protease that trims the proteins during assembly of an icosahedral capsid. e) A energy dependent motor used to package the genome into larger icosahedral capsids. Answer: c 16) A scaffolding protein is important for assembly of an icosahedral capsid….. a) but does not bind to the viral genome. b) but does not become part of the final virion. c) and helps to cut the genome into unit lengths. d) and binds to the host cell receptor. e) and assists the virion in exiting the host cell. Answer: b
17) A packaging sequence is involved in which of the following assembly processes? a) The assembly of the capsid around the genomic nucleic acid. b) The correct binding of capsid proteins to each other.
c) The insertion of the viral glycoproteins in the envelope. d) The acquisition of the envelope by the capsid. e) The packaging of the matrix proteins into the virion. Answer: a
18) In a helical nucleocapsid, which of the following MOST affects the LENGTH of the capsid? a) the (mu) value b) the (rho) value c) the size of the genome and the P (pitch) of the helix d) the size of the capsid protein e) None of the above. Answer: c
19) Enveloped virions assemble and acquire their envelope by which of the following mechanisms? a) The nucleocapsids interact directly with the cytoplasmic tails of the envelope glycoproteins and bud through the cellular membrane. b) The nucleocapsids interact with the matrix protein, which interact with the cytoplasmic tails of the envelope glycoprotein, and the virion buds through the cellular membrane. c) The envelope is assembled de novo around the nucleocapsid by cellular enzymes. d) The virion acquires the envelope after it leaves the host cell from extracellular vesicles. e) Both a and b are used by viruses. Answer: e
20) Viral proteins that assemble between the nucleocapsid and the envelope are called a) matrix proteins b) envelope glycoproteins c) scaffolding proteins d) core proteins e) packaging proteins
Question Type: True/False
21) It is possible to get high resolution images of enveloped virus particles using x-ray diffraction.
Answer: False
22) Some viruses particles have a rigid capsid surrounding an internal membrane. Answer: True
23) Cryoelectron microscopy uses computer reconstruction of images of multiple virions to produce a high resolution image of a virion or capsid. Answer: True.
24) Viral envelopes often have very different lipid compositions than the cellular membranes that they originate from. Answer: False
Question type: Essay 25 ) Describe the concept of “quasi-equivalence” as it applies to icosahedral capsid structure. Answer: Quasi-equivalence describes the situation in icosahedrons with triangulation numbers higher than 1 and that use a single protein to assembly their capsid. In these capsids, the protein must interact in a 5-fold symmetry at the 12 vertices and in a 6-fold symmetry in the hexagonal faces. Therefore its interactions are not always identical but depend on the protein’s location within the capsid. 26) Virions are often described as being energetically “metastable”. What does this mean and why is it important for entry and uncoating of the viral genome into the next host cell? Answer: Virons are described as “metastable” because they are not at their lowest, most stable, energy state. If they were, they would not be able to “pop open” to release the genome in the next host cell. Instead, they are like a “Jack-in-the-box”, primed to spring open and release the genome after some triggering event. The triggering event that causes the virion to open and release the genome is often the interaction with the host cell receptor or some other change, like a drop in pH, that occurs during attachment and entry. Often proteolytic cleavage of a virion protein is involved in setting up the metastable state and “setting the spring” that will eventually allow the virion to pop open.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 03
Question type: Multiple Choice
1) Which of the following types of genomes is most commonly found in viruses that can infect fungi? a) ssDNA b) dsDNA c) ssRNA d) dsRNA e) All of the above are found. Answer: d 2) The name of a virus family in the Latin classification system has which of the following endings? a) -viridae b) -virales c) -virinae d) -virus e) -virusdae Answer: a
3) The family classification scheme for DNA bacteriophages is not very useful for describing the evolutionary relationships between these viruses. What is the best explanation for this? a) DNA bacteriophages can infect more than one host species. b) DNA bacteriophages have a wide variety of virion structures. c) The viral genomes are genetic mosaics due to recombination. d) There are too many bacteriophages to classify into families. e) These viruses do not have an evolutionary relationship to each other. Answer: c
4) Which of the following is a type of nucleic acid NOT found as the genome of a virus that can infect vertebrates? a) ssDNA b) dsDNA
c) ssRNA d) dsRNA e) All of the above are found. Answer: e
5) Most viruses that infect plants have the following type of genome? a) ssDNA, positive sense b) ssDNA, negative sense c) ssRNA, positive sense d) ssRNA, negative sense e) None of the above. Answer: c
6) What is a possible explanation for why ssDNA viruses have genomes less that 10kb in size? a) ssDNA is not as physically stable as dsDNA. b) ssDNA is not transcribed by host cells. c) ssDNA can form hairpin structures because of base-pairing. d) Larger pieces of ssDNA can not be replicated. e) Larger pieces of ssDNA can not easily enter the host cell. Answer: a
7) An interesting observation is that many highly pathogenic and deadly human viruses have the following type of genome? a) ssDNA, positive sense b) ssDNA, negative sense c) ssRNA, positive sense d) ssRNA, negative sense e) dsRNA Answer: d
8) Which of the following virus families have the ability to synthesize reverse transcriptase? a) Retroviruses b) Caulimoviruses c) Hepadnaviruses d) None of the above are correct. e) All of the above are correct.
Answer: e
9) What distinguishes a satellite virus from a satellite nucleic acid? a) A satellite virus encodes its own capsid protein while a satellite nucleic acid does not. b) A satellite virus packages its own replication protein while a satellite nucleic acid does not. c) A satellite virus requires a helper virus while a satellite nucleic acid does not. d) Genomes of satellite viruses are smaller than those of satellite nucleic acids. e) Satellite viruses do not encode any proteins while satellite nucleic acids do. Answer: a
10) What is a ribozyme? a) A molecule of RNA that is independently capable of replicating without cellular enzymes. b) A molecule of RNA that codes for an enzyme. c) Another name for a small infectious molecule of RNA d) A virus that uses a small piece of RNA as its genome. e) A molecule of RNA that can carry out an enzymatic process. Answer: e
11) According to the RNA World hypothesis, which of the following subcellular entities may have evolved first? a) Retroviruses b) RNA Viruses c) Viroids d) DNA Viruses e) Bacteriophages Answer: c
12) According to the RNA World hypothesis, which of the following enzymes may have evolved first? a) DNA-dependent RNA polymerase b) DNA-dependent DNA polymerase c) RNA-dependent RNA polymerase d) RNA-dependent DNA polymerase e) self-replicating RNAs Answer: e
13) Which of the following virus families contains viruses with the longest ssRNA genomes? a) Picornaviruses b) Coronaviruses c) Flaviviruses d) Togaviruses e) Bromoviruses Answer: b
14) What is approximately the largest size of a double-stranded DNA genome of a virus that infect vertebrates? a) 25 kbp. b) 50 kbp c) 100 kbp d) 300 kbp e) 500 kbp Answer: d
15) Almost all of the viruses with positive-strand RNA genomes and enveloped virions infect which group of hosts? a) Bacteria. b) Vertebrates c) Plants d) Fungi e) Algae. Answer: b
16) Which of the following may be a factor in explaining why viral ssRNA genomes are not usually as long as the dsDNA genomes? a) It is much more difficult to package a large ssRNA genome into a capsid. b) Long ssRNA molecules form too many secondary structures that inhibit replication. c) Long RNA genomes are difficult to translate. d) Long RNA genomes are difficult to transcribe. e) Long pieces of RNA are easily broken by mechanical damage. Answer: e
17) The advantage of using a helical instead of an icosahedral nucleocapsid to package a ssRNA genome is….. a) it is more efficient to envelope a helical nucleocapsid than an icosahedral capsid. b) it is easier to produce a helical nucleocapsid than an icosahedral capsid. c) it better protects the genome from degradation inside the cell. d) it requires a smaller protein to build than an icosahedral capsid. e) it requires fewer copies of the nucleocapsid protein than an icosahedral capsid. Answer: c
18) There are a number of small DNA viruses that are highly dependent on their host cells for transcription and replication enzymes. Which of the following could explain the evolutionary origins of these viruses? a) They originated from fragments of the genomes of larger more independent viruses. b) They originated from intracellular plasmids found in bacteria. c) They originated from the genomes of intracellular organelles, such as mitochondria. d) They originated from fragments of cellular DNA that broke away from the cell genome. e) All of the above could be correct. Answer: d
19) The RNA World hypothesis is supported by the observation that: a) there are viruses that still use RNA as their genomic nucleic acid. b) some viruses can covert RNA to DNA. c) some RNA molecules have enzymatic activity. d) some viruses encode RNA-dependent RNA polymerases. e) All of the above support the RNA World hypothesis. Answer:
20) Which of the following characteristics are NOT one of the most important criterion used to classify viruses into families? a) topology of genome (linear or circular) b) strandedness of genome (double or single stranded) c) type of nucleic acid used in genome (DNA or RNA) d) structure of virion e) species of host infected Answer: e
Question Type: True/False
21) There are several types of viruses with enveloped virions that can infect plants. Answer: False
22) Retroviruses are the only virus family known to package two copies of its genome. Answer: True.
23) Viroids do not require a helper virus in order to replicate and cause disease. Answer: True
Question type: Essay
24) Why is the type of disease caused not the best criteria to use when classifying a virus? Answer: The disease caused by a specific virus is not usually related to the evolutionary history of that virus. Viruses with very different types of genomes, virion structures, and replication pathways can cause the same type of disease. For example, there are at least 5 different viruses that cause a form of hepatitis in humans and these viruses are in 5 different families. Families, which are based on genome and virion structure, represent evolutionary relationships between viruses.
25) Mimivirus, which infects an amoeba, is the largest known dsDNA virus and has a genome larger than some free living bacteria and archae. Even though it encodes many of its own enzymes and even tRNAs, it still does not produce its own ribosomes. Describe the possible evolutionary origin of such a large and complex viruses. Answer: Mimiviruses, along with poxviruses, are thought to have possibly once been independently replicating cells that lost the ability to make their own ribosomes and took on an intracellular parasitic life style. These viruses are capable of synthesizing and processing their mRNAs using mechanisms very similar to those used by the host cell. Another hypothesis is that they may have been precursors to the eukaryotic cell nucleus by at one point becoming incorporated into a prokaryotic cell.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 04
Question type: Multiple Choice 1) Before the viral genome can be transcribed or replicated in a new host cell it must…. a) be trimmed by cellular nucleases. b) be transported through the receptor mediated endocytosis pathway. c) be processed through the cellular exocytosis pathway. d) enter the host cell nucleus and be bound by cellular histone proteins. e) be uncoated in the appropriate compartment of the correct cell type. Answer: e
2) Unenveloped viruses must get their genome past the hydrophobic cell membrane. Some accomplish this by doing which of the following? a) They cause the plasma membrane to lyse. b) They insert viral proteins into a vesicle membrane. c) They inject their genome into the nucleus via the nuclear pore complex d) They create a pore through the membrane and extrude the genome directly into the cytoplasm e) They create a clatherin coated pit during entry Answer: d
3) Because of the rigid plant cell wall, the entry of plant viruses is difficult. Which of the following is a description of how plant viruses move between individual cells within in a whole plant? a) They move between cells using plasmodesmata. b) They cause the formation of syncytia. c) They use the receptor mediated endocytosis pathway. d) They rely on insect vectors to transfer virions between the cells in a single host. e) They produce movement proteins that can create holes in the plant cell wall, allowing movement of the virions between cells. Answer: a
4) Which of the following is the best description of a syncytia? a) A cellular structure that viruses us to move within a host cell.
b) A fusion of two cells causes by viral envelope glycoproteins. c) A structure between two plant cells that viruses can use for cell to cell movement. d) A vesicle involved in the receptor mediated endocytosis pathway. e) A protein that is involved in the transport of proteins into the nucleus. Answer: b
5) Orthymyxoviruses and paramyxoviruses both bind to which receptor on the surface of which host cells? a) an immunoglobulin family receptor protein b) the CD4 protein c) the carbohydrate sialic acid d) the neuraminidase enzyme e) a multiple membrane spanning transport protein Answer: c
6) Which of the following is an example of a virus that requires two different host cell receptors to complete its entry into the host cell? a) HIV-1 b) Adenovirus c) Polio (picornavirus) d) Influenza virus (orthomyxovirus) e) Both HIV an Adenovirus require two cell receptors for entry. Answer: e
7) Which of the following organelles is used as a sorting and recycling station in the receptor mediated endocytosis pathway? a) Early endosome. b) Clatherin-coated vesicle. c) Lysosome. d) Golgi apparatus. e) Caveolae Answer: a
8) Most viruses must exit the endosome before it fuses with a lysosome. Why? a) Their envelope will not fuse easily with the lysosomal membrane. b) To avoid the very low pH in the lysosome, which causes destructive conformational changes.
c) To avoid being degraded by lysosomal proteases and nucleases. d) To enhance their movement towards the nucleus of the cell. e) The pH of the lysosome is too high to induce membrane fusion. Answer: c
9) Which of the following is an accurate description of cavelolae? a) Small, flask-shaped invaginations of the plasma membrane enriched in cholesterol. b) Vesicles surrounded by a cage of clatherin proteins. c) Regions of the plasma membrane rich in cell signaling molecules. d) A cytoskeletal network that is involved in transport of vesicles to the nucleus. e) A cellular motor protein that is involved in intracellular transport. Answer: a 10) The major different between class I fusion proteins and class II fusion proteins is that …. a) class I protein mediate fusion at the plasma membrane and class II protein mediate fusion with the endosome membranes. b) only class I proteins contain fusion peptides. c) only class II proteins have a transmembrane domain. d) only class I proteins undergo large conformation changes within the protein during entry. e) class I proteins are found in unenveloped virus particles while class II proteins are found in enveloped particles. Answer: d
11) Adenoviruses use which of the following entry mechanisms? a) The fibers on the virion can penetrate the endosome membrane can cause it to lyse open. b) An interaction between the penton base of the virus and the cellular integrin proteins causes the endosome membrane to lyse open c) The capsid forms a pore through the cell membrane and extrudes the genome into the cytoplasm d) The viral envelope fuses at the plasma membrane after binding to the host integrin protein. e) The viral envelope fuses with the nuclear membrane after binding to the nuclear pore complex. Answer: b
12) Inhibition of the M2 protein of influenza with the drug amantadine will block which step of virus entry?
a) fusion of the viral envelope with the endosome membrane. b) movement of the RNA genome segments through the nuclear pore c) the conformational change that the HA proteins exhibit in response to the drop in pH d) binding to sialic acid on the surface of the host cell e) unpacking of the viral RNA genome segments from the virion Answer: e
13) Why would some viruses have the enzyme neuraminidase, which can cleave their receptor sialic acid from membranes, in their envelopes? a) It removes sialic acid from the viral envelope so that it doesn’t interfere with binding to the next host cell. b) It allows virions to mature their envelope proteins so that they can attach to the next host cell. c) It prevents the virions from attaching to dead cells, which would not lead to a productive infection. d) It removes sialic acid from the host cell membranes, which exposes their high affinity protein receptor. e) It allows the released virus particles to move more easily through the extracellular matrix.
14) Many large DNA viruses use which of the following cellular components to get their nucleocapsid near to the host cell nucleus a) intermediate filaments b) nuclear pore complex c) actin filaments d) microtubules e) importins Answer: d
15) What mechanism do most retroviruses, but not HIV, use to get their genome into the host cell nucleus? a) They actively inject their genome into the nucleus through the nuclear pore complex. b) These viruses do not need to enter the nucleus to replicate. c) They attach their genome to importin proteins which carry them into the nucleus. d) They wait until the cell enters mitosis and the nuclear envelope breaks down. e) The genome is bound to viral proteins that contain nuclear localization signals that move the genome through the nuclear pore complex. Answer: d
16) Which of the following describes the function of dynein?
a) It is a protein involved in importing cargo into the nucleus through the nuclear pore complex. b) It is a motor protein that moves along microtubules towards the nucleus. c) It is a motor protein that moves along microtubules towards the cell periphery. d) It is a cell structure used to pass virus particles directly between host cells. e) It a cellular membrane protein used as a cell receptor by many viruses.
Answer: b
17) Which of the following statements is a good explanation for the observation that many different rhinovirus strains can all use the same host cell receptor? a) The receptor binding site is buried at the base of a narrow canyon on the viral capsid which is inaccessible to antibody proteins. b) The recptor binding site is the most exposed area of the capsid which is highly accessible to antibody proteins. c) The amino acid sequence of the canyon region of the capsid is highly variable. d) The amino acid sequence on the antibody exposed surfaces of the capsid is highly variable. e) The amino acid sequence on the exposed areas of the capsid are highly conserved in each strain. Answer: a
18) A soluble form of the CD4 protein was once investigated as a treatment for HIV infection. How would this protein work to block infection. a) It would raise the pH of the endosome and prevent activation of the fusion protein. b) It would bind to the cell membrane and prevent fusion of the HIV virion with the plasma membrane. c) It would interact with the host cell receptor and prevent binding by the virion glycoproetin. d) It would interact with the HIV envelope glycoprotein and block its interaction with the host cell receptor. e) It would inhibit entry of the viral genome into the cell nucleus. Answer: c
19) As part of an experiment, you take a solution of purified influenza virus particles and lower the pH of the solution to 5.5. You then add the virus to a culture of the appropriate host cell. What do you think would happen? a) The HA protein would become inactivated and the virus would not be able to enter the host cell. b) The viral genome would be degraded and the virus would not be able to start the infection. c) The HA protein would be able to bind more tightly to the host cell receptors.
d) The cell would not be able to take up the virus particles into clatherin coated pits. e) The virus particles would not be able to be transported into the nucleus. Answer: a
Question Type: True/False
20) The interaction between the viral particle and the host cell receptor is a major determinant of the species specificity of viral infections. Answer: True
21) Most DNA viruses replicate in the cytoplasm of the host cell, since the ribosomes they need to translate their mRNAs are located in this cellular compartment. Answer: False
22) It would be correct to say that in a topological sense the nucleocapsid of an enveloped virion has never left the cytoplasm of a host cell. Answer: True
23) The diameter of the opening in the nuclear pore complex is much too narrow to allow passage of any virus particles directly into the nucleus. Answer: False
Question type: Essay
24) Enveloped viral particles require activation energy in order to penetrate the host cell. Describe the two events that these viruses can use to provide this activation energy. Answer: Some enveloped viruses use the interaction between the host cell receptor and an envelope glycoprotein, which induces a conformational change in the viral glycoprotein and provides the necessary energy for fusion. Other viruses require the drop in pH that occurs in endosomes, which causes conformation changes in the viral glycoproteins and provides energy for membrane fusion.
25) Describe what a fusion peptide is and how it is involved in mediating membrane fusion between the viral envelope and the cell membrane?
Answer: A fusion peptide is a hydrophobic 10-12 amino acid region at the N-terminus of the transmembrane subunit of an viral envelope glycoprotein. During entry of an enveloped virus, the viral glycoprotein is activated by either binding to the host cell receptor or the drop in pH in the endosome. This activation causes a conformational changes or rearrangement in the glycoprotein and exposes the fusion peptide. This peptide is then inserted into the host cell membrane and mediates fusion of the viral envelope with the host membrane.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 05
1) Which of the following structures found on E. coli cells is required for infection with a ssRNA phage? a) Cell wall b) Lipopolysaccharide c) F-pili d) Cell surface receptor e) All of the above are required. Answer: c
2) The discovery of the ssRNA phages was useful to scientists working on which of the following processes: a) Structure of ribosomal RNA b) Translation of messenger RNA c) Structure of proteins d) Transcription of messenger RNA e) Replication of DNA Answer: b
3) Why are ssRNA phages used as an index organism to detect the presence of pathogenic enteroviruses in the sewage treatment process? a) The RNA phage are smaller than the pathogenic viruses. b) The RNA phage are easier to inactivate than the pathogenic viruses. c) The RNA phage are more stable than the pathogenic viruses. d) The RNA phage are easier to quantify using a plaque assay than the pathogenic viruses. e) The RNA phage are easier to see with an electron microscope than the pathogenic viruses Answer: d
4) Translational readthrough occasionally occurs in the coat protein gene of the ssRNA phage Q. Which of the following describes this process? a) The stop codon (UGA) is read as a tryptophan codon (UGG). b) The RNA-dependent RNA polymerase reads into the next gene.
c) The RNA-dependent RNA polymerase inserts an extra base in this gene. d) The ribosome shifts back one base and reads a different reading frame. e) The ribosome shifts forward one base and reads a different reading frame. Answer: a
5) How is the structure of an RNA phage virion different from the structure of the virion of many dsDNA phages? a) They have much shorter tails than the DNA phages. b) The heads do not use icosahedral symmetry. c) The icosahedral head has a very large triangulation number. d) They are solely composed of a helical nucleocapsid. e) They lack the tail structure used to inject the genome into the host cell. Answer: e
6) Which of the following proteins in the virions of the ssRNA phages binds to the F-pilus during virus attachment and entry? a) Lysis protein b) Attachment protein c) Coat protein d) Maturation protein e) Replicase protein Answer: d
7) When an RNA phage virion is assembled with either a defective or missing maturation protein, which of the following occurs? a) The viral RNA genome is more sensitive to RNAse degradation. b) The virion is more sensitive to protease degradation. c) The virion is unstable and disassembles easily in the environment. d) The virion is not able to carry out genome replication. e) The tail cannot inject the genome into the host cell. Answer: a
8) Once the RNA genome of Q is released into the host cell, which of the following describes the first step in the viral replication cycle?
a) Translation of the genome by viral ribosomes to produce proteins. b) Translation of the genome by cellular ribosomes to produce proteins. c) Replication of the genome by a viral enzyme. d) Replication of the genome by a cellular enzyme. e) Cleavage of the genome into two fragments. Answer: b
9) The bacteriophage MS2, which has a ssRNA genome, must produce many more copies of the coat protein than of the replicase and lysis proteins. Which of the following genome features controls how much of each protein is produced? a) Translational control sequences at the 3’ end of the genome b) Translational control sequences at the 5’ end of the genome c) Secondary structure of the RNA genome d) The strength of the transcriptional promoters e) The location of the transcriptional terminators Answer: c
10) Which of the following genes from the ssRNA phage MS2 is translated immediately upon entry of the viral genome into the host cell? a) Maturation protein gene b) Lysis protein gene c) Coat protein gene d) Replicase gene e) A1 gene Answer: c
11) In the ssRNA phage MS2, the replicase and lysis proteins are NOT produced immediately upon entry of the viral genome. Which of the following mechanisms is the primary explanation for why this happens? a) The start codons for these genes are buried in a very stable stem-loop structure. b) They have Shine-Dalgarno sequences that do not bind well to the ribosome. c) They both contain non-canonical TTG start codons. d) The genes encoding these proteins are uncoated from the capsid until later. e) The initiator tRNA does not bind well to the start codons of these genes. Answer: a
12) In the ssRNA phage MS2, translation of the lysis protein gene is dependent on which of the following events? a) Replication of the viral genomic RNA. b) Initiation of translation of the replicase gene. c) Binding of the coat protein to the nucleation site on the genome. d) Termination of translation of the coat protein gene. e) Initiation of translation of the maturation gene. Answer: d
13) Site directed mutagenesis of the MS2 genome was carried out to abolish the MJ stem structure that is just upstream of the start codon of the replicase gene. Which of the following describes the result of this experiment? a) The coat protein was unable to bind to the viral genome. b) The maturation protein was unable to bind to the stem-loop. c) The ribosome could no longer bind to the start codon for the replicase gene. d) The replicase protein was unable to bind to the viral genome. e) Translation of replicase gene increased in the absence of coat protein translation. Answer: e
14) What is the function of Host Factor during the replication of the Q RNA genome? a) It delays the folding of the RNA into its final secondary structure. b) It makes the 3’ end of the genome more accessible to the replicase enzyme. c) It adds a non-template A nucleotide to the 5’ end of the minus strand. d) It facilitates binding of the replicase protein to the coat protein start codon. e) It prevents binding of the replicase enzyme to the 5’ end of the genome. Answer: b
15) In the ssRNA phage MS2, binding of the coat protein to which of the following RNA structures acts to initiate packaging of the viral RNA into the capsids. a) The 5’ end of the genome b) The 3’ end of the genome c) The MJ stem loop d) The start codon of the coat protein gene e) The operator stem loop
Answer: e
16) In the ssRNA phage MS2, the replicase protein binds to the start codon of the coat protein gene. Which of the following describes the reason for this binding? a) It prevents replication and translation from occurring simultaneously. b) It initiates synthesis of the minus-strand copy of the genome. c) It enhances binding of the ribosome to the coat protein gene. d) It disrupts the stem-loop structure that prevents replication of the viral genome. e) It exposes the 3’ end of the genome which allows the replicase to begin RNA synthesis. Answer: a
17) The viral polymerase complex from the RNA phage Q contains which of the following host cell proteins? a) Host Factor b) S1 ribosomal protein c) EF-Tu translational factor d) EF-Ts translational factor e) All of the above are part of the complex. Answer: e
18) In the ssRNA phage Q the synthesis of the plus strand RNA genome from the negative strand template does not require the ribosomal S1 protein. Which of the following explains why? a) The minus strand is shorter and takes less time to replicate b) The minus strand lacks the secondary structure that prevents replication. c) There is no competition between binding of the replicase enzyme and the ribosome. d) The replicase enzyme is more processive when copying the minus strand. e) The minus strand has a lower GC content than the plus strand. Answer: c
19) In the ssRNA phage MS2, the maturation protein is only produced after which of the following events occurs? a) The synthesis of the negative strand of the viral genome. b) The synthesis of the positive strand of the viral genome. c) Packaging of the viral genome into new capsids. d) Translation of the coat protein.
e) Folding of the newly synthesized genome into the stable secondary structure. Answer: b
20) The replicase enzyme of the ssRNA phage Q has been used by scientists to do which of the following? a) Synthesize RNA molecules from a DNA template. b) Measure small amounts of target RNA molecules in a sample. c) Measure the levels of pathogenic viruses in drinking water. d) Amplify DNA molecules in a sample. e) Fuse two pieces of RNA together. Answer: b
Question Type: True/False
21) Replication and translation can occur simultaneously on a single molecule of genomic RNA from the ssRNA phage MS2. Answer: False
22) During the replication cycle of the ssRNA phage MS2, the lysis gene can not be translated in the absence of translation of the coat protein gene. Answer: True.
23) Replication of the RNA genome by the replicase enzyme from the phage Q is completely independent of host cell proteins. Answer: False.
24) The translation of the maturation protein from a newly synthesized positive strand genome in the phage MS2 depends on delayed folding of the RNA into its final secondary structure. Answer: True
Question type: Essay
25) The RNA phages do not use a tail assembly to inject their genome through the cell wall of the host cell. How do they get their genome into the host cell? Answer: The RNA phage can only infect male E. coli cells, which contain the F-pilus. The structure of the F-pilus is different than the rest of the host cell and does not contain the thick cell wall. The RNA phage uses the maturation protein to bind to the F-pilus. While the exact mechanism of entry is not known, it is thought that the F-pilus is retracted back into the host cell, bringing the RNA genome along with it.
26) Why must the ssRNA phage, like MS2 and Qb, prevent the viral genome from simultaneously being translated by a ribosome and replicated by the replicase enzyme? Describe the mechanism that these viruses use to prevent this from happening. Answer: Ribosomes translate the RNA genome in the 5’ to 3’ direction while the replicase enzyme moves in the 3’ to 5’ direction. If both of these processes were happening on the same genome at the same time the two complexes would meet and not be able to complete their processes. To avoid this from happening the replicase enzyme can bind to the viral RNA at two internal sites – one of which is the start site for translation of the coat protein. This is also where the ribosome binds to begin translation of the coat protein gene. This competition prevents a single genome from being replicated and translated at the same time.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 06
Question Type: Multiple Choice
1) Which of the following was used to distinguish different bacteriophages before the development of the electron microscope in the 1930’s? a) Western blot b) DNA sequence c) DNA restriction analysis d) X-ray crystallography e) Plaque morphology Answer: e 2) What distinguishes the small bacteriophage X174 from many other bacteriophages? a) The virion has a very large head. b) The virion has a very long tail. c) It has a single-strand DNA genome. d) It has a single-strand RNA genome. e) It has a double-strand RNA genome. Answer: c
3) Which of the following bacteriophages had its entire genome sequenced first? a) MS2 b) X174 c) Lambda phage d) T4 e) T3 Answer: b 4) Several different mRNAs are produced from the X174 genome using which of the following mechanisms? a) Multiple transcription promoters
b) Multiple transcription terminators c) Multiple translation start sites d) Multiple stop codons e) Both a and b are correct Answer: e 5) The phage X174 can tolerate mutations in the non-structural region of its genome more easily than in the structural region of the genome. Which of the following explains why? a) Not all of the proteins coded in this region are packaged into the mature capsid. b) Single-stranded DNA is not as easily mutated as double-stranded DNA. c) Many of the non-structural proteins have more than one function. d) Some of the non-structural proteins are non-essential for virus replication. e) The presence of overlapping reading frames in this region of the genome. Answer: d 6) Which of the following is used as the primary host cell receptor for the phage X174? a) Glucose on lipopolysaccharide b) A membrane protein c) The cell wall d) The F-pili e) The internal membrane Answer: a 7) Entry of the viral genome for X174 appears to occur at which locations on the host cell? a) The surface of the F-pili b) Cell wall adhesion regions c) The base of the flagella d) Regions of high lipopolysaccharide e) All of the above Answer: b
8) Which of the following describes the function of the H protein (pilot protein) in the microviruses? a) It forms the spikes on the capsid.
b) It is the scaffolding protein for assembly. c) It is carries out DNA replication. d) It regulates mRNA transcription. e) It helps the viral DNA enter the host cell. Answer: e
9) Why must the microviruses produce dsDNA before viral genes can be expressed? a) Only dsDNA can be packaged into virions. b) DsDNA is more stable than ssDNA. c) Only dsDNA is a substrate for transcription by the host RNA polymerase. d) Only dsDNA is a substrate for replication by the host DNA polymerase. e) The viral regulatory proteins can only bind to double-stranded DNA. Answer: c
10) Which of the following bacteriophages has a genome composed of ssDNA? a) lambda phage b) X174 c) T7 d) MS2 e) Q Answer: b 11) Which of the following processes was studied by working with the phage X174? a) Transcription of mRNA b) Splicing of mRNA c) Translation of mRNA d) Replication of DNA e) Lysogeny Answer: d 12) Which of the following describes the first step in the replication cycle of the phage X174? a) Conversion of ssDNA into dsDNA. b) Translation of the viral genome into protein. c) Transcription of the viral DNA by the cellular RNA polymerase.
d) Transcription of the viral DNA by the viral RNA polymerase. e) Integration of the viral DNA into the host chromosome. Answer: a 13) Stage I DNA replication in the bacteriophage X174 is carried out entirely by host cell proteins. Why? a) DNA replication is required for penetration of the viral genome into the host cell. b) The bacteriophage X174 does not encode any of its own DNA replication proteins. c) The phage genome has become integrated into the host genome. d) Only the host cell proteins can replicate a ssDNA genome. e) Stage I DNA replication occurs before any viral proteins are expressed. Answer: e 14) Abundant synthesis of the E protein from the bacteriophage X174 would lead to premature lysis of the host cell. Which of the following mechanisms controls the synthesis of the E protein? a) The mRNA is transcribed from a weak promoter. b) The open reading frame has a weak ribosome binding site. c) The secondary structure of the mRNA prevents translation of the E protein. d) The repressor protein prevents transcription of the mRNA. e) There is a strong transcriptional terminator upstream of the E gene. Answer: b 15) The A protein of the phage X174 is required for which of the following processes? a) Synthesis of the double-stranded replicative form DNA. b) Packaging of the viral protein into the newly formed capsids. c) Assembly of the viral capsid. d) Synthesis of the plus-strand DNA via rolling circle replication. e) Entry of the viral DNA into the host cell. Answer: c 16) In the bacteriophage X174, which of the following events occurs at the same time as the ssDNA is packaged into the procapsid? a) Proteolytic maturation of the capsid proteins. b) Removal of the external scaffolding protein D.
c) Removal of the internal scaffolding protein B. d) Addition of the spike proteins to the capsid. e) Synthesis of the second DNA strand. Answer: c
17) When is the external scaffolding protein D removed from the procapsid? a) After lysis of the host cell b) During packaging of the viral DNA into the procapsid. c) When the internal scaffolding protein B is removed from the procapsid. d) Before the viral DNA is package into the procapsid e) During entry into the next host cell Answer: a
18) Which of the following statements is NOT true? a) Both microviruses and gokushoviruses package a ssDNA genome. b) Microviruses use two different scaffolding proteins while gokushoviruses only use one. c) The genomes of the gokushoviruses are much smaller than the microviruses. d) Both microviruses and gokushoviruses infect free living bacterial cells. e) Both microviruses and gokushoviruses package their genomes into small icosahedral capsids. Answer: d
19) How does the E protein cause lysis of the host cell? a) It degrades the cell wall components before cell wall assembly. b) It makes the cell wall more resistant to osmotic pressure. c) It breaks critical bonds in the cell wall components. d) It activates a cellular enzyme that can break down the cell wall. e) It inhibits a cellular protein that synthesizes the cell wall. Answer: e
Question Type: True/False
20) Because gokushoviruses infect bacteria that can parasitize eukaryotic cells, they may have been the evolutionary source for eukaryotic viruses.
Answer: True 21) The bacteriophage X174 has several weak transcriptional terminators which leads to mRNAs with different 5’ ends. Answer: False 22) The scaffolding proteins of the bacteriophage X174 remain as part of the final mature capsid structure. Answer: False.
23) Microviruses are the only known non-satellite viruses requiring two separate scaffolding proteins. Answer: True. 24) The ssDNA phage X174 does not encode DNA binding proteins to regulation gene expression from the viral genome. Answer: True
Question type: Essay 25) Mutations in the internal scaffolding protein B of the ssRNA phage X174 cause abnormally small 9S and 6S particles to form in infected cells. Explain how this provides information about the assembly pathway of this virus. Answer: The 9S particles represent pentamers of the major capsid protein. The 6S particles represent pentamers of the spike protein G. This result suggests that these pentamers are intermediates in the assembly pathway to a complete virion and that the internal scaffolding protein B is required to assemble these intermediates into the final capsid. The function of the B protein is to facilitate interactions between the 9S and 6S intermediates and without a functional internal scaffolding protein B the 9S and 6S intermediates accumulate in the infected cell. 26) The genome of the X174 phage is very compact and contains several overlapping open reading frames. Explain how this can be both an evolutionary advantage and disadvantage for the phage.
Answer: The advantage of using overlapping reading frames is that the phage can code for more proteins with less genome sequence. This supports the concept of genetic economy. It also allows the virus to have a smaller virion to transport the smaller genome. The major disadvantage of overlapping reading frames is that some bases in non-structural region of the genome are part of the coding sequences for two, three, or even four different proteins. Mutating one of these bases will potentially change a codon, and therefore an amino acid, in more than one viral protein.
27) Describe the proteins required for both Stage I DNA and Stage II DNA replication and the role that each plays in the virus replication cycle of the bacteriophage X174. Answer: Stage I DNA replication occurs at the start of the virus replication cycle before any viral proteins have been produced and is therefore carried out completely by host cell proteins (primosome components, SSB, DNA polIII, DNA polI and ligase). It is used to convert plus-strand ssDNA into the double-stranded replicative form DNA via synthesis of the complementary minus-strand. This replicative form DNA is now the template for production of viral mRNAs and production of more plus-strand progeny genomes. Stage II DNA replication is initiated by the viral A protein and requires a few host cell proteins (rep, SSB, and DNA polIII). Stage II replication is used to produce more ssDNA plus-strand genomes which can either be used as templates for Stage I DNA replication or packaged into capsids as progeny genomes.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 07
Question type: Multiple Choice
1) Bacteriophage T7 was isolated from what source? a) Unprocessed waste from a sewage treatment plant b) Commercially available treatment for intestinal infections c) Soil found on a farm d) Water samples taken from a polluted river e) Animal manure. Answer: b
2) What is the size and composition of the T7 bacteriophage genome? a) 4000 nt of ssDNA b) 4000 nt of ssRNA c) 5,000 bp of dsDNA d) 40,000 bp of dsDNA e) 200,000 bp of dsDNA Answer: d
3) What genetic technique helped scientists in the 1970s to map the genes in the genome of bacteriophage T7? a) Restriction enzyme mapping b) DNA sequencing c) Conditional-lethal mutants d) Southern blotting e) Site-directed mutagenesis Answer: c
4) How are the genes in the genome of the bacteriophage T7 arranged in the genome? a) By when they are expressed during the viral replication cycle. b) By their function during the viral replication cycle.
c) By the amount of GC bases they contain. d) By their size, shortest to longest. e) Both a and b are correct.
Answer: e
5) Which part of the T7 virion binds to the lipopolysaccharide molecules on the outer cell membrane of the host cell? a) The vertices of the icosahedral head. b) The tail fibers. c) The portal protein. d) The regions of three-fold symmetry on the icosahedral head. e) The envelope glycoprotein. Answer: b
6) The entry of the genome of the bacteriophage T7 is dependent on which of the following processes? a) Division of the infected host cell. b) Replication of the viral genome by host DNA polymerase. c) Translation of the viral genome by the host ribosomes. d) Transcription of viral genes by the viral RNA polymerase. e) Transcription of viral genes by the host RNA polymerase. Answer: e
7) What is unique about the RNA polymerase encoded by the bacteriophage T7? a) It depends on host cell proteins for its function. b) It is composed of a single polypeptide. c) It is composed of many polypeptides. d) It can transcribe host genes in addition to viral genes. e) It can only transcribe the Class I genes on the T7 genome. Answer: b
8) One of the first proteins produced during the infection cycle of bacteriophage T7 inhibits the cellular enzymes EcoB and EcoK. Why is this important for the phage?
a) This prevents transcription of the cellular genes. b) This allows transcription of the viral genes. c) This prevents the viral proteins from being degraded. d) This prevents the viral genome from being degraded. e) This shuts down host cell genome replication. Answer: d
9) What is interesting about the promoters that direct transcription of the Class II and Class III genes from bacteriophage T7? a) They are very rich in GC basepairs. b) They are much longer and more complex than the host gene promoters. c) They can only be recognized by the viral RNA polymerase. d) They can be recognized by either the host or viral RNA polymerase. e) They are not very highly conserved. Answer: c
10) What is the function of cleavage of the mRNAs from bacteriophage T7 by the host ribonuclease III? a) It processes the transcript into smaller more stable mRNAs. b) It produces a sequence that is recognized by the host cell ribosomes. c) It degrades the viral mRNAs after they have been translated into proteins. d) It removes introns from the viral mRNAs and produces a mature mRNA. e) It produces RNA primers required for viral DNA replication. Answer: a
11) Which of the following enzymes is NOT involved in replication of the bacteriophage T7 genome? a) Single-Strand DNA binding protein b) Lysozyme c) DNA ligase d) RNA polymease e) RNA primase/helicase Answer: b
12) What would be observed in a cell infected with a T7 phage mutated in gene 3 (endonuclease gene). a) No Class II mRNAs. b) No Class III mRNAs. c) Incomplete entry of the viral genome. d) Concatamers of the viral genome. e) Incomplete virus capsids. Answer: d 13) The removal of the RNA primer leaves a gap in the newly synthesized viral genomic DNA. How does the bacteriophage T7 solve this problem? a) It produces concatemers of the viral genome. b) It circularizes the viral genome. c) It uses a special DNA polymerase to fill in the gaps. d) It leaves the RNA as part of the packaged viral genome. e) It uses a protein as a primer instead of RNA. Answer: a
14) What is the role of the viral RNA polymerase in the replication of the bacteriophage T7 genome? a) It binds to the single-stranded DNA and prevents reannealing. b) It helps to unwind the two strands of the viral genome. c) It produces the RNA primer on the leading strand. d) It produces the RNA primer on the lagging strand. e) It can switch from RNA synthesis to DNA synthesis. Answer: c
15) The host cell protein thioredoxin binds to the DNA polymerase of bacteriophage T7 and improves which of the following? a) speed b) accuracy c) processivity d) Both a and b are correct e) Both a and c are correct. Answer: e
16) Holin is a small membrane-specific protein produced by the bacteriophge T7. Which of the following describes the function of this protein? a) It ensures the replication of the entire T7 genome. b) It helps the T7 phage particles lyse the host cell. c) It creates the portal in the phage head where the viral genome is packaged. d) It degrades the host cell wall during entry of the viral genome. e) It cleaves the viral genome during packaging. Answer: b
17) The bacteriophage T7 produces a protein with an array of acidic amino acids that acts as a DNA mimic. Which of the following describes the function of this protein? a) It competitively inhibits the host restriction endonucleases. b) It binds to the viral genome and helps to package it into the head. c) It acts as a primer for DNA replication. d) It assists the entry of the viral genome into the host cell. e) It binds to the host cell RNA polymerase and directs it to transcribe viral genes. Answer: a 18) Infection of a F+ cell with the bacteriophage T7 leads to an abortive infection. Which of the following steps in the replication cycle is where the cycle is halted? a) Entry of the viral DNA into the host cell. b) Transcription of the Class I genes. c) Transcription of the Class II and III genes. d) Translation of the Class II and III mRNAs. e) Replication of the viral genome. Answer: d 19) The RNA polymerase from bacteriophage T7 has become a useful tool in molecular biology. Which of the following describes how it can be used? a) To express high levels of a foreign protein in a bacterial cell. b) To measure small amounts of target RNA molecules in a sample. c) To measure the levels of pathogenic viruses in drinking water. d) To amplify DNA molecules in a sample. e) To fuse two pieces of RNA together.
Answer: a Question Type: True/False 20) The genome of the bacteriophage T7 has circularly permuted ends. Answer: False. 21) Incubation of bacterial cells infected with the phage T7 with an inhibitor of protein synthesis will allow only the Class I mRNAs to be produced. Answer: True. 22) The bacteriophage T7 is dependent on the host cell DNA polymerase for replication of the viral DNA. Answer: False. 23) Bacteriophage T7 expresses an exonuclease which degrades the host cell DNA in order to provide nucleotides for viral DNA replication. Answer: True. 24) The promoters of the Class II and Class III genes in the bacteriophage T7 have the same -10 and -35 sequences as the promoters for host cell genes. Answer: False Question type: Essay 25) The removal of the RNA primer leaves a gap in the newly synthesized viral genomic DNA. How does the bacteriophage T7 solve this problem? Answer: The bacteriophage forms large linear DNA concatemers via a terminal repeat of about 150bp. Recombination between these terminal repeats may create the concatemers which leads to a single copy of the repeat between each viral genome in the concatemer. Processing of the genome concatemers depends on several viral proteins including the gene 3 endonuclease and the T7 RNA polymerase. When the T7 RNA polymerase transcribes the Class III genes on the
concatemers it reads through a weak terminator into the next genome copy. When the RNA polymerase pauses at a specific sequence in terminal repeat it forms a special DNA structure which recruits the proteins that process the ends of the viral genome. This allows single genome copies to be produced and packaged into preformed virion heads. 26) How does the bacteriophage T7 inhibit the host cell RNA polymerase and why is this advantageous to the virus? Answer: Bacteriophage T7 produces the gp0.7 protein from one of the Class I genes that can add a phosphate group to a specific tyrosine amino acid on one of the subunits of the host RNA polymerase. This inhibits the transcription of host cell genes, which allows all of the energy, nucleotides, and amino acids to be shunted to viral protein synthesis and not used to make cellular proteins. This also shuts down expression of the Class I genes, which are transcribed by the host RNA polymerase. However, since these genes have already been expressed in the virus life cycle, it does not hurt the replication of the phage. Transcription of the Class II and Class III genes are solely dependent on the viral RNA polymerase.
27) Describe how the RNA polymerase from bacteriophage T7, along with specific DNA sequences taken from the late T7 genes, can be used to produce high levels of a foreign protein in a bacterial cell. Answer: The T7 RNA polymerase specifically recognizes the promoter sequences from the late T7 genes. Expression plasmids exist that contain a late T7 promoter sequence along with the efficient ribosome binding site from the T7 late genes. The open reading frame of the desired protein can then be inserted downstream from these sequences. Then the resulting plasmid is inserted into host E. coli cells that contains the gene for the T7 RNA polymerase behind the IPTG inducible lac promoter. These E. coli cells can then be cultured without expressing the foreign protein, in case it is toxic to the host cell. When the cells reach a high enough density, they are treated with IPTG. This turns on expression of the T7 RNA polymerase which then transcribes the gene for the foreign protein, causing high levels of the protein to be expressed.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 08
Question type: Multiple Choice
1) Which of the following terms describes a bacteriophage that can either produce new virus particles or exist as a repressed integrated viral genome? a) Lysogenic b) Temperate c) Prophage d) Lytic e) Lysogen Answer: b
2) Which of the following terms describes a bacterial cell that has a repressed copy of a bacteriophage genome integrated into its chromosome? a) Lysogenic b) Temperate c) Prophage d) Lytic e) Lysogen
Answer: e 3) What is the function of the cos sites in the phage genome? a) They function as the origin of DNA replication b) They bind to the cI repressor c) They bind to the N antiterminator d) They circularize the genome e) They are the sites of integration with the host chromosome Answer: d 4) Which of the following statements about the transcripts from phage that terminate at the transcriptional terminators tL1 and tR1 is FALSE?
a) They are expressed at immediate-early times. b) The encode the proteins N and cro. c) They are expressed first in the transcriptional program. d) They contain NUT sequences. e) They can be antiterminated by the Q protein. Answer: e 5) The N and Q proteins from phage both have which of the following functions? a) Recombination of the viral genome b) Repressors of transcription initiation c) Activators of transcription initiation d) Repressors of transcription termination e) Unwinding of the viral genome Answer: d 6) The Q protein from phage activates expression of head and tail genes using which of the following mechanisms? a) It causes anti-termination at the transcriptional terminator tL1 b) It activates transcription from PR’. c) It causes anti-termination at the transcriptional terminator tR’. d) It inhibits activity of the N protein. e) It inhibits the activity of the cI repressor. Answer: c 7) The cI repressor of the phage binds to several locations on the viral genome. Which of the following is the term that describes these binding sites? a) Operators b) Cos sites c) Promoters d) Terminators e) AttP sites Answer: a
8) In order to transcribe the late structure genes found on the left hand side of the phage genome, which of the following must occur? a) The phage genome must be integrated into the host chromosome. b) The phage genome must be linear. c) The phage genome must be circularized d) The phage genome must be replicated into many copies. e) The phage genome must be ligated into concatmers. Answer: c 9) How does the binding of the phage cI repressor to OR1 and OR2 block transcription from PR? a) It prevents the RNA polymerase from transcribing down the gene. b) It blocks binding of the RNA polymerase to the -10 and -35 sites on the promoter. c) It terminates transcription at an earlier terminator. d) It leads to the degradation of the RNA produced from PR. e) It activates a promoter that produces an antisense transcript. Answer: b 10) Why is binding of the phage cI repressor to OR1 and OR2 necessary for transcription from PRM? a) It facilitates binding of the RNA polymerase to PRM. b) It blocks transcription from PL which competes for the RNA polymerase. c) It prevents transcription of an antisense RNA. d) It stabilizes the transcript from PRM. e) It allows read through a transcriptional terminator. Answer: a 11) The phage will lysogenize the host cell if which of the following proteins is produced in sufficient levels during infection? a) N b) CI c) Q d) Integrase e) Cro Answer: b
12) When bacterial cells that have an integrated prophage in their genomes are treated with UV light, it leads to cleavage of the cI repressor. Which of the following host cell proteins activates the autoprotease activity of the cI repressor? a) DNA excision repair enzyme b) LexA c) RecA d) GroES e) Exonuclease III Answer: c 13) How does the cro protein from phage help to establish a lytic infection? a) It inhibits the integrase enzyme. b) It activates the excision enzyme. c) It binds to OL1 and blocks transcription from PL d) It binds to OR1 and blocks transcription from PR e) It binds to OR3 and blocks transcription from PRM. Answer: e 14) What is the function of the cII protein from phage? a) It represses transcription from PR. b) It activates transcription from PRM. c) It activates transcription from PRE. d) It inhibits cellular proteases that cleave the cI repressor. e) It antiterminates transcription at tL1. Answer: c 15) What is the function of the Int protein from phage? a) It mediates site specific recombination between attP and attB. b) It ligates the ends of the viral chromosome. c) It binds to multiple sites within the origin or replication. d) It recruits the cellular DNA replication enzymes to the viral genome. e) It acts as a scaffolding protein for virion assembly. Answer: a
16) Retroregulation limits expression of the Int protein during lytic growth. The mechanism of retroregulation involves which of the following? a) Binding of an antisense RNA that inhibits translation of the int mRNA. b) Degradation of the Int protein by cellular proteases. c) Inhibition of transcription from Pint. d) Specific degradation of the int mRNA by Exonuclease III. e) Termination of transcription upstream of the int coding region. Answer: d 17) DNA replication of the genome of the phage takes place through a rolling circle mechanism. Which of the following describes the products of this type of DNA replication? a) Individual circular dsDNA genomes. b) Individual linear dsDNA genomes. c) Concatemers of dsDNA genomes. d) Individual circular ssDNA genomes. e) Individual linear ssDNA genomes. Answer: c
18) Which of the following describes the function of the H protein, sometimes known as the tape measure, during assembly of the virion? a) It controls the amount of viral DNA packaged into the head. b) It controls the length of the tail. c) It controls the size of the head. d) It cleaves the viral DNA and produces the cos sites. e) It attaches the tail to the head. Answer: b 19) The cellular complexes GroES and GroEL are involved in the assembly of the phage virion. Which of the following describes their function during assembly? a) They package the viral genome into the head. b) They act as chaperones in the formation of the portal vertex. c) They act as a scaffold for the assembly of the tail. d) They acts as a scaffold for the assembly of the head. e) The cleave concatemers of the viral genome during assembly.
Answer: b 20) The R and S proteins from phage can form complexes called holin and spanin. Which of the following describes the process that these complexes participate in? a) Assembly of the virion. b) Replication of the viral genome. c) Packaging of the viral genome into the head d) Excision of the viral genome from the host chromosome. e) Lysis of the host cell to release virions. Answer: e
Question Type: True/False 21) The cIII protein from phage inhibits cellular proteases that would degrade the cII protein. Answer: True
22) CRISPR elements are places in the bacterial chromosome where phage genomes integrate during lysogeny. Answer: False 23) When phage infects E. coli cells that are metabolically active and in the logarithmic phase of growth, the virus will go lytic in most of the cells that it infects. Answer: True 24) When there are high levels of the cI repressor of phage then both PR and PRM are at maximal levels of transcription. Answer: False 25) The phage immediate-early proteins N and cro are expressed only when the virus lysogenizes the host cell. Answer: False
26) If a phage lysogen were superinfected with the same strain of phage, the cI repressor would inhibit lytic replication from the incoming phage genome. Answer: True
Question type: Essay 27) Explain how the binding affinity of the phage cI repressor to the three rightward operators (OR1, OR2, OR3) controls transcription from both PR and PRM? Answer: The phage cI repressor binds to the three operators with the following affinities: OR1 > OR2 = OR3. Low levels of cI bind to OR1 first, which blocks access of the RNA polymerase to PR and inhibits transcription from PR. As higher levels of cI build up, the cI repressor binds to OR2, which is facilitated by cooperativity between the cI dimers. The binding to OR2 activates the weak PRM promoter by facilitating binding of the RNA polymerase. As very high levels of cI build up, the repressor finally binds to OR3, which blocks transcription from PRM and serves as an autoregulatory mechanism to maintain constant levels of cI in the lysogenic cell. 28) Explain the mechanisms by which treatment of a phage lysogen with UV light leads to the induction of the prophage and the production of virus particles. Answer:Treatment of host cells with UV light induces the SOS gene pathway, which serves to repair damage in the cellular genome. The expression of the SOS genes is normally inhibited by the cellular LexA repressor. Induction of the SOS genes requires activation of the “co-protease” activity of the RecA protein, which enhances the autoprotease activity of the LexA repressor. The LexA repressor cleaves itself into two domains, which inactivates is repressor activity and allows the SOS genes to be expressed. In addition to activating the autoprotease activity of the LexA protein, RecA can also activate a similar activity in the repressor cI. This leads to the cleavage of cI into two domains. Inactivation of cI removes the repressor from the operators and activates the expression from PR and PL, which allows the lytic growth program to begin.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 09
Question type: Multiple Choice
1) Archaea are singled-celled microorganisms that share which of the following characteristics with eukaryotic cells? a) Initiate translation of proteins with a methionine, not N-formyl-methionine. b) Contain histone-like proteins to condense their genomic DNA. c) Use a TATA-binding protein to initiate transcription of their genes. d) Have similar enzymes involved in DNA replication . e) All of the above are correct. Answer: e
2) What information was used to identify the three domains of life? a) Sequence of the 16S ribosomal RNA b) Sequence of the mitochondrial genome c) Sequence of the cytochrome c gene d) Chemical structure of the cell wall e) Chemical structure of phospholipids Answer: a
3) Which of the following terms specifically describes archaeal organisms that can grow above 80oC? a) Thermophile b) Hyperhalophile c) Hyperthermophile d) Methanogen e) Extremophile Answer: c
4) Viruses that infect archaeal cells have been isolated from all of the following environments EXCEPT:
a) Hot springs with temperatures over 80oC b) Environments with a pH of 0 c) Solfataric fields that emit sulfur gases d) The surface of the moon e) Environments with salt concentrations over 1.5M Answer: d
5) The filaments attached to one end of the Sulfolobus spindle-shaped virus 1 are thought to be involved in which of the following processes? a) Degradation of the host cell wall b) Attachment to the surface of host cells c) Injection of the genome into the host cell d) Movement of the virus particle through the environment e) Maintaining the structure of the virion Answer: b 6) The archaea virus SSV-1, which infects a host organism that lives at 80oC, has a positively supercoiled genome. What is the advantage of this? a) It reduces local unwinding of the DNA. b) It makes it easier for DNA to be unwound during replication. c) It makes it easier for DNA to be unwound during transcription. d) It prevents tangling of the genomic DNA. e) It allows histone proteins to condense the genome. Answer: a
7) Into which of the following genes in the host cell genome does the archaea virus SSV-1 integrate its genome? a) DNA polymerase b) RNA polymerase c) Transfer RNA d) Translation initiation factor e) Ribosomal RNA Answer: c
8) Which of the following techniques can be used to induced an integrated copy of the archaea virus SSV-1 to begin expressing viral genes? a) Exposure of cells to low pH b) Exposure of cells to high salt concentrations c) Superinfection with the same strain of virus d) Growth of cells at lower temperatures e) Exposure of cells to UV light Answer: e
9) Which of the following characteristics is common to many of the viruses that infect archaeal cells and distinguishes them from the phages that infect bacteria. a) They release mature virions without lysing the host cell. b) Their viral genomes are very high in AT basepairs. c) Their viral genomes are linear. d) Their viral genomes are composed of double-stranded RNA. e) Their virions are composed of icosahedral capsids. Answer: a
10) What is the function of the large pyramidal structures that are produced during infection with the archaeal virus SIRV-2, which is a member of the Rudivirus family? a) They are sites of viral gene expression. b) They lyse the host cell and release virions from the cell. c) They are part of the virion assembly complex. d) They are structures involved in viral DNA replication e) They are involved in inhibiting host cell functions. Answer: b
11) What is unusual about the virion of the Acidianus two-tailed virus? a) The virion contains two tails, one at each end of a lemon-shaped virion. b) The two tails can be of different lengths. c) The only requirement for tail production is temperatures above 75oC. d) The tails are elongated after the virion leaves the host cell. e) All of the above are correct. Answer: e
12) Some of the viruses that infect archaeal cells have linear dsDNA genomes with covalently closed ends. What is a major advantage of this feature? a) It makes the genome more stable under low pH conditions. b) It allows the genome to be more easily packaged into the virion c) It allows the genome to be more easily integrated into the host cell genome. d) It allows the genome to use a self-priming mechanism for DNA replication. e) All of the above are correct. Answer: d
13) Which of the following can be found at the ends of the genome of a virus that infects archaeal cells? a) Covalently bound protein b) Inverted terminal repeats c) Telomeric-like repeat sequences d) Covalently closed ends e) All of the above can be found. Answer: e
14) Viruses that infect archaeal cells have been observed to have all of the following virion shapes EXCEPT: a) Bottle shaped with a wide and a narrow end b) Spherical c) Brick shaped d) Filamentous e) Lemon-shaped Answer: c
15) Which of the following is a description of an IS element? a) A short transposable DNA sequence b) A region of DNA where transcription begins c) A telomeric-like sequence at the ends of the DNA d) A region of the host chromosome where the viral DNA integrates e) A region of DNA that acts as an origin or replication Answer: a
16) Even though the two archaeal viruses HHPV-1 and HRPV-1 are clearly related to each other, based on genome and virion structures, they have one major difference. Which of the following describes this difference? a) One can undergo lysogeny while the other can only carry out lytic infection. b) One infects hyperthermophilic hosts while the other infects a hyperhalophilic host. c) One packages a dsDNA genome while the other packages a ssDNA genome. d) One appears to encode an obvious DNA polymerase while the other does not. e) One has a linear genome while the other has a circular genome. Answer: c
17) Even though many of the viruses that infect archaeal cells do not kill their host, they often do which of the following? a) Shut down host protein synthesis b) Increase the cell doubling time c) Decrease the cell doubling time d) Shut down genome replication e) Inhibit synthesis of host cell membranes Answer: b
18) The extrusion of the tails on the Acidianus two-tailed virus requires which of the following? a) Temperatures above 75oC b) An exogenous source of energy c) Cofactors from the host cell d) Cofactors from the virus e) High salt concentration Answer: a
Question Type: True/False 19) Archaea cells contain a nucleus like eukaryotic cells. Answer: False 20) Most archaea viruses resemble bacteriophages with an icosahedral head and a helical tail.
Answer: False. 21) Rudiviruses, a family of archaea viruses, are different from most other archaea viruses in that they lyse the host cell to release mature virions. Answer: True 22) Infection of the archaeal cell Acidianus with the virus ATV at the suboptimal temperature of 75oC leads to a productive lytic infection rather than lysogeny. Answer: True 23) Some of the viruses that infect host cells in the euryarchaeota phyla have similar virion structures as the head-tail viruses in the Myoviridae and Siphoviridae families. Answer: True Question Type: Essay 24) Many of the viruses that infect archaeal cells primarily carry out a lysogenic infection. Even if they do enter a productive infectious cycle, they can release new virions without killing the host cell. What might be the evolutionary advantages of these lifestyle features? Answer: The host cells for many of these archaeal viruses live in very extreme environments that have either high temperatures, high salt concentrations or very low pH. The populations of host cells in these environments may not be large and finding another host cell to infect may be difficult. In addition, the virus particles themselves may not be stable for very long outside of the host cell. By entering a lysogenic state and integrating the viral genome into the host cell chromosome, these viruses are automatically passed down from cell to cell through cell division. If the host cell becomes stressed by a change in environmental conditions, then the virus can briefly enter a lytic state and release new virions to find new host cells. Being able to release virions while not killing the host cell allows the original viral genome to be maintained in its current host. 25) In comparing the genomes of the viruses that infect archaeal cells, very few of the viral genomes have genes encoding an identifiable DNA polymerase. Give two possibilities that explain this observation.
Answer: One possibility is that these viruses do not encode their own DNA polymerase but instead use the DNA polymerases of their host cells to carry out the replication of their genomes. Instead of encoding a polymerase, they would encode unique viral protein that would just direct the host cell proteins to replicate the viral genome. This is similar to the mechanisms used by the smaller DNA viruses that infect eukaryotic cells, like parvoviruses, polyomaviruses and papillomaviruses. The second possibility is that they encode DNA polymerases that do not resemble known DNA polymerases based on amino acid sequence. This would make the function of the genes encoding these enzymes impossible to identify as DNA polymerases.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 10
Question type: Multiple Choice
1) All of the following describe a method of introducing Cucumber Mosaic Virus into a healthy plant EXCEPT…. a) Grafting an infected branch b) Insect feeding c) Watering with a virus containing solution d) Mechanical inoculation e) Infection of seeds Answer: c
2) Which of the following statements about cucumber mosaic virus is FALSE? a) It has an enveloped helical nucleocapsid. b) It has a wide range of host species that it can infect. c) Its genome is composed of positive-strand RNA. d) It is transmitted by aphids. e) It can cause asymptomatic infections in some plants. Answer: a
3) The coat protein of cucumber mosaic virus contains a negatively charged domain localized on the internal side of the capsid. Which of the following describes the purpose of this domain? a) It maintains the structure of the capsid. b) It associates with the positive charge of the viral RNA. c) It is involved in release of the viral genome into the host cell. d) It interacts with the host cell receptor. e) It is involved in movement of the capsid across the plant cell wall. Answer: b
4) Which of the following describes the structures of the genomic RNA segments from cucumber mosaic virus?
a) They have a 5’ cap and a 3’ poly A tail. b) They have a 5’ IRES and a 3’ poly A tail. c) They have a 5’ cap and a 3’ terminal tRNA-like structure. d) They have a 5’ phosphate and a 3’ terminal tRNA-like structure. e) They have a protein covalently bound to the 5’ end and a 3’ poly A tail. Answer: c
5) Which of the following describes a feature of plant viruses, like cucumber mosaic virus, that is rare or absent in animal viruses? a) Segmented genomes are each packaged into a single virion. b) Viral particles are transmitted to new hosts via an insect vector. c) Viral genomes are composed of ssRNA with a negative sense. d) Viral genomic RNA has a 5’ cap. e) Segmented genomes are each packaged into separate virions. Answer: e 6) Which of the following enzymes can transfer an amino acid to the 3’ end of the genome of cucumber mosaic virus? a) Elongation factor Tu b) Aminoacyl tRNA synthetase c) Nucleotidyltransferase. d) Ribosomal protein S1. e) Methyltransferase Answer: b
7) Which of the following characteristics of the cucumber mosaic virus influences the aphid species that can transmit the virus? a) Amino acid sequence of the coat protein. b) The replication efficiency of the RNA-dependent RNA polymerase. c) The specificity of binding to the host cell receptor. d) The sequence of the 3’ end of the viral genomic RNA. e) The sequence of the IRES at the 5’ end of the genomic RNA. Answer: a
8) The methyltransferase domain of the polymerase subunit 1a in the cucumber mosaic virus is responsible for doing with of the following? a) Separating strands of the viral RNA during replication. b) Replicating the viral genome. c) Adding the 5’ cap to the viral RNA genome segments. d) Movement of the viral genome through the plasmodesmata. e) Inhibiting host ribonucleases. Answer: c
9) Which of the following describes the first step in the replication cycle of the cucumber mosaic virus? a) Synthesis of minus-strand copies of the genome. b) Synthesis of plus-strand copies of the genome. c) Copying of viral genome into dsDNA. d) Copying of the viral genome into mRNA. e) Translation of the genome into protein. Answer: e
10) In an infected plants, the cucumber mosaic virus replicase complex is associated with the membrane surrounding which of the following cellular organelles? a) Golgi apparatus b) Nucleus c) Mitochondria d) Central Vacuole e) Chloroplast Answer: d
11) Which of the following has been used as a system to study brome mosaic virus replication? a) Bacterial cells b) Yeast cells c) Insect cells d) Animal cells e) Human cells Answer: b
12) What is the role of the plasmodesmata in the replication of cucumber mosaic virus? a) They allow release of progeny virions from host cells. b) They are the sites of entry of capsids into the host cell. c) They are the sites of viral replication inside of plant cells. d) They allow movement of virus genomes between neighboring cells. e) They are involved in assembly of progeny virions. Answer: d
13) How has reassortment played a role in the evolution of cucumber mosaic virus? a) It has allowed swapping of RNA segments between strains. b) It has allowed swapping of regions of the genome between strains c) It has increased mutations in the RNA genomes. d) It has maintained stability of the viral genome. e) It has increased genetic bottlenecks. Answer: a
14) All of the following describe a function of the movement protein from cucumber mosaic virus EXCEPT: a) It allows the viral RNA to move between host cells. b) It interacts with the host cytoskeleton. c) It dilates the plasmodesmata. d) It binds to viral genomic RNAs. e) It causes the viral RNA to be taken up by aphids. Answer: e
15) Which of the following describes the hypersensitive response in plants infected with the cucumber mosaic virus? a) The virus moves into the vascular tissue and causes a systemic infection. b) The virus causes an asymptomatic infection. c) Virus replication is limited to a local region of infection. d) The plant is completely resistant to the virus. e) Virus replication only occurs in the newest tissues on the plant. Answer: c
16) Plant defenses against RNA viruses involved which of the following? a) siRNAs b) RISC c) Dicer d) Host RNA-dependent RNA polymerase e) All of the above are correct. Answer: e
17) Which of the following statements about satellite RNAs found in cucumber mosaic virus infections is FALSE? a) They require a cucumber mosaic virus for replication. b) They are packaged into cucumber mosaic virus capsids. c) They are small linear RNA molecules. d) They encode several functional proteins. e) They can increase the symptoms produced by cucumber mosaic virus. Answer: d
18) Which of the following proteins from cucumber mosaic virus acts at the RNA-dependent RNA polymerase? a) Protein 1a b) Protein 2a c) Protein 2b d) Movement Protein e) Coat Protein Answer: b Question Type: True/False 19) In cucumber mosaic virus, productive infection requires simultaneous entry of all three major RNA segments, each packaged into a separate virion. Answer: True
20) The 5’-terminal 200nts on the cucumber mosaic virus genome function as a promoter for the synthesis of the minus-strand RNA. Answer: False 21) Most cultivars of cucumber are resistant to the cucumber mosaic virus, which means they can be infected but do not show any symptoms of the infection. Answer: False 22) Plants infected with cucumber mosaic virus are more tolerant to drought and cold than uninfected plants. Answer: True. 23) In lieu of an immune response, plants use RNA silencing to defend against virus infection. Answer: True Question type: Essay 24) Plant viruses, like cucumber mosaic virus, often package separate RNA genome segments into separate virions. What are the evolutionary advantages and disadvantages of this strategy? What ensures that the plants are infected with all of the necessary genome segments to begin an infection? Answer: The evolutionary advantage of packaging each separate genome segment into its own virion is that it allows the virus to maintain a relatively large genome in smaller discrete units that are more stable. It also allows the virion size to be smaller and require fewer coat proteins to be assembled. The major disadvantage is that it means that three or four separate virus particles, each with a different genome segment, must enter the host cell at the same time. The mode of infection is what ensures that all of the genome segments will enter simultaneously. Since most plant viruses are transmitted via insect feeding, it is likely that the insect will pick up many copies of the virus and deposit them in the cells of the next host plant. This ensures that one copy of each genome segment will enter the next host cell. 25) Viruses that infect plants must contend with the thick cell wall, which is impedes movement of macromolecules between cells. Describe the mechanisms that cucumber mosaic virus uses to transverse this cell wall to both initiate an infection as well as spread through the plant.
Answer: Cucumber mosaic virus is transmitted to healthy plants using aphids as a vector. When the insect feeds on the plant it breaks the cell wall and deposits virus particles into the cytoplasm of the cell. To transmit between host cells, the virus produces a movement protein that dilates the plasmodesmata, which are membrane lined channels that traverse the cell wall between cells, and transmits virus genome segments to neighboring cell. For long range movement, virus particles take advantage of the vascular system of plants. They enter the sieve cells, which are part of the phloem, and this allows the virus to invade tissues that are distant from the initial site of infection.
26) Describe how satellite RNAs of the cucumber mosaic virus are act as parasites of the virus. Answer: Satellite RNAs are small linear RNAs that do not appear to encode any functional proteins. These RNAs are dependent on cucumber mosaic virus for their replication and transmission. They are packaged into the capsids of the cucumber mosaic virus. The presence of these RNAs usually reduces the accumulation of cucumber mosaic virus particles in infected cells, which leads to a reduction of symptoms in a plant infected with both cucumber mosaic virus and the satellite RNA. Since the satellite RNA is dependent on the cucumber mosaic virus for its own replication and transmission and reduces the efficiency of viral replication, then it is acting as “a parasite of the virus”.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 11
Question type: Multiple Choice
1) Which of the following diseases is NOT caused by a member of the picornavirus family? a) Common cold b) Polio c) Hepatitis A d) Influenza e) Foot-and-mouth disease Answer: d
2) Why is it unlikely that there will ever be an effective vaccine against the rhinovirus, the major cause of the common cold? a) The immune system is not very effective at attacking rhinoviruses. b) There are over 100 different serotypes of rhinovirus. c) The immune system does not protect the nose. d) The common cold is too fast for the immune system to fight off. e) Antibodies can not bind to the rhinovirus virion very well. Answer: b
3) The killed Salk and live Sabin vaccines have been used successfully to nearly eliminate which of the following viruses from the human population? a) Polio b) Smallpox c) Measles d) Hepatitis A e) Foot-and-mouth disease Answer: a
4) Many of the picornaviruses use host cell receptors that have which of the following characteristics?
a) They are phospholipids. b) They are carbohydrates. c) They belong to the immunoglobulin superfamily. d) They are integrins. e) They are ion channels. Answer: c 5) Some picornaviruses have depressions, called “canyons”, on the surface of the virions. Which of the following describes the role that these depressions play? a) They release the viral genome into the host cell. b) They bind to the host cell receptor. c) They maintain the stability of the capsid. d) They bind to antibodies. e) They adhere to the envelope. Answer: b 6) Entry of the poliovirus genome into the host cell involves all of the following EXCEPT… a) Binding to a host cell receptor b) Extrusion of the hydrophobic N-terminus of VP1 c) Conformational change of the virion d) Loss of the internal VP4 protein e) Acidification of the endosome Answer: e 7) The 5’ end of the poliovirus genomic RNA contains all of the following EXCEPT… a) A 5’ cap b) An unusually long noncoding region c) A pyrimidine-rich tract d) A high degree of RNA secondary structure e) Multiple AUG start codons Answer: a 8) The poliovirus protease cleaves the cellular eIF-4G protein. Why doesn’t this affect the virus? a) The virus doesn’t use this protein as its host cell receptor.
b) The virus encodes the poly A tail as part of the genome. c) The virus encodes its own version of this cellular protein. d) The virus does not use cap-dependent translation. e) The virus encodes its own RNA-dependent RNA polymerase. Answer: d 9) How does cleavage of the host cell protein eIF-4G give the virus a competitive advantage? a) It releases translation factors that the virus needs. b) It inhibits a cellular nuclease that would degrade the viral genome. c) It prevents translation of host cell mRNAs but not viral genomes. d) It inhibits host cell defense mechanisms. e) It releases nucleotides to be used in viral genome replication. Answer: c
10) Translation initiation of the genomes of picornaviruses require all of the following EXCEPT: a) IRES at the 5’ end of the genome b) VPg protein attached to 5’ end of genome c) Pyrimidine-rich sequence upstream of an AUG d) Small subunit of ribosome e) Host cell translation initiation factors Answer: b
11) Since translation of mRNAs in eukaryotic cells produces only a single polypeptide, how do picornaviruses produce multiple proteins from their RNA genome? a) They produce multiple subgenomic mRNAs. b) Their genome consists of a multicistronic mRNA. c) They use multiple IRES regions to translate multiple open reading frames. d) They have internal translation start sites in their genome. e) They cleave a single polypeptide into individual proteins. Answer: e
12) Which of the following describes the source of the protease that cleaves the picornavirus polyprotein into individual functional proteins? a) It is a cellular protease. b) It is brought into the host cell with the virion.
c) It is part of the polyprotein. d) It is one of the capsid proteins. e) It is a complex of a viral and a cellular protein. Answer: c
13) Why do many positive-strand RNA viruses form their genome replication complexes on the surface of cytoplasmic membranes? a) Genome replication requires cellular membrane bound proteins. b) This allows the RNA to be replicated close to the site of virion assembly. c) The membrane acts as a nucleation sites to bring all of the proteins together. d) The membrane protects the viral genome during replication. e) Fatty acids are required co-factors of the viral polymerase. Answer: c
14) The VPg protein from picornaviruses has which of the following function? a) It acts as a primer for RNA synthesis. b) It is the RNA-dependent RNA polymerase. c) It is the protease the cleaves the viral polyprotein. d) It induces the formation of cellular membranes. e) It packages the viral genome into capsids. Answer: a
15) Which of the following describes the last step in the maturation of the picornavirus capsid? a) Assembly of the 5S protomer b) Packaging of the viral genome. c) Cleavage of P1 polyprotein into VP0, VP1 and VP3. d) Cleavage of VP0 into VP2 and VP4. e) Assembly of the 14S pentamer. Answer: d
16) Picornaviruses cause cytopathic effects in infected host cells by doing all of the following EXCEPT: a) Inhibiting cap-dependent translation of mRNAs. b) Degrading cellular DNA.
c) Inhibiting intracellular transport from the ER to the Golgi. d) Cleaving histone H3 protein. e) Inhibiting host cell mRNA synthesis. Answer: b 17) In the picornavirus genome, there are several A nucleotides found at the 3’ end of both the positive and negative sense strands. How are these A nucleotides used in replication of the RNA genome? a) They function as the poly A tail for translation of both strands. b) They provide energy for the RNA-dependent RNA polymerase. c) They allow the genome strands to be easily separated. d) They basepair with the U nucleotide bound to the VPg protein. e) All of the above are correct. Answer: d
18) The ability of picornaviruses to cause pathogenesis in specific tissues can be localized to which of the following regions of the viral genomic RNA? a) The RNA-dependent RNA polymerase coding region. b) The 3’ noncoding region. c) The non-structural protein coding region. d) The capsid protein coding region. e) The 5’ noncoding sequence. Answer: e
Question Type: True/False
19) Once the viral genome has entered the host cell, poliovirus does not require any of the virion proteins to carry out its infectious cycle. Answer: True
20) The poly A tail found at the end of the picornavirus genome is created using the same mechanism as the poly A tails on host cell mRNAs. Answer: False
21) The 3C proteinase from picornaviruses can cleave itself out of the intact polyprotein. Answer: True
22) The RNA-dependent RNA polymerase from picornaviruses does not require a primer. Answer: False
23) Hepatitis A produces less cytopathic effects in infected cells than other picornaviruses. Answer: True
Question type: Essay
24) Explain how the rhinovirus capsid can evolve to evade the immune system yet can still bind and recognize the same host cell receptor. Answer: Rhinoviruses have a capsid structure that has both a “canyon” region and an exposed ridge. Antibody molecules, which are a major component of antiviral immunity, can bind to the exposed ridge but are not narrow enough to bind in the canyon. The host cell receptor, on the other hand, is a narrow protein that can bind to the base of the canyon. This allows the amino acid residues on the surface of the virus to vary over time and allows the virus to evade the binding of antibodies. Yet the amino acids at the base of the canyon have selective pressure to remain the same so that they can still interact with the host cell receptor and allow virus entry into host cells. 25) Instead of a 5’ cap on the viral genomic RNA, genomes of the picornaviruses have a covalently bound protein. In addition, the viral 3C protease cleaves a major component of the cap binding complex. This situation should inhibit translation initiation of the picornaviral RNA into protein. Explain how the virus “solves” this problem. Answer: Instead of using cap-dependent translation, which requires the 5’ cap on the RNA and the cellular cap binding complex, picornaviruses use a cap-independent process for initiating translation of the viral genome. They have a very long 5’ noncoding sequence that has a high degree of secondary structure which functions as a internal ribosome entry site (IRES). This IRES can bind to cellular proteins, some of which are involved in translation initiation, which then bring in the small subunit of the ribosome. This allows the ribosome to be deposited near the correct AUG to begin translation of the picornavirus genome, bypassing the need for the 5’ cap and the cap binding complex.
26) Poliovirus virions enter cells through a pH independent mechanism at the cell surface, which is an unusual pathway for a naked virion. Describe the entry mechanism and explain why this is this important for a virus that uses the oral-fecal transmission route? Answer: Poliovirus capsids bind to the host cell receptor on the surface of the cell. This binding induces a conformational change in the capsid that includes the release of the VP4 protein and the extrusion of a hydrophobic tail of the VP1 protein. It is thought that the hydrophobic tail of VP1 forms a channel through the cell membrane which allows viral RNA to pass through the membrane and into the cytoplasm of the host cell. The reason that poliovirus must use a pH independent pathway is that when it infects a new host it enters through the gastrointestinal tract. If the virion used a pH dependent pathway, then it would be affected by the low pH in the stomach acid. This would cause the capsid to change conformation prematurely and prevent it from entering the correct host cells.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 12
Question type: Multiple Choice
1) Which of the following diseases is caused by a member of the flavivirus family? a) Yellow Fever b) Dengue Fever c) West Nile Encephalitis d) Hepatitis C e) All of the above. Answer: e
2) Which of the following describes the primary mechanism of transmission of the flavivirus Hepatitis C? a) Mosquito bites b) Contaminated blood transfusions c) Aerosols d) Contaminated food and water e) Animal bites Answer: b
3) How was Yellow Fever Virus introduced into the New World from Africa? a) Infected animals were imported. b) Tires containing infected mosquitoes were imported. c) Migrating birds brought it. d) It came over on slave trading ships. e) Walter Reed released it from a laboratory. Answer: d
4) The yellow fever vaccine strain has 32 amino acid mutations in comparison to the wildtype pathogenic virus strain. Which of the following genes contains the majority of these amino acid substitutions?
a) Polymerase b) Capsid protein c) Envelope glycoprotein d) Protease e) Helicase Answer: c
5) Which of the following techniques was used to isolate the flavivirus Hepatitis C virus? a) Molecular cloning of the viral cDNA b) Purification of virus particles c) Antibody staining with patient serum d) Plaque assay e) Southern blotting Answer: a
6) In the mature flavivirus virion, the fusion peptide on the E protein is buried in the dimer interface. Which of the following conditions causes the fusion peptide to become exposed? a) Uptake of the virion via receptor mediated endocytosis. b) Interaction with the sialic acid residues on the surface of the cell. c) Binding to the host cell receptor on the surface of the cell. d) Drop in pH in the endosome. e) Binding to the host cell membrane. Answer: d
7) The hydrophobic region of the flavivirus capsid protein is thought to do which of the following? a) Bind to the host cell receptor. b) Interact with the viral envelope. c) Insert into the host cell membrane. d) Interact with and condense the genomic RNA. e) Bind to other capsid proteins. Answer: b
8) Which of the following describes the phenomenon of antibody-dependent enhancement?
a) Antibodies bound to a flavivirus particle allows entry into a cell via the Fc receptor. b) Antibodies bound to the host cell receptor make it unable to bind a flavivirus particle. c) Antibodies bound to infected cells cause the immune system to kill them. d) Antibodies bound to a flavivirus particle allow it to be removed by the immune system. e) The overproduction of antibodies during a flavivirus infection Answer: a
9) Which of the following conditions is required to induce fusion of the flavivirus envelope with the host cell membrane? a) Increase in pH b) Decrease in pH c) Binding of envelope protein to the host cell receptor d) Uptake of the virion into a vesicle. e) Proteolytic degradation of the virion. Answer: b
10) Which of the following statements comparing flaviviruses with togaviruses is FALSE? a) Flaviviruses have a T=3 capsid while togaviruses have a T=4 capsid. b) Flaviviruses have smaller virions that togaviruses. c) Flaviviruses do not produce subgenomic RNAs like togaviruses. d) Flaviviruses have enveloped virions but togaviruses have naked virions. e) Flaviviruses produce a single-polyprotein while togaviruses produce more than one. Answer: d
11) Which of the following statements comparing flaviviruses with picornaviruses is FALSE? a) They both use an IRES to initiation translation of the viral genome. b) They both have enveloped virions c) They both encode the structural proteins at the 5’ end of the genome. d) They both produce their proteins from a single open-reading frame. e) They both produce viral proteases to cleave the polyprotein. Answer: b
12) The nonstructural proteins of flaviviruses are produced on the rough ER and have membrane spanning domains. Which of the following explains why the nonstructural proteins are localized to cellular membranes?
a) Fatty acids are a required cofactor for RNA synthesis. b) Viral RNA replication can only occur in the lumen of the ER. c) Membranes serve to localize the viral replication complex. d) The viral replication proteins must be glycosylated before they are active. e) The nonstructural proteins require proteolytic processing by lysosomal enzymes. Answer: c
13) Flavivirus virions obtain their envelopes from the cellular membranes of which of the following organelles? a) Endoplasmic Reticulum b) Nucleus c) Golgi apparatus d) Plasma membrane e) Mitochondria Answer: a
14) Which of the following proteins from flaviviruses has the RNA-dependent RNA polymerase activity? a) NS1 b) NS2 c) NS3 d) NS4 e) NS5 Answer: e
15) Which of the following cellular proteases helps to process the polyprotein of flaviviruses? a) Chymotrypsin b) Trypsin c) Furin d) Cathepsin D e) Papain Answer: c 16) When is the “pr” region cleaved by the protease furin from the prM protein of flaviviruses?
a) During translation of the structural proteins. b) When the virion acquires the envelope from the ER. c) As the capsid is being assembled in the cytoplasm. d) After the virion moves through the trans Golgi network. e) After release of the virions from the host cell. Answer: d
17) West Nile Virus was introduced into the United States in 1999 and became an endemic infection over the next several years. Which of the following wild animal populations does this virus circulate in? a) Bats b) Bees c) Birds d) Beetles e) Bears Answer: c
18) Which of the following describes the reason why the precursor to the capsid protein from flaviviruses has a membrane spanning domain? a) So that it is localized on the membranes where viral RNA replication takes place. b) So that it islocalized on the membranes where the virions obtain their envelope. c) So that it is close to where the other structural proteins are localized. d) So that it will be translated by ribosomes associated with the ER. e) All of the above are correct. Answer: e
Question Type: True/False
19) A cloned DNA copy of the yellow fever virus can be used to produce infectious viral RNA. Answer: True
20) Infection with a second strain of Dengue fever virus within two years of having had the first strain causes Dengue Hemorrhagic Fever.
Answer: True
21) Since flaviviruses replicate in the cytoplasm of the host cell, they do not need to encode a methyltransferase enzyme to produce the 5’ cap on the viral genomic RNA. Answer: False
22) In a flavivirus infection, newly synthesized positive-strand RNA genomes can only be packaged into new virions. Answer: False
23) Once the West Nile Virus became endemic in the United States, 20% of the population has seroconverted to the virus. Answer: False
Question type: Essay
24) Describe the events that events that lead West Nile virus from moving from a local epidemic to becoming endemic in the United States. Answer: West Nile virus was originally isolated from Uganda and is found in several parts of the world including the Middle East, Europe and Asia. The first outbreaks of West Nile Virus in the US were in the New York City region in 1999 when dead birds were seen in high numbers. Over the course of the next several years, the virus moved westward eventually causing infections in birds and human in all 48 contiguous states. An increase in the mosquito population was thought to have enhanced the movement of West Nile across the country. The number of people exposed and infected with West Nile appears to have leveled off, though an increase in either infected mosquitoes or birds could lead to sporadic regional outbreaks.
25) Describe the final processing steps that the flavivirus virion goes through in order to be converted from an immature virion into a mature infectious virion. Answer: The nucleocapsid buds into the lumen of the ER to obtain the envelope. The immature virion then progresses through the exocytosis pathway to eventually be released from the host cell. Movement of the virion through the low pH environment of the trans Golgi network causes the surface proteins of the virion to fold down into the flattened structure and exposes the furin cleavage site. This allows furin to cleave the prM protein into the final M protein. However, the
“pr” peptide is not released from the virion until after the virion leaves the cell and is exposed to the neutral pH outside the host cell.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 13
Question type: Multiple Choice
1) Which of the following is the correct description for the term arboviruses? a) Viruses that are all in the togavirus family. b) Viruses that all have an RNA genome. c) Viruses that are all capable of infecting the liver. d) Viruses that can all cause diseases in humans. e) Viruses that all use an insect as a transmission vector. Answer: e 2) What is the definition of a “dead-end” host for an arbovirus? a) A vertebrate host that does not transmit the virus efficiently. b) An insect vector that dies before it can transmit the virus. c) A vertebrate host that does not get sick when infected with the virus. d) An insect vector that poorly replicates the virus. e) A virus that can not replicate in the lungs of the host Answer: a
3) Which of the following members of the togavirus family is not transmitted via mosquitoes? a) Sindbis virus b) Equine Encephalitis virus c) Rubella virus d) Ross River virus e) Semliki Forest virus Answer: c
4) Which of the following members of the Togavirus family caused an epidemic in the Indian Ocean region in 2005? a) Ross River virus b) Sindbis virus
c) Venezuelan encephalitis virus d) Chikungunya virus e) Rubella virus Answer: d
5) Which of the following describes an interesting feature of the envelope of a togavirus? a) There are 240 copies of the envelope protein in the envelope. b) The envelope proteins are arranged with icosahedral symmetry. c) The envelope is composed of a lipid bilayer. d) The envelope is inside the capsid. e) The envelope only contains one type of protein. Answer: b
6) Which of the following components of the togavirus virion bind to the host cell receptor? a) Lipid envelope b) Capsid protein c) HA protein d) E1 glycoprotein e) E2 glycoprotein Answer: e
7) If you add togavirus virions to host cells and then lower the pH of the medium, what will happen? a) The virions will become inactivated. b) The virus will bind more tightly to the host cell receptor. c) The virions will fuse to the plasma membrane of the cell. d) The virus will be released from the host cell receptor. e) The virions will be taken up by receptor mediated endocytosis. Answer: c
8) During entry of a togavirus virion, which of the following events may help disrupt the nucleocapsids and release the genomic RNA into the host cell? a) Uptake of the virion into the endosome. b) The increase in pH inside the endosome.
c) Degradation of the capsid proteins by the viral protease. d) Binding of the ribosomes to the genomic RNA. e) Binding of viral polymerase to the genomic RNA. Answer: d 9) The open reading frame that takes up the 5’ end of the togavirus genome encodes which of the following? a) The nonstructural proteins. b) The capsid proteins. c) The IRES sequence. d) The envelope proteins. e) The proteins that shut down host defenses. Answer: a
10) How are the structural proteins in togaviruses expressed? a) They are translated from the negative-sense strands after genome replication. b) They are translated directly from incoming genomes. c) They are translated from a subgenomic RNA. d) They are only translated from newly synthesized full-length genomes. e) None of the above are correct. Answer: c
11) Which of the following allows the production of the P1234 nonstructural protein in a togavirus? a) Ribosomal frameshifting. b) Production of the subgenomic mRNA. c) Proteolytic cleavage. d) Readthrough of a stop codon. e) Initiation of translation at a downstream start codon. Answer: d
12) Which of the following describes the mechanism used by togaviruses to switch from synthesizing negative-strand genomes to making positive-strange genomes? a) Phosophorylation of the polymerase protein.
b) Dephosphorylation of the polymerase protein. c) Glycosylation of the polymerase protein. d) Methylation of the polymerase protein. e) Proteolytic cleavage of the polymerase protein. Answer: e 13) In an experiment, mutation of bases at the very 5’ end of the togavirus genome reduces the amount of the negative-strand of the genome produced. What does this result suggest? a) That the virus genome contains an IRES sequence. b) That the packaging sequence is only found at the 5’ end of the genome. c) That the replication complex binds to both ends of the genome. d) That the genome forms a covalently closed circle for replication. e) That a protein is used as a primer for genome replication. Answer: c
14) An experiment was done in togaviruses where the nsP2 protein was mutated so that it can proteolytically cleave the P123 protein very quickly. Which of the following describes the results of this experiment? a) Inability of the virus to produce negative-strand genomes. b) Inability of the virus to produce positive-strange genomes. c) Inability of the virus to produce subgenomic mRNAs. d) Faster replication of the virus genome. e) Production of higher levels of virus particles. Answer: a
15) During infection with a togavirus, the subgenomic mRNAs represent the complementary strand of which of the following? a) The full-length positive-strand genome. b) The 3’ half of the positive-strand genome. c) The 3’ half of the negative-strand antigenome. d) The 5’ half of the positive-strand genome. e) The 5’ half of the negative-strand antigenome. Answer: e
16) Which of the following describes the mechanism used to regulate the various functions of the RNA-dependent RNA polymerase from togaviruses? a) Proteolytic cleaveage. b) Post-translational phosphorylation. c) Post-translational glycosylation. d) Interaction with viral cofactors. e) Interaction with viral structural proteins. Answer: a
17) How does a togavirus ensure that only full length genomes are packaged into the virions? a) Only full length genomes will fit into the capsid. b) Only full length genomes are produced near the site of assembly. c) Only full length genomes can bind to the envelope glycoproteins. d) Only full length genomes contain the packaging signal. e) Only full length genomes can be processed by the viral nuclease. Answer: d
18) Translation of the subgenomic mRNA from togaviruses occurs on ribosomes that are located on or in which of the following cellular compartments? a) Mitochondria b) Nucleus c) Cytoplasm d) Trans-Golgi vesicle e) Endoplasmic reticulum Answer: e
Question Type: True/False 19) Most arthropod-borne viruses can replicate in both insect cells and mammalian cells. Answer: True
20) Infection of vertebrate cells with a togavirus does not cause cytopathic effects but leads to a persistent infection instead. Answer: False
21) The P123 version of the polymerase protein from togaviruses can autocatalytically cleave itself into the individual nonstructural proteins. Answer: False
22) The subgenomic mRNA from togaviruses is synthesized from a subgenomic negative-strand RNA. Answer: False
23) The production of the subgenomic mRNA allows togaviruses to synthesize 10 times more structural proteins than non-structural proteins. Answer: True
24) One of the advantages of the alphavirus vector that uses a double subgenomic RNA for expressing foreign proteins is that it does NOT need a helper virus to produce virions. Answer: True
Question type: Essay 25) The togaviruses have their non-structural protein coding sequences at the 5’ end of the viral genome while the picornaviruses and the flaviviruses have the non-structural protein coding sequences at the 5’ end. Explain how this difference is important in the replication cycle of the togaviruses. Answer: In eukaryotic cells, only the first open reading frame at the 5’ end of the mRNA is translated. This means that whatever proteins are coded for at the 5’ end of the viral genome will be produced immediate upon entry. Because the genomes of the togaviruses have two separate open reading frames, it is critical that the nonstructural proteins are produced at the start of the infection. Once these proteins are synthesized, then they can copy the genome into the negative sense antigenome. This can then be copied into the subgenomic RNA, which is then translated to produce the capsid and envelope proteins. If the nonstructural proteins were coded for at the 3’ end of the genome, they would never be synthesized during the viral replication cycle.
26) Alphaviruses, which are members of the togavirus family, have been developed as useful vectors for the expression of proteins in various human and insect cells. Describe two situations where alphaviruses could be used as vectors in biology or medicine. Answer: 1) They have been used to produce high levels of foreign proteins in various cell types. This is better than using bacterial cells because the proteins will receive their normal posttranslational modifications (phosphorylation, glycosylation). One example of this is to produce proteins from unrelated viruses that could be used as vaccines. 2) Infection of insects with a virus that expresses an RNAi construct against other mosquito borne pathogens, such as yellow fever or West Nile Virus. 3) Alphaviruses could express a toxic protein to kill off mosquitoes or other insects. 4) Because alphaviruses infect neurons in their vertebrate hosts, they have been used to study live neurons in culture. These viruses could eventually be developed as gene therapy vectors for introducing genes into neurons.
27) There are two proposed mechanisms for how togaviruses assemble their virions. Describe the two mechanisms and any available evidence that supports them. Answer: One of the proposed mechanisms of togavirus virion assembly involves formation of complete nucleocapsids in the cytoplasm. These nucleocapsids then associate with the tails of the envelope glycoproteins, which bind to a hydrophobic pocket on the capsid protein. As the nucleocapsid buds through the plasma membrane, the association between the tail of one glycoprotein with one of the capsid proteins produces the same T=4 iscosahedral structure in the envelope that is seen in the capsid. The observation of preformed nucleocapsids in the cytoplasm of infected cells by electron microscopy supports this model. The second mechanism suggests that the capsid proteins bind to the genomic RNA in a complex that is not as structured as the complete nucleocapsid. These complexes also bind to the tails of the glycoproteins. The association between each capsid protein with a glycoprotein nucleates the assembly of the nucleocapsid as it buds through the plasma membrane allowing the capsid to form during the budding process.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 14
Question type: Multiple Choice
1) All of the following are diseases which can be caused by members of the coronavirus family EXCEPT: a) Bronchitis b) Hepatitis c) Arthritis d) Gastroenteritis e) Encephalitis Answer: c
2) Which of the following is a coronavirus that emerged as a serious human pathogen in Asia in 2003? a) Ebola b) SARS c) Chikungunya d) Coxsackie Virus e) West Nile Virus Answer: b
3) The majority of known coronaviruses have been isolated from which of the following vertebrates? a) Bats b) Mice c) Humans d) Pigs e) Birds Answer: a
4) Which of the following describes the structure of the coronavirus virion?
a) Naked helical capsid b) Naked icosahedral capsid c) Icosahedral nucleocapsid surrounded by an envelope d) Helical nucleocapsid surrounded by an envelope e) None of the above. Answer: d 5) The 5’ two-thirds of the coronavirus genome contains which of the following? a) IRES sequence b) Non-structural protein coding sequences c) Capsid protein coding sequences d) Envelope protein coding sequences e) Binding sites for the viral polymerase Answer: b
6) Which of the following coronavirus proteins is responsible for virus entry and is the primary determinant of host range? a) Spike (S) protein b) Envelope (E) protein c) Membrane (M) protein d) Hemagglutinin-Esterase (HE) protein e) Nucleocapsid (N) protein Answer: a
7) Which of the following describes the mechanism used by coronaviruses to produce the ORF1b protein? a) Read through a translational stop codon b) Ribosomal frameshifting c) RNA editing d) Antitermination of transcription e) Translation initiation at a downstream start codon Answer: b
8) Which of the following statements about the proteinases from coronaviruses is FALSE?
a) They are encoded in the nonstructural region of the viral genome. b) They are cysteine proteinases. c) They are packaged into the virion. d) They first cleave themselves out of the polyprotein. e) They primarily cleave the non-structural polyprotein into mature proteins. Answer: c
9) Which of the following is an enzymatic function found in the nonstructural proteins of a coronavirus? a) Methyltransferase b) Helicase c) RNA-dependent RNA polymerase d) Ribonuclease e) All of the above. Answer: e
10) What is unique about the structure of the subgenomic RNAs produced by the coronaviruses? a) They each have their own IRES sequence. b) They have a protein covalently attached to the 5’ end. c) They are synthesized from a full-length negative strand copy of the genome. d) The first 60 to 100 nucleotides at the 5’ end is the same. e) They have a tRNA structure at their 3’ end. Answer: d
11) The TRS sequence on the coronavirus genome is involved in which of the following processes? a) Synthesis of the full length negative strand copy of the genome. b) Transcription of the subgenomic negative strands. c) Synthesis of the full-length positive strand genomes. d) Packaging of the viral genome into the capsid. e) Translation of the genome into protein. Answer: b
12) The membrane proteins of coronaviruses are glycosylated in which of the following cellular compartments?
a) Cytoplasm b) Endosome c) Lysosome d) Smooth ER e) Golgi apparatus Answer: e
13) Which of the following processes does NOT contribute to the evolution of coronaviruses? a) Genome Reassortment b) Random point mutations c) Error rate of the RNA-dependent RNA polymerase d) Selection in new host species e) RNA-RNA recombination Answer: a
14) Enveloped virus-like particles can be formed in cells when only the M and E protein from a coronavirus are expressed. What does this indicate? a) That these proteins can not associate with the nucleocapsid. b) That these proteins can not associate with each other. c) That these proteins are sufficient for assembly and budding of virions. d) That these proteins require HE and S for virion formation. e) All of the above are correct. Answer: c
15) The complex RNA structure called a pseudoknot in the genome of coronaviruses is involved in which of the following processes? a) Translation initiation of the nonstructural proteins. b) Translation initiation of the structural proteins. c) Replication of the positive strange genomes. d) Packaging of the genome into the capsid. e) Ribosomal frameshifting from ORF1a to ORF1b. Answer: e
16) Which of the following might explain the potentially low barrier to species jumping seen in coronaviruses? a) The large size of the RNA genome. b) The modular nature of the Spike glycoprotein. c) The ability of one virus to bind to multiple host cell receptors. d) The ability of the virus to reassort its genome segments. e) The high number of envelope glycoproteins found on the virion. Answer: b
17) How do coronavirus enveloped virions get released from the host cell? a) The viral envelope fuses with the plasma membrane, releasing the virion. b) They lyse open the host cell. c) Virus containing vesicles fuse with the plasma membrane, releasing virions. d) They bud from the surface of the host cell. e) All of the above are mechanisms used by coronaviruses. Answer: c 18) Which of the following have made it difficult to create a cDNA clone of the entire coronavirus genome that can be used in reverse genetics experiments? a) The genome is too short to be cloned. b) The genome contains regions that are resistant to cloning. c) The viral RNA can not be converted to DNA. d) The viral RNA from coronaviruses is not infectious. e) Reverse genetics does not work with coronaviruses. Answer: b
Question Type: True/False
19) Coronaviruses have the longest RNA genome of any known virus. Answer: True
20) Even though some coronavirus virions have a hemagglutinin-esterase protein, they still cannot bind to sialic acid. Answer: False.
21) The negative-strand RNA templates account for over 10% of the RNA molecules found in a coronavirus infected cell. Answer: False
22) If the Spike protein from some coronaviruses is incorporated into the plasma membrane of host cells, it can cause cell fusion and the formation of syncytia. Answer: True
23) The subgenomic mRNAs in the coronaviruses are synthesized from subgenomic negativestrand templates. Answer: True
Question type: Essay
24) Unlike the other positive-strand RNA viruses that have simpler genomes, coronaviruses produce a nested set of sub-genomic mRNAs, each of which is translated into a single protein. Explain why the virus needs to produce so many subgenomic mRNAs. Answer: In eukaryotic cells, almost all mRNAs are monocistronic and only the first open reading frame at the 5’ end of the mRNA will be translated. When the ribosome reaches the first stop codon, it falls off of the mRNA and will not translate a downstream open reading frame. This means that for each of the coronavirus structural proteins to be produced, it must be at the 5’ end of one of the subgenomic RNAs. The mechanism that coronaviruses use to ensure this is to have a nested set of subgenomic RNA that all have the same 3’ end but have their 5’ ends at a different position. The results is that each structural protein open reading frame is at the 5’ end of one of the nested set of subgenomic mRNAs, which will allow it to be translated.
25) Describe the two alternative hypotheses for how a bat coronavirus evolved to infect humans and cause the SARS epidemic in 2003. Which one does the evidence appear to support? Answer: Hypothesis one is that a bat coronavirus could have jumped into a different species of animal that served as a intermediate host. This intermediate host served to amplify the virus, which could have led to it mutating into a form that could infect humans. The virus would then have jumped from the intermediate host into humans and had the capacity to then be transmitted from human to human. The second hypothesis that a bat coronavirus was passed to humans but was not in a form that was pathogenic. The virus then jumped from humans to the intermediate
host, which amplified the virus and allowed it to mutate into a form that was more pathogenic to humans. This final version then moved back to human where it was highly transmissible and pathogenic. This second more complicated pathway is supported by viral genome sequences of viruses isolated from various human and animal hosts throughout the epidemic.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 15
Question type: Multiple Choice 1) All of the following viruses are members of the order Mononegavirales EXCEPT…. a) Rabies b) Influenza c) Measles d) Ebola e) Sendai virus Answer: b
2) Which of the following statements about rabies is FALSE? a) The virion has a bullet shape. b) It is usually transmitted through the bites of bats or domestic dogs. c) The vaccine can be administered after infection has occurred. d) Infection with the virus has a 50% mortality rate in untreated individuals. e) Infection of humans causes an encephalitis. Answer: d
3) Which of the following virion proteins mediates the coiling of the rhabdovirus nucleocapsid to form the bullet-shaped virion? a) The HN (hemagglutinin/neuraminidase) protein b) The F (fusion) protein c) The M (matrix) protein d) The N (nucleocapsid) protein e) The L (RNA polymerase) protein Answer: c
4) Which of the following is a difference observed between the paramyxoviruses and the rhabdoviruses? a) One has a negative-strand genome and one has a positive-strand genome.
b) One has a naked virion and one has an enveloped virion. c) One has a helical nucleocapsid and one has an icosahedral nucleocapsid. d) One packages the RNA-dependent RNA polymerase and the other doesn’t. e) One fuses the envelope at the plasma membrane and one fuses the envelope with the endocytotic membrane. Answer: e
5) In the paramyxoviruses, cleavage of the F0 protein into two subunits F1 and F2 is important for which of the following? a) Formation of the envelope. b) Glycosylation of the protein. c) Creation of the transmembrane domain. d) Exposing the fusion peptide. Answer: d
6) Which of the following statements about paramyxoviruses is FALSE? a) The N protein can bind to a variable number of nucleotides in the genome. b) The RNA-dependent RNA polymerase is a virion protein. c) Every protein coded for in the genome is packaged into the virion d) The N protein protects the genome from ribonuclease digestion. e) Naked genome-length RNA is never found within the cell. Answer: a
7) What is the function of the neuraminidase enzyme during infection with Sendai virus, a member of the paramyxovirus family? a) It helps the assembly of the envelope. b) It attaches to the host cell receptor. c) It is involved in evasion of the host immune system. d) It facilitates exit of the virions. e) It is involved with transcription of viral mRNAs. Answer: d 8) Which of the following statements about the leader sequence at the 3’ end of the paramyxovirus genome, is FALSE?
a) It is translated into a short polypeptide. b) It is transcribed into a short positive-strand RNA. c) The transcript produced from the leader contains a packaging signal for the positive-strand antigenome. d) It contains the binding site for the RNA polymerase to begin transcription. e) The transcript produced from the leader lacks a 5’ cap. Answer: a
9) Which of the following describes a major difference between the positive-strand RNA viruses and negative-strand RNA viruses? a) Only positive-strand viruses must package their polymerase in their virion. b) Only negative-strand viruses must package their polymerase in their virion. c) Only positive-strand viruses must encode a polymerase in their genome. d) Only negative-strand viruses must encode a polymerase in their genome. e) Both kinds of RNA viruses both encode and package a polymerase. Answer: b
10)Synthesis of mRNAs in paramyxoviruses occurs through a single-entry mechanism, which is where the RNA-dependent RNA polymerase can only start transcription from the 3’ end of the genome. Which of the following is a consequence of this mechanism? a) More negative-strand genomes are produced than positive-strand antigenomes. b) The RNA-dependent RNA polymerase binds to both end of the genome for genome replication c) The RNA-dependent RNA polymerase binds to both ends of the genome for transcription d) More mRNA is produced from the coding regions at the 5’ end of the genome. e) More mRNA is produced from the coding regions at the 3’ end of the genome. Answer: e 11) There are two sequence elements at the 3’ end of the genomes of paramyxoviruses that are required for mRNA transcription and genome replication. These two sequences are 78 nucleotides apart. How can the polymerase bind to both of these sequence elements at the same time? a) There are cellular proteins that bridge the two sequences. b) There are viral proteins that bridge the two sequences. c) The two sequences are both on the same side of the helical nucleocapsid. d) The polymerase protein is large enough to bind both sequences. e) The polymerase does not need to bind to both sequences simultaneously.
Answer: c
12) Which of the following conditions during infection with a paramyxovirus causes the RNAdependent RNA polymerase to switch from start-stop transcription to production of full-length positive-strand antigenomes? a) Levels of the mRNAs transcribed. b) Concentration of the N protein. c) Proteolytic cleavage of the polymerase protein. d) Phosphorylation of the polymerase protein. e) Levels of the L protein. Answer: b 13) How is the poly(A) tail added to the 3’ ends of the mRNAs produced during infection with a paramyxovirus? a) The viral polymerase stutters at a poly(U) sequence. b) The cellular poly(A) polymerase adds it. c) Paramyxovirus mRNAs do not have poly(A) tails. d) The viral poly(A) polymerase adds it after the mRNA is released from the template. e) The entire poly(A) tail is encoded in the genome. Answer: a
14) What mechanism do the paramyxoviruses use to produce 5 different proteins from a single gene on their genome? a) Use of alternative start codons. b) Read-through of a stop codon. c) Ribosomal frameshifting d) RNA editing e) Both RNA editing and alternative start codons are used. Answer: e
15) Which of the following describes the process of RNA editing as used by the paramyxoviruses? a) Removal of an introns and splicing together of the exons. b) Splicing together of two separate RNAs.
c) Removal of one or two nucleotides from the 5’ end of the mRNA. d) Addition of one or two non-template nucleotides to the mRNA. e) Removal of one or two nucleotides from the middle of the mRNA. Answer: d
16) Mutation of the RNA editing site in the genome of a paramyxovirus will have which of the following effects? a) It eliminates the production of the P protein. b) It eliminates the production of the V protein. c) It causes the production of the P protein. d) It causes the production of the V protein e) It eliminates mRNA splicing. Answer: b
17) Which of the following proteins from paramyxovirus virions interacts with the tails of the envelope glycoproteins during assembly of virions? a) N protein b) C protein c) L protein d) M protein e) F protein Answer: d Question Type: True/False 18) Rhabdoviruses can infect a wide variety of hosts including insects, plants and vertebrates. Answer: True 19) New paramyxoviruses have emerged from fruit bats by being transmitted to domestic livestock and then to humans. Answer: True
20) The F protein of the paramyxovirus measles is responsible for both binding and fusion of the virion to the host cell. Answer: False 21) Subacute sclerosing panencephalitis (SSPE) is a common complication of measles where the virus infects the nervous tissue immediately after causing the typical measles virus symptoms. Answer: False 22) Because measles virus can infect B and T lymphocytes, it can lead to strong immunosuppression. Answer: True 23) Most of the genomes of the paramyxoviruses have been shown to have genomes lengths that are exact multiple of 8 nucleotides. Answer: False Question type: Essay 24) Describe the two models that explain how the monopartite negative-strand RNA viruses produces individual mRNAs. Which of the two models does the experimental evidence support? Answer: The multiple-promoter model states that the viral RNA-dependent RNA polymerase can begin synthesis of the viral mRNAs at any of the intergenic sequences. This would predict that transcription of each mRNA is independent of any of the upstream or downstream coding regions. The single-entry model states that the viral RNA-dependent RNA polymerase would always start RNA synthesis at the 3’ end of the negative-strand genome. It would then pause at each intergenic region and either disengage from the template to restart synthesis at the 3’ end or continue on to transcribe the next protein coding region. To demonstrate which of these two mechanisms is correct, where a thymine dimer was introduced into a gene and it inhibited transcription of all the downstream genes, which supports the single-entry model. 25) Describe two major differences between transcription and genome replication in paramyxoviruses. Answer: When the levels of the nucleocapsid protein builds up in the infected cell, the viral polymerase switches from producing subgenomic mRNAs to producing full-length positive-
strand antigenomes. One major difference is that the nucleocapsid protein only binds and encapsidates the full-length antigenome and genome copies. The subgenomic mRNAs are not bound by the nucleocapsid protein. The second major difference is that during genome replication the viral RNA polymerase does not pause at the intergenic regions and stutter to create the polyA tail. It continues through and produces an authentic full-length copy of the genome with no stops or reinitiation.
26) The order of the genes in the genomes of paramyxoviruses and rhabdoviruses is highly conserved. Is there a benefit to the virus for this specific gene order? Answer: Because the viral genes are transcribed with polarity, meaning that more mRNA is produced from genes located at the 3’ end of the negative-strand genome than from the genes at the 5’ end, the order of genes is related to the relative amounts of the proteins required during the infection. Because the N gene is at the 3’ end and the viral polymerase always restarts transcription from that point, more of the mRNA encoding the nucleocapsid protein will be made. Since large amounts of the nucleocapsid protein are required for packaging of viral genomes, this is a benefit. The L gene is at the 5’ end and is transcribed the least frequently. Since the L gene encodes the viral RNA-dependent RNA polymerase and only a few copies of this protein are required per virion, this is beneficial as well.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 16
Question type: Multiple Choice
1) Marburg virus is named after which of the following? a) A river in Africa. b) A country in Africa. c) A town in Africa. d) A town in Germany. e) A country in Europe. Answer: d
2) Which of the following animals appears to be the reservoir for filovirus infections? a) monkeys and primates b) bats c) racoons d) domestic livestock e) insects Answer: b
3) The virions of filoviruses are very different than the virions of other negative-strand RNA viruses. Which of the following describe this difference? a) They are enveloped. b) They are spherical. c) They are narrow and elongated. d) They don’t contain a matrix protein. e) They use a helical nucleocapsid. Answer: c
4) Which of the following viruses has NOT been associated with lethal human disease? a) Marburg b) Ebola Sudan
c) Ebola Zaire d) Ebola Reston e) None of the above. Answer: d 5) All of the following are similarities between filoviruses and paramyxoviruses EXCEPT…. a) They have enveloped virions. b) They have negative-strand RNA genomes. c) They have long thin virions. d) They encode the nucleocapsid gene at the 3’ end of the genome. e) They encode the polymerase gene at the 5’ end of the genome. Answer: b
6) The intergenic regions in the Ebola virus genome contains signals for all of the following processes EXCEPT…. a) Transcription reinitaiton. b) Trancription termination. c) Polyadenylation. d) RNA polymerase disengagement. e) Genome replication. Answer: e
7)All of these proteins are associated with the nucleocapsids of Ebola virus EXCEPT which of the following? a) NP - nucleoprotein b) VP40 – matrix protein c) L – viral RNA polymerase d) VP35 – polymerase cofactor e) VP30 – transcription activator Answer: b
8) All of the following factors can affect the efficiency of transcription of the mRNAs in the Ebola virus EXCEPT…. a) Strength of the polymerase binding site.
b) Location of the gene in the genome. c) RNA secondary structure at 3’ end of gene. d) RNA secondary structure in the intergenic region. e) Presence of overlapping genes. Answer: a
9) Inclusion bodies inside the cytoplasm of cells infected with Ebola virus are sites for which of the following processes? a) Formation of viral envelopes. b) Transcription of viral mRNAs. c) Formation of viral nucleocapsids. d) RNA editing of viral mRNAs. e) Translation of viral proteins. Answer: c
10) Budding of Ebola virus particles occurs at sites on the plasma membrane where which of the following is present? a) Insertion of viral glycoproteins in the cell membrane. b) Binding of the matrix protein with the cytoplasmic face of the cell membrane. c) High concentrations of the host cell receptor. d) Lower concentrations of phospholipids. e) Where both glycoproteins and matrix protein are located. Answer: e
11) Which of the following proteins from Ebola virus resembles the matrix proteins from other RNA viruses? a) VP24 b) VP40 c) VP30 d) L e) VP35 Answer: b
12) Which of the following describes one of the important roles for the VP30 protein of Ebola virus?
a) Activation of mRNA synthesis. b) Assembly of enveloped virions. c) Packaging of the viral genomic RNA. d) Binding to the host cell receptor. Answer: a
13) The VP30 protein from Ebola virus activates synthesis of the NP mRNAs by doing which of the following? a) Helps bring nucleotide triphosphates to the viral RNA polymerase. b) Acts as a helicase to unwind the RNA template. c) Counteracts the negative effects of a stem-loop at the 5’ end of the mRNA. d) Participates in the RNA editing process. e) Causes the RNA polymerase to bind to the NP promoter more tightly. Answer: c
14) In wildtype Ebola virus infections, only 20% of the envelope glycoprotein contains the transmembrane domain. Which of the following mechanisms controls the production of this membrane form of the protein? a) Alternative mRNA splicing b) RNA editing c) Ribosomal frameshifting d) Reading through a stop codon e) Proteolytic cleavage Answer: b
15) Scientists produced a mutant Ebola virus that does not express any of the soluble form of the envelope glycoprotein (sGP) but can only express the membrane bound form (GP). Which of the following explains the results of infecting cells with this mutant? a) It caused the cells to release more virus from the cell. b) It resulted in virus particles with higher levels of GP. c) It allowed the immune system to attack the virus. d) It caused the virus to produce smaller plaques. e) It reduced the cytopathic effect caused by the virus. Answer: d
16) During an outbreak of Ebola virus, which of the following as NOT been shown to be a major source of transmission between individuals? a) Preparation of bodies for burial. b) Reuse of needles and syringes. c) Sexual transmission. d) Aerosol droplets. e) Contact with contaminated blood. Answer: d 17) All of the following describe a feature of the pathogenesis of the filoviruses EXCEPT….. a) Induction of immunosuppression. b) Infection of macrophages and monocytes. c) Increased endothelial permeability. d) Induction of cytokine release. e) Problems with motor neurons and movement. Answer: e Question Type: True/False 18) Marburg virus, a member of the filovirus family, has a higher mortality rate than either Ebola Zaire or Ebola Sudan. Answer: False 19) The total number of recorded filovirus infections has not yet exceed 3000 cases. Answer: True 20) There is a concern that filoviruses could be used as agents of germ warfare. Answer: True 21) Labs that have Biosafety Level 2 are allowed to work with live infectious filoviruses. Answer: False
22) Most filoviruses have been isolated from monkeys taken from Asia. Answer: False 23) Filovirus infections are resistant to both treatment with interferon and ribavirin. Answer: True Question type: Essay 24) Explain the system that has allowed scientists to produce infectious filoviruses using transfection of several plasmids into cells. Answer: The first component of this system is a plasmid that contains a DNA copy of the entire Ebola genome. The genome cDNA is positioned next to a promoter for the bacteriophage T7 RNA polymerase so that when it is transcribed it will contain the authentic 5’ end. This plasmid also contains a ribozyme sequence at the 3’ end of the cDNA that produces an authentic 3’ end for the genome. In addition to the plasmid that can produce the negative sense genome, plasmids that express the nucleocapsid, polymerase, VP30 and VP35 genes from a T7 promoter are also transfected into cells. Finally, a plasmid that produces the T7 RNA polymerase is transfected so that each gene is transcribed from each plasmid. This allows authentic Ebola nucleocapsids to be produced in transfected cells and allows scientists to study replication of the virus and the production of mutant virus particles. 25) The GP protein of Ebola virus is unusual from the glycoproteins from other negative-strand RNA viruses in two major ways. Describe these differences. Answer: The first is that the actual GP open reading frame as coded for in the Ebola genome lacks a transmembrane domain and only produces a soluble form of the protein which is not incorporated into the virion envelopes but instead is secreted out of the infected cell. In order to produce a membrane-bound form of the protein, RNA editing of the viral mRNA as it is being synthesized must take place. This causes a change in the reading frame of the mRNA and produces the membrane bound form to be incorporated into viral envelopes. This occurs about 20% of the time. Another major difference is that the GP protein does not have to be cleaved by a cellular protease in order for the virus to be infectious. When the furin cleavage site was mutated so that it could no longer be cleaved, the virus particles produced were still infectious and were still pathogenic in monkeys. This is very different than the glycoproteins from other viruses which are dependent on cleavage for both infection and pathogenesis.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 17
Question type: Multiple Choice
1) Which of the following describes a similarity between bunyaviruses and flaviviruses? a) They both have positive-strand RNA virus genomes. b) They both have negative-strand RNB virus genomes. c) They both have members that are transmitted by insects. d) The both have members that only replicate in insects. e) The both similar virion structures. Answer: c
2) How are bunyaviruses maintained in nature over time? a) They can be maintained in mosquito eggs. b) They can stay viable in the soil. c) They are maintained in water samples. d) They cause persistent infections in humans. e) All of the above. Answer: a
3) Which of the following describe the differences between bunyaviruses and filoviruses? a) Bunyaviruses have a monopartite genome and filoviruses are segmented. b) Bunyaviruses have a segmented genome and filoviruses are monopartite. c) Bunyaviruses have a naked virion and filoviruses are enveloped. d) Bunyaviruses have an enveloped virions and filoviruses are naked. e) Only filoviruses can be transmitted via an insect vector. Answer: b
4) What is the definition of ambisense coding? a) One of the viral segments is positive-sense RNA and the other is negative sense. b) One of the viral segments is DNA and the other is RNA. c) One end of a viral segment is positive-sense RNA and the other is negative-sense.
d) One viral segment codes for structural proteins and the other codes for non-structural proteins. e) Only one viral segment is packaged into each viral particle. Answer: c
5) Which of the following bunyaviruses is NOT transmitted by an insect vector? a) Tomato spotted wilt virus b) Crimean-Congo hemorrhagic fever virus c) Rift Valley Fever virus d) Hantaan virus e) La Crosse virus Answer: d
6) Which of the following is a type of human illness NOT caused by a member of the bunyavirus family? a) fever b) encephalitis c) hemorrhagic fever d) fatal respiratory syndrome e) arthritis Answer: e
7) How many genome segments do bunyaviruses have? a) 1 b) 2 c) 3 d) 5 e) 8 Answer: c
8) Viruses, such as bunyaviruses, that use ambisense coding, do which of the following to produce their mRNAs? a) They translate the positive end of the viral segment first. b) They translated the negative end of the viral segment first. c) They copy the positive end of the viral segment into mRNA first.
d) They copy the negative end of the viral segment into mRNA first. e) They translate the entire ambisense viral segment into protein first. Answer: d
9)Which of the following are typically the largest proteins coded for by RNA viruses? a) The nucleocapsid protein. b) The RNA polymerase. c) The matrix protein. d) The envelope glycoproteins. e) The regulatory protein. Answer: b
10) Which of the following describes an interesting feature of the envelope glycoproteins from bunyaviruses? a) They are exported out to the plasma membrane of the cell. b) They are retained in the Golgi membrane. c) They are not glycosylated. d) They are cleaved into three segments. e) 80% of the proteins made are secreted out of the cell. Answer: b
11) Bunyaviruses that have been reassorted for the M segment have lost their virulence. Which of the following describes the conclusion from this experiment? a) The envelope proteins are responsible for virulence. b) The RNA polymerase is responsible for virulence. c) The non-structural protein is responsible for virulence. d) The nucleocapsid protein is responsible for virulence. e) Virulence is not controlled by any of the above. Answer: a
12) The S genome segment from bunyaviruses encodes which of the following proteins? a) The RNA polymerase protein. b) The envelope glycoproteins. c) The nucleocapsid protein.
d) Both the nucleocapsid protein AND the non-structural protein. e) Either b or d can be correct, depending on the virus. Answer: e
13) What do bunyaviruses use to prime the transcription of their viral mRNAs? a) A cellular protein b) A viral protein c) Fragments of cytoplasmic capped mRNAs. d) Fragments of nuclear capped mRNAs. e) The do not use primers for mRNA transcription. Answer: c
14) Bunyavirus mRNAs can be translated while they are still being transcribed by the viral RNA polymerase. Why has this been shown to be important for this group of viruses? a) Transcription prevents premature termination of translation. b) Translation prevents premature termination of transcription. c) It allows the virus to use attenuation as a regulatory mechanism. d) The virus can translate the structural protein on the rough ER ribosomes. e) It prevents cellular ribosomes from translating cellular mRNAs. Answer: b
15) In the bunyaviruses, which of the following viral proteins is proposed to regulate the transition from production of mRNAs to genome replication? a) The N (nucleocapsid protein) b) The M (matrix protein) c) The G (glycoprotein) d) The L (polymerase protein) e) The NS (non-structural protein) Answer: a
16) In the RNA viruses with segmented genomes, which of the following explains antigenic shift? a) Lack of RNA editing by the RNA-dependent RNA polymerase. b) Lack of proof-reading by the RNA-dependent RNA polymerase.
c) Exchange of the glycoproteins between two virions. d) Exchange of genome segments between two virions. e) All of the above are correct. Answer: d
17) Which of the following could be the source of new pathogenic bunyavirus infections in humans? a) Acquisition of new viruses from bats. b) Evolution of viruses that over stimulate the immune system. c) Reassortment between two viruses in mosquitoes. d) Transovarial transmission of a bunyavirus. e) Infection of domestic animals. Answer: c
18) A reverse genetics system for bunyaviruses has been established by doing which of the following? a) Expressing negative-strand viral genomes in mosquito cells. b) Expressing negative-strand viral genomes in mammalian cells. c) Expressing positive-strand viral genomes in mosquito cells. d) Expressing positive-strand viral genomes in mammalian cells. e) By transfecting mammalian cells with naked negative-strand viral RNA. Answer: d Question Type: True/False 19) The bunyavirus Sin Nombre caused a severe respiratory infection in Asia in 2003. Answer: False 20) The mechanism for how bunyaviruses package one of each of their genome segments is well understood. Answer: False
21) The genome segments of bunyaviruses can form panhandles and circularize due to complementary 3’ and 5’ ends. Answer: True 22) Bunyaviruses appear to use a pH dependent mechanism for entry into host cells. Answer: True 23) Bunyavirus mRNAs are translated while they are still being transcribed. Answer: True 24) Synthesis of the positive-strand antigenome of bunyaviruses uses the same capped primer as the synthesis of the mRNAs. Answer: False Question type: Essay 25) Bunyaviruses remove the 5’ ends of cellular mRNAs. Describe the mechanism that these viruses use to do this and how the virus uses these RNA fragments. What advantage does this provide to the virus? Answer: The L protein (RNA polymerase) of bunyaviruses binds to the 5’ end of a cellular mRNA in the cytoplasm of the infected cell and cleaves the mRNA 10-18nts from the 5’ end. The RNA polymerase then aligns the 3’ end of the RNA fragment with the 3’ end of the viral genome segments and uses this fragment as a primer for viral mRNA synthesis. This provides two advantages to the virus. Since the virus does not encode its own methyltransferase enzyme activity, it gives the viral mRNAs a cap which improves the efficiency of translation. In addition, by removing the caps from the cellular mRNAs, it prevents them from being translated and gives the virus an advantage when competing for ribosomes. 26) Explain how genetic drift and shift can lead to the emergence of new strains of bunyavirus that are pathogenic in humans. Answer: Antigenic drift is caused by the poor fidelity of the RNA-dependent RNA polymerase when copying the viral genome. This leads to the introduction of point mutations throughout the viral genome. This can lead to new virus strains which are not recognized by the immune systems of previously infected patients and the emergence of new infections. Even so, data
suggests that there is not a high level of genome variability among disease isolates, suggesting that only some genotypes are pathogenic in humans. Antigenic shift is potentially more dangerous since it involves the reassortments of viral genome segments. The new progeny virions produced will have the capacity to make entirely new proteins from newly acquired genome segment. While there is evidence that only closely related viruses can reassort their genome segments, there is also evidence that this has led to the emergence of at lease only highly pathogenic virus in humans.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 18
Question type: Multiple Choice
1) Which of the following viruses was responsible for the death of 20 million people in 19181920? a) Ebola virus b) Influenza virus c) Smallpox virus d) Rift Valley Fever virus e) Measles virus Answer: b
2) Many of the symptoms caused by infection with the influenza virus, including fever, headache and malaise, are actually the result of which of the following? a) Factors produced by the virus during infection. b) Direct damage to the cells of the lung. c) Infection of the liver. d) Loss of ciliated epithelium. e) The effect of cytokines induced by the virus. Answer: e
3) Influenza produces 11 different proteins from 8 genome segments. How many of these proteins are packaged into the viral particle? a) 7 b) 8 c) 9 d) 10 e) 11 Answer: c
4) Genome segments 7 and 8 from influenza virus can produce two different proteins using which of the following mechanisms?
a) Ambisense coding. b) RNA editing. c) Readthrough of a stop codon. d) Alternative mRNA splicing. e) Use of alternative start codons. Answer: d
5) Cleavage of the HA protein of influenza by cellular proteases is important for which of the following? a) Activation of the fusion peptide. b) Creation of the sialic acid binding site. c) Release of the envelope proteins from the Golgi. d) Attachment of the envelope to the capsid. e) Insertion of the HA protein into the membrane. Answer: a
6) Which of the following describes the function of the M2 protein from influenza virus? a) It induces the fusion of the viral envelope with the cell membrane. b) It binds to the host cell receptor for viral entry. c) It acts as an ion channel to allow H+ ions to enter the virion. d) It helps to initiate transcription of viral mRNAs. e) It cleaves off the 5’ caps from the cellular mRNAs. Answer: c 7) Several of the protein from influenza virus interact with the cellular protein -importin. Why is this necessary for virus infection? a) It allows the viral proteins to by glycosylated in the Golgi. b) It is important for entry of the viral genomes into the cell. c) It transports the viral proteins to the plasma membrane. d) It transports the viral proteins into the nucleus. e) It is involved in fusion of the viral envelope with the endosome. Answer: d
8) Which of the following describes a difference between transcription and genome replication in the influenza virus? a) Transcription requires the PB2 protein while genome replication does not. b) Transcription produces a shorter positive strand mRNA while replication produces a fulllength antigenome. c) Transcription produces a poly(A) tail at the 3’ end of the viral mRNA while genome replication does not. d) Transcription requires a primer derived from a cellular pre-mRNA while genome replication does not. e) All of the above are correct. Answer: e 9) Treatment of influenza infected cells with actinomycin D and -amanitin, which inhibit the activity of the cellular RNA polymerase II, shut down the synthesis of viral mRNAs. Which of the following describes the mechanism of this inhibition? a) The viral RNA-dependent RNA polymerase is also inhibited by these compounds. b) The virus needs a supply of nuclear pre-mRNAs to snatch caps from. c) These inhibitors reduce the supply of nucleotides for transcription. d) The cellular RNA polymerase synthesizes the viral mRNAs. e) This leads to the degradation of the viral RNA genome segments. Answer: b 10) How is the poly(A) tail added to the 3’ ends of the mRNAs produced during infection with a influenza virus? a) The viral polymerase stutters at a poly(U) sequence. b) The cellular poly(A) polymerase adds it. c) Influenza virus mRNAs do not have poly(A) tails. d) The viral poly(A) polymerase adds it after the mRNA is released from the template. e) The entire poly(A) tail is encoded in the genome. Answer: a
11) The abundance of which of the following proteins from influenza virus controls whether the virus is producing mRNAs or full-length positive antigenomes. a) PB1 protein b) PB2 protein c) PA protein
d) Nucleocapsid protein. e) Matrix protein Answer: d
12) The NS2 protein from influenza can bind and inhibit cellular proteins involved in polyadenlyation of mRNAs. Why doesn’t this affect the virus? a) Influenza virus mRNAs don’t have poly(A) tails. b) Influenza virus uses a stuttering mechanism to add the poly(A) tail. c) All of the viral mRNAs are polyadenylated before the NS2 protein is made. d) Influenza virus encodes its own poly(A) polymerase that isn’t affected by NS2. e) The virus encodes the poly(A) tail in the genome. Answer: b
13) Which of the following describes the function of the NS1 protein made during an influenza virus infection? a) Inhibition of cellular antiviral defenses. b) Activation of viral RNA polymerase. c) Transport of nucleocapsids out of the nucleus. d) Inhibition of cellular RNA polymerase. e) Inhibition of antibody production. Answer: a
14) New reassorted influenza viruses are USUALLY transmitted to human from which of the following pathways? a) A reassortment of two avian viruses that is directly transmitted from birds to humans. b) A reassortment of an avian virus and a human virus that is transmitted from a pig. c) A reassortment of two pig viruses that is directly transmitted from pigs to humans. d) A reasortment of a human virus and a pig virus that is transmitted from a bird. e) A reassortment of two human viruses that is directly transmitted from a human. Answer: b
15) Why are reassorted influenza viruses usually more likely to cause a severe worldwide pandemic? a) They are more immunosuppressive than other influenza viruses.
b) They contain new segments that produce more pathogenic proteins. c) They can infect different types of cells. d) They have acquired new glycoproteins for which there is no prior immunity. e) They have acquired mutations that allow them to evade the immune system. Answer: d
16) Most animal influenza viruses do not infect humans. Which of the following can explain this observation? a) Animal viruses fail to destroy ciliated epithelium in that host. b) Animal viruses do not induce specific cytokines in the host. c) Animal viruses bind to a different form of sialic acid than human viruses. d) The HA proteins of animal viruses are activated by the protease furin. e) Both c and d are correct. Answer: e
17) What function does the neuraminidase protein of influenza virus carry out? a) It binds to sialic acid and helps the virus enter the host cell. b) It helps release virions from virus producing cells. c) It is involved in the glycosylation process of the NA protein. d) It cleaves the HA protein into two functional domains. e) It helps the virus evade the immune system. Answer: b Question Type: True/False 18) While often confused with milder upper-respiratory infections caused by rhinoviruses and coronaviruses, the symptoms of influenza infection are more severe. Answer: True 19) Most seasonal outbreaks of human influenza are caused by the influenza C virus. Answer: False 20) Virions of the influenza virus can be either spherical or filamentous in shape.
Answer: True 21) Influenza is unusual for an RNA virus because it replicates in the nucleus. Answer: True 22) Since influenza virus replicates in the nucleus of the infected cell, it uses the cellular polyadenlyation enzymes to add the poly(A) tail on the viral mRNAs. Answer: False 23) During an influenza virus infection, the spliced mRNAs are produced in higher abundance than the unspliced mRNAs. Answer: False 24) Prophylatic treatment of a patient with an antiviral drug to influenza is the best way to prevent infection. Answer: False Question type: Essay 25) Influenza virus is unusual for an RNA virus because it replicates in the nucleus of the host cell. Describe the two processes that influenza uses the nucleus to accomplish. For which of these two is replication in the nucleus essential? Answer: Influenza replicates in the nucleus of the host cell for two reasons:1) it snatches caps from cellular pre-mRNAs to use as primers for synthesis of viral mRNAs and 2) it uses the host cell mRNA splicing enzymes to carry out alternative splicing of mRNAs produced from two genome segments, 7 and 8. The splicing enzymes only exist in the nucleus of the host cell, so this is the process that is absolutely dependent on the virus replicating in the nucleus. However, the virus could snatch caps from mature cellular mRNAs in the cytoplasm, similar to bunyaviruses, if it replicated in the cytoplasm instead. 26) Explain the role that antigenic drift and shift play in the ability of influenza to cause new outbreaks. Which one is thought to have caused the 1918 strain of influenza to emerge?
Answer: Antigenic drift consists of the gradual changes of amino acids due to lack of fidelity of the RNA-dependent RNA polymerase. These amino acid changes, particularly in the HA and NA protein, make these external protein unrecognizable by the immune response to previous influenza viruses. This explains why infection with influenza does not lead to a life long immunity to the virus. Antigenic shift is a larger change in the HA and NA proteins. This involves the swapping of two or more genome segments when two viruses infect the same cell. These reassorted viruses have completely different HA and NA proteins. Since few people have any prior immunity to these reassorted viruses, they are usually the cause of worldwide pandemics. While it was thought that the deadly 1918 strain was due to antigenic shift, after the genome was recovered and sequenced, it was actually due to antigenic drift, since only a few amino acids in several crucial proteins were changed.
26) Influenza virus is one of the only RNA viruses that replicates in the nucleus of the host cell. How does this virus regulate transport of viral nucleocapsids into and out of the nucleus at various times during the infection? Answer: At the start of an infection with influenza, virions are dissembled due to the low pH in the endosome. This releases the nucleocapsids into the cytoplasm where the exposed nuclear localization signal on the NP protein causes the import of the nucleocapsids into the nucleus. In addition, most of the viral proteins contain a nuclear localization signal which allows them to be transported back into the nucleus after they are synthesized in the cytoplasm. As nucleocapsids form in the nucleus of the infected cell, they must be transported out of the nucleus so that they can bud from the plasma membrane and become enveloped. The newly made nucleocapsids interact with the M1 protein. Next, the NS2 protein, which contains a nuclear export signal, binds to the M1 protein and allows the nucleocapsids to be exported out of the nucleus and into the cytoplasm for final assembly and release.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 19
Question type: Multiple Choice
1) Which of the following factors affect the abundance of the viral proteins produced during infection with a reovirus? a) Length of the mRNA. b) Sequences surrounding the start codon. c) Length of the 5’ noncoding sequences. d) Secondary structure in the 5’ noncoding sequences. e) All of the above are correct. Answer: e
2) Which of the following describes the type of type of nucleic acids found in reovirus genomes? a) single-stranded positive-sense RNA b) single-stranded negative-sense RNA c) double-stranded RNA d) single-stranded DNA e) double-stranded DNA Answer: c
3) How has the creation of reassortant viruses helped in the study of reoviruses? a) It allows for the infection of new hosts via antigenic shift. b) It allows for the association of a specific viral protein with its function. c) It allows scientists to measure the size of the various genome segments. d) It allows for easier identification of specific virion protein. e) It allows for the creation of new gene therapy vectors. Answer: b
4) Which of the following describes an interesting feature of the reovirus virion? a) It has two envelopes – one inner and one outer. b) The envelope has icosahedral symmetry, same as the underlying capsid.
c) Each genome segment is wrapped into a helical nucleocapsid. d) The capsid consists of two concentric shells, both with icosahedral symmetry. e) The mature virion has open passages at each of the twelve vertices. Answer: d
5) Which of the following is NOT a host cell protein that can be used as a receptor by a reovirus? a) Cathepsin b) Sialic Acid c) JAM-A d) Integrin e) None of the above. Answer: a
6) Which of the following is the first step in the expression of reovirus proteins during the infection? a) Translation of the incoming RNA segment into protein. b) Copying of the positive strand of each genome into a negative strand. c) Copying of the negative strand of each segment into an mRNA. d) Capping of the positive strand of each genome segment. e) Translation of the positive strand of each genome segment.
Answer: c
7) What is the source of the nucleotide triphosphates used to make reovirus mRNAs? a) They are produced by enzymes inside the core virion. b) They diffuse into the core virion from the cytoplasm. c) RNA synthesis occurs in the cytoplasm, where the nucleotides are located. d) The viral RNA polymerase transports them into the core virion. e) They are brought inside the virion from the previous host cell. Answer: b
8) All of the following are enzymatic activities found within the virion core of reoviruses EXCEPT…. a) RNA-dependent RNA polymerase activity.
b) RNA helicase activity c) Phosphatase to remove 5’ end of mRNAs d) Methyltransferase. e) Peptidyl transferase. Answer: e
9) Which of the following reovirus proteins is implicated in selective inhibition of PKR activation in infected cells? a) 1 b) 3 c) 1 d) 2 e) 1 Answer: b
10)Which of the following mechanisms explain how reovirus mRNAs acquire their poly(A) tail? a) They do not have poly(A) tails but use other sequences to functionally substitute. b) Cellular enzymes add the poly(A) tail c) Viral enzymes in the virion core add the poly(A) tail. d) The encode a poly(A) tail in each genome segment. e) The RNA polymerase stutters at a poly(U) region at the end of each genome segment. Answer: a
11)Which of the following describes the mechanism used by reoviruses to ensure that one of each of the 10 genome segments is package into the virion? a) Reoviruses do not have a specific mechanism to ensure packaging of each genome segment into the virion. b) Each double-stranded RNA segment has a unique packaging sequence. c) One of each double-stranded RNA segments binds to the capsid proteins. d) One of each mRNA is assembled into a virus factory. e) None of the above are correct. Answer: d
12) Which of the following is used as the template for the production of more reovirus genome segments in the virus factories?
a) Double-stranded RNA. b) Single-stranded negative sense RNA. c) mRNAs. d) Single-stranded positive sense RNA. e) Both “c” and “d” are correct. Answer: e
13) Which of the following accounts for the majority of the viral mRNA synthesized in a reovirus infected cell? a) mRNA made from single-stranded negative RNA segments. b) mRNA made from incoming double-stranded RNA segments. c) mRNA made from newly synthesized double-stranded RNA segments. d) mRNA made from RNA segments found in the cell nucleus. e) mRNA made from virions found in the lysosome. Answer: c
14) Infection of a cell with a reovirus can activate which of the following cellular proteins or processes? a) NF-B b) IRF-3 c) Apoptosis d) Caspases e) All of the above are correct. Answer: e
15)Reoviruses cause cell-cycle arrest in infected cells. At what point in the cell cycle do these viruses halt the cell cycle? a) Between mitosis and G1. b) Between G1 and S. c) Between S and G2 d) Between G2 and mitosis. e) All of the above. Answer: d
16) Reoviruses keep their genome sequestered inside the inner capsid throughout the entire infectious cycle. Which of the following is the best explanation for why do they not release the genome segments out into the cytoplasm? a) The double-stranded RNA segments activate the interferon response. b) There are cellular enzymes that specifically degrade double-stranded RNA. c) The RNA segments can not be translated by the cellular ribosomes. d) Double-stranded RNA is sequestered into special compartments within the cytoplasm. e) There are cellular proteins that will bind double-stranded RNA and inhibit it. Answer: a
17) Reoviruses have been used to study viral pathogenesis in mice. Using virus reassortants, which of the following has been shown to be a major determinant for infection of the nervous system in a mouse? a) Activation of the host cell immune system. b) Binding of the virus to different host cell receptors. c) Activation of the interferon system in host cells. d) The rate of viral mRNA synthesis in host cells. e) The rate of genome synthesis in host cells. Answer: b
18) Reoviruses can cause myocarditis in infected mice but it is through a different mechanism than used by most other viruses that cause this disease. Which of the following describes the reason reoviruses destroy heart muscle? a) Reoviruses induce cytopathic effects in heart muscle. b) Reoviruses induce apoptosis in the heart muscle. c) Reoviruses induce the interferon in the heart muscle. d) Reoviruses induce the immune system to destroy the heart muscle. e) Reoviruses induce the RNAi pathway in heart muscle. Answer: a Question Type: True/False 19) Some reoviruses are transmitted by insects and are therefore examples of arboviruses. Answer: True
20) The RNA-dependent RNA polymerase of reoviruses is released into the cytoplasm along with the double-strand RNA segments. Answer: False 21) There is evidence that the noncoding sequences on reovirus genome segments are highly conserved. Answer: True 22) Most reovirus virions must be partially degraded by proteases in the lysosome before infection. Answer: True 23) Infectious subvirion particles are intermediates in the assembly of reovirus virions. Answer: False 24) Reoviruses replicate more poorly in transformed cells than in normal cells. Answer: False 25) Reovirus capsid proteins assemble around positive-strand RNA segments before completion of genome replication. Answer: True Question type: Essay 26) Reoviruses use double-strand RNA to encode their genome. Why is this a problem for a virus that infects mammalian cells and how does the virus prevent this problem? Answer: Double-stranded RNA (dsRNA) is a potent inducer of the antiviral interferon pathway. Since mammalian cells do not produce large quantities of dsRNA, it is a signal to the cell that there is a virus infection. The effects of interferon are numerous, but the end result is that it will shut down protein production in cells. This would be a problem for the virus since it would not be able to produce any of its own proteins. In order to prevent setting off the interferon pathway,
reoviruses maintain their dsRNA genome segments inside of their capsid at all times during the infectious cycle. At the start of the infection, the virion does not completely dissociate and the dsRNA segments are kept inside the core of the capsid. Only the single-stranded positive-strands of RNA strands are released into the cytoplasm to be used as mRNAs. At the end of the infection the capsid forms around the positive strands and they are only converted into dsRNA after the capsid has sequestered them from the cell. This prevents the dsRNA from activating the interferon response in the host cell. 27) The human pathogenic virus, rotavirus, is a member of the reovirus family and causes severe diarrhea in children. Describe the adaptations that rotavirus virions have which allow them to survive the human gastrointestinal tract. Answer: The capsid of reoviruses has two concentric shells, which make it particularly hardy and allows it to survive the gastrointestinal tract. In fact, not only is the virion resistant to the effects of the low pH and proteases found in the gut, the virus actually requires that the virion be partially proteolytically degraded, either in the stomach of the infected person or in the lysosome of the infected host cell, in order to be infectious. This degradation releases some of the proteins from the outer shell of the virion and opens up passages so that nucleotides can enter the virion and the mRNAs can leave. Finally, the use of double-stranded RNA makes the viral genome very stable, since like double-stranded DNA, having two strands allows the genome to be more resistant to nucleases and other conditions that might lead to the degradation of the genome.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 20
Question type: Multiple Choice
1) Which of the following describes the type of nucleic acid used in the genomes of parvoviruses? a) Single-stranded DNA. b) Double-stranded DNA. c) Positive-sense single-stranded RNA. d) Negative-sense single-stranded RNA. e) Double-stranded RNA. Answer: a
2) Which of the following distinguishes the parvoviruses from adenoviruses and polyomaviruses? a) They have naked capsids. b) They replicate in the nucleus. c) They require the cellular DNA polymerase. d) They cannot induce the cell to enter S phase. e) They have a DNA genome. Answer: d
3) Which of the following distinguishes the dependoviruses from the autonomous parvoviruses? a) Dependoviruses require the host cell DNA polymerase. b) Dependoviruses require the host cell RNA polymerase. c) Dependoviruses require coinfection with an adenovirus. d) Dependoviruses are packaged in the virion of another virus. Answer: c
4) Which of the following describes the major difference between the gene expression strategies between different members of the parvovirus family? a) Some use alternative mRNA splicing and some do not.
b) They use different numbers of transcriptional promoters. c) Some use alternative start codons and some do not. d) Some use RNA editing and some do not. Answer: b
5) Which of the following describes a major difference between how the genomes of autonomous parvoviruses and dependoviruses are packaged? a) They both package either the positive or negative sense strand. b) Autonomous parvoviruses package only the positive sense strand while dependoviruses package double-stranded DNA. c) Autonomous parvoviruses package only the negative sense strand while dependoviruses package only the positive sense strand. d) Autonomous parvoviruses package only the positive sense strand while dependoviruses package only the negative sense strand. e) Autonomous parvoviruses package only the negative sense strand while dependoviruses package either the positive or negative sense strand. Answer: e
6) Which of the following describes the structures found at the ends of the parvovirus genomes? a) Self-complementary hairpin structures. b) 5’ cap structures and 3’ poly(A) tails. c) 5’ triphosphate. d) Covalently attached proteins. e) The genome is circular so it has no ends. Answer: a
7) What major function does coinfection with an adenovirus provide to adeno-associated virus, a member of the dependovirus group of parvoviruses? a) It helps the parvovirus package new virions. b) It helps the parvovirus enter the nucleus. c) It induces the host cell to enter S phase. d) It provides a DNA polymerase for genome replication. e) It provides an RNA polymerase for gene expression. Answer: c
8) Which of the following steps has been shown to be blocked in cells that are nonpermissive for parvoviruses? a) Binding of the virion to the correct receptor. b) Uncoating of the virion. c) Transcription of viral mRNAs. d) Synthesis of viral proteins. e) Replication of the viral genome. Answer: b
9) How do parvoviruses solve the problem of replicating the ends of linear DNA molecules? a) They do not have a double-stranded DNA genome. b) They circularize their genome so that there are no ends. c) They use a covalently bound protein as a primer. d) They have self-complementary ends that serve as primers. e) They encode a special DNA polymerase that can replicate ends of DNA. Answer: d
10) Which of the following describes the first step in the replication cycle of the autonomous parvoviruses? a) Translation of the incoming genome into proteins. b) Transcription of the incoming genome into early mRNAs. c) Synthesis of double-stranded DNA from the incoming genome. d) Alterative splicing of the incoming genome. e) Integration of the incoming genome into the host chromosome. Answer: c
11) Which of the following is NOT a function of the NS1 protein from minute virus of mice, an autonomous parvovirus? a) Stimulates transcription from its own p4 promoter. b) Stimulates transcription from the p38 promoter. c) Unwinds DNA hairpins during genome replication. d) Nicks viral DNA during genome replication. e) Regulates splicing of the viral mRNAs. Answer: e
12) Which of the following describes the fate of the AAV parvovirus genome in the absence of a helper virus? a) It is degraded. b) It integrates into a nonspecific location on a human chromosome. c) It integrates into a specific location on chromosome 19. d) It is replicated, just more slowly in the absence of the helper virus. e) It is maintained as an episome in the nucleus of the infected cell. Answer: c
13) Which of the following is an advantage of the parvovirus AAV genome integrating into the human genome? a) The viral genome is passed on to daughter cells. b) The viral genome disrupts the gene for an antiviral protein. c) The viral genome can be more easily transcribed by the cellular RNA polymerase. d) The viral genome can never be excised to begin a productive infection. e) The viral genome becomes stabilized by histones in the chromatin. Answer: a
14) The problem with replicating the ends of linear DNA is due to which of the following? a) That DNA polymerase does not require a pre-existing primer. b) The removal of the primer from the 3’ end of the new DNA strand. c) The removal of the primer from the 5’ end of the new DNA strand. d) That the primer is composed of RNA rather than DNA. e) That DNA polymerases can not synthesize DNA in the 5’ to 3’ direction. Answer: c
15) The Rep78 protein from the parvovirus adeno-associated virus has all of the following protein domains or enzymatic functions EXCEPT…. a) DNA binding domain. b) Helicase domain. c) Coiled-coil domain. d) Actin binding domain. e) Zinc finger domain. Answer: d
16) Which of the following diseases is NOT caused by a parvovirus? a) Panleukopenia b) Aplastic crisis in anemia patients c) Erythema infectiosum d) Birth defects e) Neurological problems. Answer: e
17) Which of the following does NOT explain why parvoviruses replicate better in tumor cells than in normal cells? a) Tumor cells have a reduced interferon response than normal cells. b) Tumor cells bind to more parvovirus virions than normal cells. c) Tumor cells have reduced DNA damage response than normal cells. d) Tumor cells go through the cell cycle more quickly than normal cells. e) None of the above. Answer: b
18) Which of the following viral proteins is responsible for the integration of the genome of the parvovirus adeno-associate virus into the host chromosome? a) Rep40 b) Rep78 c) VP1 d) VP2 e) integrase Answer: b Question Type: True/False 19) Parvoviruses can only productively infect cells that are NOT going through the cell cycle. Answer: False
20) The dependoviruses, which are a group of parvoviruses, require coinfection with an adenovirus or herpesvirus to undergo a productive infection. Answer: True 21) The oncotropism exhibited by parvoviruses means that they replicate more efficiently in tumor cells. Answer: True 22) The absence of the minor capsid proteins in parvovirus virions does not reduce infectivity. Answer: False 23) The parvovirus genome must first be converted to double-stranded DNA before it can be transcribed into mRNAs. Answer: True 24) Eukaryotic cellular chromosomes use the same mechanism as the parvoviruses to maintain the ends of their linear DNA. Answer: False Question type: Essay 25) Explain why the ends of DNA can not be completely replicated and how the parvoviruses use the self-complementary ends to solve this problem. Answer: All DNA polymerases require a pre-existing 3’ OH group to begin DNA synthesis on. This is usually obtained from a primer which is laid down at the 5’ end of the newly replicated DNA strand. When this primer is removed, the DNA polymerase can not fill in the gap at the 5’ end. If this situation were allowed to continue, then the DNA would get shorter after each round of replication. Parvoviruses solve this problem by having self-complementary ends to their genomes. The ends of the genome base-pair and produce a 3’ OH group that can be used as a primer for replication. Since there is no RNA primer used, there is no gap produced when the primer is removed. A series of steps that involve nicking of the DNA strand and refolding of the hairpin ends allows this self-priming mechanism to be used to completely replicate the ends of each viral genome.
26) When researchers first isolated the DNA genomes from the virions of the adeno-assocaited virus, a member of the dependovirus group of parvoviruses, they thought they were doublestranded. Explain why and how they were able to determine the correct genome structure. Answer: Adeno-associated virus packages either the positive-sense strand of DNA or the negative-sense strand of DNA into each virion. While a single virion will only have a singlemolecule of single-stranded DNA in each particle, a collection of particles will have nearly an equal number of both positive and negative sense strands. When the DNA was released from the particles it reannealed to its complementary strand and the genome appeared to be doublestranded. This was puzzling because the AAV particles are not large enough to hold a doublestranded DNA molecule. When the researchers used conditions, such as high temperature or high pH, where the two strands could not reanneal, they observed the result of single-stranded DNA molecules.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 21
Question type: Multiple Choice
1) The simian virus 40 (SV40) was isolated from which of the following? a) Mouse tissue extracts. b) Monkeys used for HIV research. c) Hepatitis virus B vaccine. d) Cells used to produce poliovirus vaccine. e) Human adenoidal tissue. Answer: d
2) Under which of the following conditions do polyomaviruses cause tumors in their hosts? a) Injection of high titers in young animals. b) Injection of high titers in older animals. c) Exposure to the virus via an aerosol. d) Exposure to particularly tumorigenic strains of the virus. Answer: a
3) Which of the following describes the structure of the polyomavirus capsid? a) 72 capsomeres composed of hexamers of VP1 b) 72 capsomeres composed of pentamers of VP1 c) 60 capsomeres composed of hexamers of VP1 d) 60 capsomeres composed of pentamers of VP1 e) 12 capsomeres composed of pentamers of VP1 with the remaining capsomeres composed of hexamers of VP1 Answer: b
4) Which of the following cellular proteins are packaged into the polyomavirus virions? a) Tubulin monomers. b) Actin monomers. c) Histone octomers.
d) Myristylated proteins. e) Transcription factors. Answer: c
5) If the histone proteins are removed from genome of SV40, which of the following will happen? a) The DNA becomes supercoiled. b) The DNA becomes nicked. c) The DNA assumes a relaxed circle form. d) The DNA becomes denatured. e) Nothing happens to the DNA. Answer: a
6) Which of the following enzymes can permanently remove supercoiling from circular DNA molecule? a) Histones b) Restriction endonuclease c) DNA ligase d) Topoisomerase I e) DNA gyrase Answer: d
7) The intergenic region on the SV40 chromosome contains DNA sequences that control which of the following processes? a) Early gene transcription. b) Late gene transcription. c) DNA replication. d) mRNA splicing. e) All of the above EXCEPT “d” are correct. Answer: e
8) The nuclear localization signal on which of the following proteins directs the SV40 genome into the nucleus of the infected cell? a) Importin
b) VP1 c) VP2 d) Histone 2A e) Large T antigen Answer: b
9) Which of the following mechanisms is used by SV40 to produce several proteins from a single transcription unit? a) Use of alternative start codons. b) RNA editing. c) Alternative mRNA splicing. d) Ribosomal frameshifting. e) All of the above. Answer: c
10) The SV40 large T antigen contains all of the following functional protein domains EXCEPT: a) Transactivation domain b) DNA helicase domain c) ATPase domain d) Spliceosome binding domain e) DNA binding domain Answer: d 11) The large T antigen from SV40 can bind to all of the following cellular proteins EXCEPT…. a) Poly(A) polymerase b) DNA polymerase c) p53 d) pRb e) p300 Answer: a
12) SV40 induces the infected cell to enter the S phase of the cell cycle. What purpose does this serve for the virus? a) The virus requires the breakdown of the nuclear envelope.
b) The virus requires the cellular splicing enzymes present during S phase. c) The virus requires transcription factors made during S phase. d) The virus requires the RNA polymerase II only present during S phase. e) The virus requires the DNA replication enzymes made during S phase. Answer: e
13) The small T antigen of SV40 regulates the cell cycle of the host cell by DIRECTLY doing which of the following? a) Turning on transcription of cyclin D1. b) Turning on the activity of the MAP kinase. c) Inhibiting the activity of the PP2A phosphatase. d) Phosphorylating the transcription factor AP1. e) Inactivating the p53 protein. Answer: c
14) The SV40 middle T antigen can activate cell metabolism and the cell cycle by doing which of the following? a) Binding to MAP kinase and activating it. b) Interacting with the cellular c-Src protein. c) Inactivating the PP2A phosphatase. d) Interacting with the pRb protein. e) Binding to and cleaving the p300 protein. Answer: b
15) Binding of the large T antigen of SV40 to the cellular protein pRb causes which of the following to occur? a) Degradation of the cellular protein p53 b) Activation of the apoptosis pathway. c) Replication of viral DNA d) Dissociation of the transcription factor E2F. e) Blocks progression through the cell cycle. Answer: d
16) Which of the following describes a function of the large T antigen from SV40?
a) Binds to early promoters and inhibits transcription of early mRNAs. b) Induces new transcription factors that leads to late gene transcription. c) Binds to the viral origin of replication and separates the DNA strands. d) Binds to the cellular p53 protein, which prevents apoptosis. e) All of the above are correct. Answer: e 17) Which of the following must occur in nonpermissive cells which become transformed by the polyomavirus SV40? a) The viral origin of replication must become inactivated. b) Cellular DNA becomes packaged into virions. c) The early viral genes become integrated into the host chromosome. d) The Rb protein becomes bound to E2F. e) The large T antigen proteins become degraded. Answer: c Question Type: True/False 18) Most individuals who were born in the US between 1941 and 1961 have been accidentally injected with SV40 contaminated poliovirus vaccine. Answer: True 19) Polyomaviruses are a major infectious cause of human cancers. Answer: False 20) Studying the circular genomes of polyomaviruses allowed scientists to study the different properties of supercoiled DNA. Answer: True 21) The enhancer sequence on the SV40 chromosome is located on the opposite side of the genome from the intergenic region. Answer: False
22) If the smallest introns in the SV40 genome are lengthened, then the levels of the Large Tantigen increase. Answer: False 23) SV40 will only transform cells which are nonpermissive for productive viral infection. Answer: True Question type: Essay 24) While SV40 can not cause tumors in monkeys or humans, it can transform rodent cells. Explain the molecular mechanisms that cause this to happen. Answer: When SV40 infects monkey or human cells, which are permissive for viral replication, the virus completes the entire infectious cycle and produces new virions. This leads to the death of the host cell. Cells that die from virus infection can not become transformed and cause tumors. When SV40 infects mouse or rat cells, the virus is able to only complete part of the infectious cycle yet can not produce new virions. This does not lead to the death of the host cell. Since the large T antigen is produced at the start of the infectious cycle and forces the cell into the S phase, the cell is left in an altered state but is not killed by the virus. If the early genes become integrated into the host chromosome, then there is a continuous supply of large T antigen, which keeps the cell in the S phase and causes transformation of the cell. 25) The polyomavirus SV40 has been used as an in vitro model for studying the biochemistry of DNA replication in mammalian cells. Explain why SV40 is a good model for studying this process. Answer: SV40 was chosen as a model for studying mammalian DNA replication because it has a small genome and the replication of the viral genome is almost completely dependent on the host cell DNA replication proteins. The only two viral components that are required to direct the cellular replication machinery to replicate the viral chromosome are the viral origin of DNA replication and the large T antigen protein. This allowed scientists to insert the SV40 origin on a plasmid, which could then be isolated in large amounts from bacteria. By mixing the origin containing plasmid with large T antigen and cellular extracts or purified proteins together in a tube with the plasmid, they could identify the components required for complete replication of DNA.
26) The large T antigen of SV40 is a highly multifunctional protein. Describe three of the most important functions that this protein has in regulating the infection of a host cell with SV40.
Answer: Large T antigen is absolutely required for infection of a host cell with SV40. The most critical functions that it performs are: 1) it binds to cellular proteins and disrupts normal regulatory events. This includes binding to the pRb protein, which releases the E2F transcription factor and allows the cell to enter the S phase of the cell cycle. This also initiates transcription of genes that produced proteins and enzymes involved in DNA replication, which SV40 will need to replicate its own DNA. Large T antigen also binds to p53, which prevents the host cell from entering apoptosis, which would lead to premature death of the cell. 2) it binds to the viral origin of replication, acts as a helicase to unwind the viral DNA, and binds to the cellular DNA polymerase and other replication proteins. This targets the cellular replication machinery to the viral DNA and allows the genome to be replicated. 3) it regulates transcription of the viral genes. T antigen binds to sites in the intergenic region and associates with the cellular transcription factor TBP, which stabilizes the transcription complex on the DNA and activates transcription of the early genes. At late times of infection, high levels of large T antigen then downregulate transcription of early genes, which allows for negative autoregulation. Finally, T antigen induces cellular transcription factors which turn on transcription of the viral late genes.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 22
Question type: Multiple Choice
1) Which of the following is thought to be the reservoir for human papilomaviruses? a) Cottontail rabbits b) Surfaces contaminated with papillomaviruses. c) Human male genital tract. d) Human female genital tract e) Both male and female genital tracts. Answer: e
2) The human papillomavirus can produce condylomas. What is the more common term to describe this type of skin lesion? a) Rash b) Genital wart c) Canker sore d) Cold sore e) Skin ulcer. Answer: b
3) Productive infections with human papillomaviruses have been difficult to study in cultured cells. Which of the following explains why? a) They only infect human cells in culture. b) They only produce a few virions per infectious cycle. c) The viral particles are difficult to purify. d) They only produce virions in differentiated keratinocytes. e) They induce a strong interferon response in infected cells. Answer: d
4) The papillomaviruses used to be classified in the same family as the polyomaviruses. Which of the following is a feature that distinguishes them from polyomaviruses?
a) Transcription of their genome only occurs on one strand. b) Their genome is composed of double-stranded DNA. c) Their virion is a naked capsid composed of 72 capsomeres. d) Their genome is associated with cellular histones in a minichromosome. e) They produce proteins that interact with pRb and p53. Answer: a 5) Which of the following cellular events causes the papillomavirus to enter “vegetative replication”? a) Induction of the apoptosis pathway. b) Entry into the S phase of the cell cycle. c) Terminal differentiation of keratinocytes. d) Cell division of the host cell. e) Transformation into a cancer cell. Answer: c
6) When the late promoter of papillomaviruses is activated, it increases production of the E1 and E2 proteins. Which of the following explains why an increase in these two proteins would contribute to vegetative replication of the virus? a) They repress transcription for the early promoter. b) They can cause the keratinocytes to become differentiated. c) They initiate DNA replication of the viral genome. d) They interact with the cellular protein pRb. e) They interact with the cellular protein p53 Answer: c
7) Which of the following proteins from papillomavirus can bind to the viral origin of DNA replication and unwind the DNA strands? a) E1 b) E2 c) E6 d) E7 e) L1 Answer: a
8) The E2 protein from papillomaviruses can bind to the viral DNA and to mitotic chromosomes. What purpose might this serve for the virus? a) It is important for regulating viral gene expression. b) It assists with the replication of the viral chromosome. c) It allows the viral DNA to be bound by cellular histones. d) It allows the viral DNA to segregate to each daughter cell. e) It improves the stability of the viral DNA. Answer: d
9) Papillomaviruses replicate in differentiated keratinocytes, which are not actively dividing. How does the virus handle this situation? a) They encode their own DNA replication enzymes. b) Plasmid replication in the basal cells produces enough copies of the viral genome. c) The viral E2 protein directly activates transcription of DNA replication genes. d) The viral E6 protein binds to the p53 protein, causing it to be degraded. e) The viral E7 protein binds to the pRb protein, forcing the cell into S phase. Answer: e
10) Cervical tumors caused by human papillomavirus do not show the typical mutations in the p53 gene that most cancer cells have. Which of the following explains why? a) The virus is not sensitive to the effects of p53. b) The E6 protein causes the degradation of the p53 protein. c) Apoptosis does not occur in cervical epithelium. d) Cervical epithelial cells do not express p53. e) The E7 protein binds to pRb, preventing it from inducing apoptosis. Answer: b
11) Which of the following describes the mechanism used by the E6 protein of papillomaviruses to remove the p53 protein. a) It causes the p53 protein to be exported out of the cell. b) It causes the p53 protein to be targeted to the lysosome. c) It causes the p53 protein to become ubiquinated. d) It acts as a protease to directly degrade the protein. e) It phosphorylates p53, which causes it to be degraded by the proteasome. Answer: c
12) The E6 proteins from highly oncogenic papillomaviruses have been shown to interact with cellular proteins, which control cell polarity and proliferation, that contain which of the following protein domains? a) Zinc-finger domain b) Activation domain c) DNA binding domain d) Homeobox domain e) PDZ domain Answer: e
13) The E7 protein from papillomavirus stabilizes the cellular p53 protein, which leads to cell cycle arrest. Which of the following explains the mechanism by which p53 causes cell cycle arrest? a) p53 activates transcription of p21, which blocks phosphorylation of pRb. b) p53 binds to pRb and causes it to release the E2F transcription factor. c) p53 binds directly to p21 and causes it to become degraded by the proteasome. d) p53 binds to the viral E6 protein, which causes it to be degraded by the proteasome. e) All of the above are correct. Answer: a
14) The cultured human cell line HeLa expresses the E6 and E7 proteins of human papillomavirus. What would happen to these cells if the expression of these proteins was shut off? a) They would continue to grow at their usual pace b) They would continue to grow, just more slowly. c) They enter the G0 phase of the cell cycle. d) They go into apoptosis and die. e) They become even more tumorigenic. Answer: d
15) Which of the following describes the form that the papillomavirus genome is found in most cervical cancer cells? a) The entire viral genome is integrated into the genome of the host cell. b) A fragment of the genome is integrated into the genome of the host cell. c) The intact viral genome remains an episomal plasmid.
d) A fragment of the viral genome remains as an episomal plasmid. e) Multiple copies of the genome are arranged in concatamers. Answer: b
16) Which of the following describes the best treatment for papillomavirus induced cervical lesions? a) Vaccination with the vaccine against HPV. b) Radical surgery to remove the uterus and cervix. c) Removal of the lesion using a laser. d) Injection of antibodies against HPV into the lesion. e) Giving the patient systemic anticancer drugs. Answer: c
17) The currently available HPV vaccines contain virus-like particles composed of which of the following? a) L1 protein alone b) L1 protein and viral DNA c) L1 and L2 proteins. d) L1 and L2 proteins and viral DNA. e) E6 and E7 proteins. Answer: a Question Type: True/False 18) In papillomaviruses, plasmid replication produces a large number of viral genomes which will be packaged into new virions. Answer: False 19) The E7 proteins from the oncogenic strains of papillomaviruses bind to pRb more tightly than the E7 proteins from nononcogenic strains of the virus. Answer: True 20) Mutations in the p53 gene are seen in over 50% of human tumors.
Answer: True 21) Very few cases of cervical cancer are caused by infection with papillomavirus. Answer: False 22) Cervical cancer cells, which have been transformed by the papillomavirus, are still capable of producing large amounts of virus particles. Answer: False 23) The Pap test, named after George Papanicolaou, screens for the presence of cancer cells in the cervix. Answer: True Question type: Essay 24) Explain the roles that plasmid replication and vegetative replication play in the life cycle of papillomaviruses as they infect stratified epithelium. Answer: Papillomaviruses initially infect the basal layer of cells in stratified epithelium. These cells are actively dividing. After an initial burst of replication that increases the number of viral genomes in each cell to 50 to 100 copies, the virus enters the plasmid replication stage. This is where the virus replicates each genome once per cell cycle so that each daughter cell will receive an equal number of viral genomes. Terminal differentiation of the epithelial cells triggers the virus to enter vegetative replication stage. This turns on transcription of the late promoter, which also increases the levels of the E1 and E2 proteins, which are involved in rapid replication of the viral genome and the producing of a high number of genomes. Finally, production of the L1 and L2 capsid proteins induces the assembly of new virions, which are shed along with the outer layer of cells. 25) Discuss the differences between the oncogenic papillomaviruses, strains 16 and 18, from the more benign virus strains that lead to higher incidence of cervical cancer. Answer: Most of the differences between the oncogenic strains of papillomavirus, particularly strains 16 and 18, and the less oncogenic strains, are in the E6 and E7 proteins, which are the primary oncogenes in papillomaviruses. Some of the differences include which cellular proteins E6 and E7 bind to and the strength of that binding. For example, the E7 protein from the
oncogenic strains of virus bind more tightly to the Rb protein than do the E7 proteins from the nononcogenic virus strains. In addition, the oncogenic E7 proteins can target Rb for ubiquination, which causes it to be degraded by the cellular proteasome. There are differences in the E6 proteins from the oncogenic strains as well. The E6 proteins from oncogenic strains, but not the more benign strains, targets the cellular p53 protein for degradation by the proteasome. Finally, the E6 proteins from the oncogenic strains can bind to cellular proteins that contain PDZ domains, which are involved in cell proliferation and cell polarity.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 23
Question type: Multiple Choice
1) Which of the following was NOT studied or discovered in adenoviruses? a) mRNA splicing b) Transcription initiation by RNA polymerase II c) Regulation of protein translation. d) Proteins involved in regulating transcription. e) Use of viruses as gene therapy vectors. Answer: c
2) Adenovirus virions are composed of which of the following components? a) Hexons composed of trimers of the hexon protein. b) Penton bases composed of five copies of the penton protein. c) Penton fibers composed of trimers of polypeptide IV. d) Basic polypeptides bound to the viral DNA. e) All of the above are correct. Answer: e
3) Adenovirus virions are transported to the nucleus of the host cell via an interaction between the hexon proteins and which of the following cellular structures? a) Nuclear matrix b) Microtubules c) Actin fibers d) Intermediate filaments e) Endocytotic vesicles. Answer: b
4) Which component of the adenovirus virion binds to the host cell receptor? a) Knob on the fiber protein. b) Penton base.
c) Hexons. d) Minor capsid proteins. e) Both “a” and “b” can bind to different receptors. Answer: e
5) What is the structure of the ends of the adenovirus genome when it is released from the virion into the nucleus? a) There are no ends – the viral genome is a closed circle. b) There is a single 5’ phosphate. c) There is a triphosphate at the 5’ end. d) The terminal protein is covalently bound to the 5’ end. e) The ends are paired to each other in a panhandle formation. Answer: d
6) What is the function of the VA RNAs produced by adenovirus? a) Inhibition of the cellular RNA polymerase III. b) Inhibition of the interferon induced PKR kinase. c) Stimulation of translation of viral mRNAs. d) Regulation of mRNA stability. e) Inhibition of the adaptive immune system. Answer: b
7) All of the following are involved in determining the type of mRNAs produced during adenovirus infection EXCEPT….. a) Transcription initiation by RNA polymerase II. b) Location of the transcriptional promoters. c) Location of the start codons. d) Alternative mRNA splicing. e) Alternative polyadenylation sites. Answer: c
8) During the cell cycle in an uninfected cell, the cellular protein Rb represses S phase genes by doing which of the following? a) Localizes histone deacetylase to E2F inducible genes.
b) Binds to the adenovirus E1A protein and releases E2F. c) Prevents binding of the cellular RNA polymerase II to E2F inducible genes. d) Binds and phosphorylates the cyclin dependent kinase. e) Prevents the binding of E2F to the promoters of S phase genes. Answer: a
9) The CR3 region, found on the13S version of the E1A protein, is involved in activation of transcription by binding to which of the following proteins? a) CBP b) TBP c) ATF d) CBP and TBP e) ATF and TBP Answer: e
10) Which of the following describes the function of the terminal protein in the replication of the genome of adenovirus? a) It ligates the viral genome into a circular molecule. b) It produces the RNA primer. c) It binds single-stranded DNA and prevents reannealing. d) It acts as the primer for DNA replication. e) It acts as the DNA polymerase. Answer: d
11) During infection with adenovirus which of the following events activates the production of the major late transcripts? a) Entry of the viral genome into the nucleus. b) Replication of the viral genome. c) Transcription of the E1A gene. d) Transcription of the E1B gene. e) Transcription of the E2 gene. Answer: b
12) There are five families of mature transcripts produced from the major late gene of adenovirus. Which of the following is the MAJOR determinant for which family is produced from the primary transcript? a) The location of the polyadenylation site. b) The location of the 5’ splice site. c) The location of the 3’ splice site. d) The location of the transcription start site. e) The location of the start codon. Answer: a
13) The E1A protein from adenovirus indirectly stabilizes the cellular p53 protein. Why is this potentially a problem for the virus? a) This will activate the adaptive immune response against virally infected cells. b) This will initiate the RNAi pathway, which leads to degradation of viral RNA. c) This will induce the apoptosis pathway, which leads to cell death. d) The virus requires active p53 protein to activate viral genes. e) The virus does not use p53, so this is not a problem at all. Answer: c
14) The proteins produced from which of the following genes from adenovirus serves to suppress apoptosis in infected cells? a) E1A b) E1B c) E2 d) E3 e) Major late gene Answer: b 15) The E2 gene encodes all of the following proteins involved in replicating the adenovirus genome EXCEPT: a) DNA polymerase b) Preterminal protein. c) Single-stranded DNA binding protein. d) Ligase e) All of these proteins are encoded by the E2 gene. Answer: d
16) The tripartite leader found on all of the transcripts produced from the major late gene of adenovirus carries out which of the following functions? a) It makes the mRNA more stable. b) It binds to the eIF4F translation factor. c) It shunts the ribosome to the correct AUG on the mRNA. d) It assists with transport of the mRNA out of the nucleus. e) It improves the efficiency of mRNA splicing. Answer: c
17) If the E1A gene is transfected into cultured cells, it causes an abortive transformation and the cells die. If the E1B gene is included with E1A, then cells become fully transformed and survive. What critical function does the E1B gene provide? a) The E1B proteins suppress apoptosis. b) The E1B proteins prevent the degradation of the p53 protein. c) The E1B proteins assist with transport of mRNAs out of the nucleus. d) The E1B proteins bind to Rb and cause the cell to enter S phase. e) The E1B proteins activate transcription from p53 inducible promoters. Answer: a Question Type: True/False 18) The E1A protein from adenovirus can act as an oncogene by inducing tumors in experimental animals. Answer: True 19) Binding of histone deacetylases to the promoters of genes leads to activation of transcription from that promoter. Answer: False 20) During DNA replication of the adenovirus genome, the virus only uses continuous synthesis, which means that it does not produce Okazaki fragments. Answer: True
21) The unique 5’ cap and 3’ poly(A) tail in the late transcripts of adenovirus allow the ribosome to begin translation at the correct start codon. Answer: False. 22) Transcription from the major late promoter of adenovirus produces a primary transcript that is over half the length of the virus genome. Answer: True 23) When rodent cells are infected with adenovirus, they produce virions and are killed by the virus. Answer: False 24) Because adenovirus produces all of the enzymes it needs for DNA replication, it is not dependent on the host cell entering the S phase of the cell cycle. Answer: False Question type: Essay 25) Adenovirus has a linear double-stranded DNA genome. Describe how adenovirus DNA is replicated so that the “end problem” is solved. Answer: Adenovirus has an unusual solution to solving the problem of completely replicating the ends of linear DNA. Unlike other DNA viruses, it uses the preterminal protein as the primer on which DNA synthesis begins. Because there is no RNA primer that is then removed there is no gap at the 5’ end of the new strand and therefore no “end problem”. The presence of a cytosine, which is covalently attached to a serine amino acid in the preterminal protein, base pairs with the guanosine on the template strand. The viral DNA polymerase then uses this protein as the primer and begins synthesis of the new strand of DNA in a continuous fashion until it reaches the end. This displaces the nontemplate strand which is bound by the viral single-strand DNA binding protein. This displaced strand forms a noncovalent circle because of basepairing of the terminal repeats, which forms a “panhandle”. This resembles the ends of the original DNA molecule and a new preterminal protein binds, allowing DNA polymerase to created a second strand of DNA.
25) A strain of adenovirus, called ONYX-015, that does not express the E1B 55K protein, is being studied as a treatment for cancer. Why does the lack of E1B 55K allows this virus to spread and kill cancer cells but not normal cells? Answer: The major function of the E1B 55K protein in adenovirus is to suppress the function of the cellular protein p53 and prevent the cell from entering apoptosis. During infection of a normal cell, the E1B protein allows the cell to stay alive long enough to complete the viral replication cycle and produce new virions. The ONYX-015 virus, which lacks the EIB 55K protein, will not productively infect normal cells because without the ability to inhibit apoptosis, the cell will die before it can produce new virus particles. However, most human tumors have a mutated or missing p53 gene, which means that they do not produce p53 and can not enter the apoptosis pathway. This means that the ONYX-015 adenovirus strain can complete the infectious cycle in these tumor cells and spread to new tumor cells. But as soon as this virus enters a normal cell, the production of new viral particles will cease and the infection will be terminated.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 24
Question type: Multiple Choice
1) Which of the following is a disease NOT caused by a member of the herpesvirus family? a) Cold sores. b) Chickenpox c) Common cold. d) Encephalitis. e) Hepatitis. Answer: c
2) Which of the following two herpesviruses have been associated with human cancers? a) Herpes simplex 1 and 2 b) Herpes simplex 1 and varicella-zoster virus. c) Epstein-Barr virus and cytomegalovirus. d) Epstein-Barr virus and Kaposis’ sarcoma virus e) Human herpesvirus virus 6 and 7. Answer: d
3) What is unusual about the structure of the genome of herpes simplex virus? a) It is a covalently closed circle. b) It has two unique sequences flanked by inverted repeats c) It has one long unique sequence flanked by terminal repeats. d) It is linear with a terminal protein bound to each of the 5’ ends. e) It consists of two DNA segments. Answer: b
4) Which of the following characteristics of the virion of herpesviruses is atypical of most enveloped viruses? a) There is an amorphous protein layer between the capsid and envelope. b) The capsid is composed of both a major and a minor protein.
c) The envelope contains multiple glycoproteins. d) The capsid has icosahedral structure. e) The DNA is packaged through a portal protein. Answer: a
5) Which of the following is NOT used a host cell receptor for herpes simplex virus? a) Proteoglycans. b) Nectin 1 c) Integrin d) Heparan sulfate. e) Herpesvirus entry mediator Answer: c 7) The genes of herpes simplex are expressed at which time point during the viral replication cycle? a) Immediate-early b) Early c) Delayed-early d) Late e) Delayed-early and late Answer: a 8) Which of the following describes the function of the -TIF/VP16 protein from herpes simplex virus? a) It shuts off expression of cellular proteins. b) It activates transcription of immediate-early genes. c) It uncoats the viral DNA at the nuclear pore. d) It represses transcription of immediate-early genes. e) It is required for the transition between a and b gene expression. Answer: b
9) Which of the following viral glycoproteins from herpes simplex virus are involved with fusion of the envelope with the cellular plasma membrane? a) gH and gL
b) gB c) gC d) gD e) All of the above. Answer: a 10) Which of the following describes the major function of the proteins made from the genes of herpes simplex virus? a) Replication of the viral DNA. b) Assembly of the capsid. c) Regulation of viral gene expression. d) Inhibition of the production of antibodies. e) Formation of the tegument and envelope. Answer: c
11) Which of the following events during assembly of herpesvirus virions causes the scaffolding proteins to be ejected from the capsid? a) Conformational change that seals the capsid. b) Cleavage of the scaffolding proteins by a cellular protease. c) Acquisition of the tegument around the capsid. d) Insertion of the portal protein into one of the 12 vertices. e) Packaging of the viral DNA into the capsid. Answer: e
12) In addition to encoding enzymes and proteins directly involved in replicating the viral genome, herpes simplex virus also encodes thymidine kinase and ribonucleotide reductase, which are absolutely required for infection of neurons. Which of the following explains what role these proteins play? a) They phosphorylate cellular proteins, which force the neuron into S phase. b) They increase the pool of nucleotide triphosphates required for DNA replication. c) They phosphorylate the tegument proteins before they are packaged into the virion. d) They cleave the concatemers of the viral DNA as they are being packaged into capsids. e) They help assemble the DNA replication complex on the viral origin. Answer: b
13) A few of the latency-associated transcripts (LATs) from herpes simplex virus have an unusual structure. Which of the following describes how they are unusual? a) They are covalently closed circular RNA. b) They have a high degree of secondary structure. c) They have two separate open reading frames. d) They represent a stable intron lariats. e) They form double-stranded RNA with the ICP0 mRNA. Answer: d
14) The EBNA1 protein is absolutely required for replication of the genome of Epstein-Barr virus during latent infection of B lymphocytes. Which of the following is NOT a function of the EBNA1 protein? a) Binds to multiple sites on the oriP. b) Serves as the primer for DNA replication. c) Directs cellular replication enzymes to the viral genome. d) Segregates the viral DNA into daughter cells. e) Enhances expression of the latency genes. Answer: b
15) Both HSV and EBV, which are members of the herpesvirus family, have mechanisms that prevent the immune system from recognizing and killing infected cells. Which of the following explains why this is important? a) Herpesviruses are maintained in the host for life in a latent infection. b) Herpesviruses are very sensitive to the effects of the immune system. c) Herpesviruses are rarely transmitted to new hosts. d) Herpesviruses infect cells that are components of the immune system. Answer: a
16) Epstein-Barr virus particles released from infected B lymphocytes have reduced infectivity for B lymphocytes but enhanced infectivity for epithelial cells. Which of the following explains this phenomenon? a) Epithelial cells have higher levels of the HVEM receptor protein. b) B lymphocytes do not contain the correct host cell receptor. c) B lymphocytes have MHCII protein, which binds to the viral gp42 protein. d) The viral envelope glycoproteins are not processed correctly in B lymphocytes.
e) Lymphocytes have different lipids in their membranes, which inhibit fusion of the viral envelope. Answer: c
17) Which of the following describes the distinguishing features of the three types of latency exhibited by the Epstein-Barr virus? a) Whether the viral DNA is integrated into the host chromosome or not. b) The number of copies of the viral genome maintained. c) The type of envelope glycoproteins on the cell surface. d) The cell types that are latently infected. e) The number and type of EBNA and LMP genes expressed. Answer: e
18) Herpes simplex virus (HSV) maintains a latent infection in neurons while Epstein-Barr virus (EBV) maintains latency in B lymphocytes. While EBV maintains a low level of viral DNA replication, HSV does not replicate its genome at all during latency. Which of the following explains this difference? a) B lymphocytes degrade some of the EBV genomes. b) Neurons are a non-dividing cell type while B cells still divide. c) HSV integrates its genome into the host cell genome while EBV does not. d) Neurons replicate much more quickly than B cells. e) Neurons live for the life of the host and never die. Answer: b
Question Type: True/False
19) During one round of infection with the herpes simplex virus, all four isoforms of the viral genome are produced. Answer: True
20) Herpesviruses hardly ever cause serious or fatal infections, even in patients with reduced immune function. Answer: False
21) The ICP27 protein from herpes simplex inhibits cellular gene expression by inhibiting mRNA splicing. Answer: True
22) The EBER RNAs encoded by the Epstein-Barr virus are synthesizes by RNA polymerase III. Answer: True
23) Epstein-Barr virus particles produced in B lymphocyes will infect other B lymphocytes with a higher efficiency than they will infect epithelial cells. Answer: False
24) The symptoms of mononucleosis, which include an enlarged spleen and fatigue, are caused by the expansion of infected B lymphocytes soon after primary infection. Answer: True
Question type: Essay
25) Describe what happens during a primary infection with herpes simplex virus I (HSVI), how the virus enters into latency, and then how the virus can be reactivated back to a lytic infection. Your answer should focus on the cell types affected by each stage of the infection. Answer: When HSVI initiates a primary infection it enters a epithelial cell, usually near the mouth. This initial infection is productive and new virions are released from the epithelial cells. The damage to the cells, in addition to the immune response to this primary infection, leads to the typical cold sore of a HSVI infection. From the epithelial cell, virions infect nearby sensory neurons. The virus enters the neuron and undergo retrograde transport along axons to the cell nucleus. Here the viral genome is maintained as a circular episome, transcription is repressed, and there is no viral DNA replication. The virus can be maintained in this latent state in the neurons for the life of the host. Sometimes a local or systemic stimuli – stress, fever, or sunlight – can induce the virus to exit the sensory neuron and travel back to the site of the primary infection, where it will infect epithelial cells an cause a new cold sore in the process.
26) Both herpes simplex virus and Epstein-Barr virus have multiple mechanisms to suppress both cellular antiviral pathways as well as allow latently infected cells to hide from the adaptive immune system. Describe two of these mechanisms used by either virus.
Answer: Herpes simplex virus: Virion host shut-off factor – degrades RNAs that encode proteins involved in the interferon pathway. ICP27 – inhibits splicing of cellular mRNA, limiting cellular antiviral effects. ICP47 – binds to the transporter of antigenic peptides (TAP1/TAP2) and blocks translocation of peptides into the ER and prevents their presentation on MHC I of infected cells. ICP34.5 – binds to protein phosphatase 1a and redirects it to remove the phosphate added to eIF2, which is part of the anti-viral effects of the interferon induced PKR kinase. ICP0 – leads to the degradation of several components of the ND10 sites, including PML. Without PML, cells can not respond appropriately to exogenous interferon. Multiple viral genes that block cellular apoptosis pathway. Epstein-Barr virus: The EBV encoded RNAs (EBERs) bind and inhibit the interferon induced PKR kinase. Micro-RNAs – target multiple cellular proteins involved in the cellular immune response as well as the adaptive immune response.
27) From an evolutionary perspective, herpesviruses have been very successful pathogens in the human population since they are so widely distributed and only cause severe disease in rare circumstances. Describe some of the biological characteristics of herpesviruses that have allowed them to be so successful. Answer: Herpesviruses have co-evolved with their specific mammalian hosts to become highly successful pathogens. Because they are large complex viruses that encode a large number of proteins, they can interact with their hosts in highly specific ways. Probably the single evolutionary advantage that herpesviruses have is that they infect their hosts for life because they maintain a latent infection. This allows them to undergo asymptomatic reactivation, which very effectively transmits the virus to naïve hosts, allowing the virus to be spread widely in the population. Most herpesviruses are transmitted to young hosts, where they rarely cause severe disease. This ensures that every member of the population is infected early in life and will maintain the virus for the life of the host. Most of the disease causes by herpesviruses is a result of recent events – maintaining good hygiene that prevents exposure to these viruses until later in life, using immunosuppressive drugs in transplant patients, and the introduction of HIV and AIDS into the human population.
28) Explain the three models proposed for how newly assembled herpesvirus nucleocapsids exit the nucleus and acquire the tegument and envelope/ Answer: Model #1 suggests that the tegument and glycoproteins associate with the inner nuclear membrane. The nucleocapsids bud through the inner nuclear membrane into the perincuclear space, acquiring the tegument and envelope. The enveloped virion is then taken up into a vesicle that moves through the secretory pathway. Model #2 states that the virion buds from the nucleus into the perinuclear space and then back out into the cytoplasm. The nucleocapsid then buds into a cytoplasmic vesicle acquiring the tegument and envelope in the process. Model #3 is a
variation of Model#2 and suggests that nucleocapsids leave the nucleus via enlarge nuclear pores. Once they are in the cytoplasm, the bud into a vesicle to acquire the tegument and envelope.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 25
Question type: Multiple Choice
1) A great deal of research has gone into making baculoviruses more pathogenic and deadly to their hosts. Which of the following explains why? a) They are investigated as germ warfare agents. b) They could be used to destroy weeds and other undesirable plants. c) They could be used as pesticides to kill insects. d) They kill bacteria and could be used as antibiotics. e) They could be used to kill cancer cells. Answer: c
2) Which of the following groups of organisms is the primary host for baculoviruses? a) mammals b) insects c) plants d) bacteria e) worms Answer: b
3) Which of the following is an unusual feature of baculovirus infections? a) They produce two distinct types of virions. b) The virion has two separate envelopes. c) The virion contains a tegument layer. d) They package more than one copy of the genome into a nucleocapsid. e) They replicate their DNA genome in the cytoplasm. Answer: a
4) How do the hosts of baculoviruses typically become infected with the virus? a) They are injected with virus by a parasitic wasp b) They hatch from an infected egg.
c) They breathe in aerosoled virus particles. d) They feed on virus contaminated plants. e) They mate with an infected host. Answer: d
5) The budded virions produced during a baculovirus infection are primarily involved in which of the following? a) Shutting down host defense mechanisms. b) Surviving the harsh conditions of the environment. c) Transmission via eggs laid by an infected female. d) Transmission between different hosts. e) Transmission of the virus between cells within a host. Answer: e
6) The occlusion bodies of baculovirus consist of a single protein. Which of the following is this protein? a) polyhedrin b) occludin c) tegument d) GP64 e) baculin Answer: a
7) All of the following describe differences between the budded and occluded virions of baculovirus EXCEPT: a) Occluded virions can survive in the environment better than budded virions. b) Occluded virions usually contain more than one viral genome. c) Occluded virions can infect a wider variety of insect species than budded virions. d) The tegument of occluded virions contains the GP41 tegument protein. e) Occluded virions are much less infectious in cultured cells. Answer: c
8) Which of the following describes the size and structure of the dsDNA genome of AcMNPV, a member of the baculovirus family?
a) Covalently closed circle of about 50kbp. b) Covalently closed circle of about 150kbp. c) Linear molecule of about 50kbp. d) Linear molecule of about 150kbp. e) Three linear segments of about 50kbp each. Answer: b 9) Treatment of baculovirus infected cells with the toxin -amanitin, which inhibits RNA polymerase II, does not reduce levels of the viral late transcripts. Which of the following explains why? a) Baculoviruses use the cellular RNA polymerase III to transcribe their late genes. b) Baculoviruses produce their own RNA-dependent RNA polymerase. c) Baculoviruses produce their own DNA-dependent RNA polymerase. d) Baculoviruses produce such high levels of the late mRNAs that the inhibition does not matter. e) Insect cells do not use RNA polymerase II to transcribe their genes. Answer: c
10) The late and very late genes of baculoviruses contain promoters that have sequences that are distinct from those of the host cell promoters. Which of the following explains why? a) These unique sequences bind the cellular RNA polymerase more tightly. b) The virus uses virus specific transcription factors to regulate viral transcription. c) These sequences are recognized by the viral DNA polymerase. d) These sequences are recognized by the viral RNA polymerase. e) These sequences form a unique secondary structure that influences transcription. Answer: d
11) Which of the following proteins from baculovirus is responsible for transactivating the viral early genes and is the major regulator of viral gene expression? a) IE-0 b) IE-1 c) IE-2 d) PE38 e) LEF-1 Answer: b
12) The homologous repeat sequencs (hrs) found in the genome of baculoviruses are involved in which of the following viral events? a) Processing of mRNAs b) Translation of mRNAs c) Enhancement of transcription. d) Initiation of DNA replication. e) Both transcription and replication. Answer: e
13) What is the function of the products of the very late genes in baculoviruses? a) Replication of viral DNA. b) Death of the host organism. c) Assembly of budded virions. d) Assembly of occluded virions. e) Lysis of the host cell. Answer: d
14) Assays that were used to study baculovirus DNA replication had to distinguish the plasmid DNA that was originally transfected into the cells from the DNA that was replicated in the eukaryotic cells. Which of the following describes how this was accomplished? a) Digestion of DNA with a methylation dependent restriction enzyme. b) Using a southern blot to distinguish the different types of DNA. c) Using electron microscopy to distinguish the different types of DNA. d) Using standard agarose gel electrophoresis to measure different sizes of DNA. e) Measuring the sizes of the large DNA with a pulsed-field gel electrophoresis. Answer: a
15) All of the following distinguish the baculovirus RNA polymerase from the eukaryotic RNA polymerase II EXCEPT: a) The baculovirus RNA polymerase is only composed of 4 protein subunits. b) The baculovirus RNA polymerase is associated with a capping enzyme. c) The baculovirus RNA polymerase only recognizes viral promoters. d) The baculovirus RNA polymerase transcribes viral DNA in the cytoplasm. e) The baculovirus RNA polymerase is required for viral gene expression. Answer: d
16) Which of the following assays was used to identify the baculovirus late expression factors? a) A Southern blot b) A reporter assay using the luciferase gene. c) A reporter assay using the chloramphenicol acetyl transferase gene d) A DNA replication assay using the restriction enzyme DpnI. e) An in vitro transcription assay. Answer: c
17) Which of the following observations was the MOST crucial in the development of recombinant baculoviruses that can express large amounts of foreign proteins? a) Baculoviruses can enter mammalian cells but can not replicate. b) The polyhedrin gene is not essential for virus replication in cell culture. c) Viruses missing the polyhedrin gene can be distinguished from wild-type viruses microscopically. d) Recombinant viruses can produce large amounts of a foreign protein when introduced into insect cells in culture. e) The polyhedrin gene has a very strong promoter that produces large amounts of mRNA late in the infection. Answer: b Question Type: True/False 18) Baculoviruses can infect and replicate in human but do not cause any disease. Answer: False 19) The tubular nucleocapsids of baculovirus allows the virion to accept a longer genome than normal. Answer: True 20) Treatment of cells infected with baculovirus with -amanitin toxin will inhibit immediateearly or early but not late viral gene expression. Answer: True
21) Polyhedrin proteins from different baculoviruses have unique and different amino acid sequences. Answer: False 22) The budded or occluded virions of baculoviruses are identical in makeup except for the number of genomes they contains. Answer: False 23) During evolution of baculoviruses they appear to have acquired several genes from the genomes of their cellular hosts via recombination. Answer: True Question type: Essay 24) Describe some of the characteristics of baculoviruses that make them able to be used as safe pesticides to kill insects that are agricultural pests. Answer: Baculoviruses are large complex viruses that only infect insects, primarily those in the Lepidopteran order (moths and butterflies). Many of the caterpillars of these insects voraciously eat and destroy agriculturally important plants. Baculoviruses can not infect mammals and humans for two reasons: 1) the guts of humans are acidic, which will not allow the degradation of the occluded virus particles, which are the particles that are usually found in the environment, and 2) human and mammalian cells do not have the correct transcription factors necessary to induce transcription of baculovirus genes. Humans have been shown to be exposed to millions of baculovirus particles naturally found on edible plants and no human infections have ever been reported. This means that baculoviruses can be sprayed on agricultural crops and will quickly kill off the caterpillars while not harming the humans who will eventually eat the plants. 25) You want to express large amounts of a foreign protein in insect cells. Describe how you would prepare a recombinant baculovirus that would be able to do this. Assume that you have the DNA encoding the foreign gene. Answer: The DNA encoding the foreign protein of interest must be inserted into a transfer vector so that it will be expressed from the polyhedrin promoter and is between DNA sequences from the viral genome that will allow the gene to be recombined into the viral genome. Transfection of the transfer vector along with baculovirus genome DNA into insect cells allows the
recombination event to occur. The virus particles that are released from these cells will contain a mixture of wild-type viruses and recombinant viruses, which contain the gene of interest. A plaque assay on this mixed population will allow the identification of the recombinant viruses, since they will lack the polyhedrin protein and will not form occlusion bodies inside of infected cells. Plaque purification of the recombinant virus will allow it to be produced in a pure population. Infection of insects cells with this recombinant virus will cause large amounts of the foreign protein to be produced, which can then be purified form the infected cells.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 26
Question type: Multiple Choice
1) For most of human existence, which of the following was the approximate fatality rate from smallpox infection in the countries where it was endemic? a) 1% b) 10% c) 25% d) 50% e) 100% Answer: c
2) Which of the following describes the process of variolation, which was an early method to prevent smallpox infections? a) Exposure of children to milkmaids infected with cowpox. b) Quarantine of smallpox victims for 40 days. c) Use of plant extracts to prevent smallpox infection. d) Blowing powdered pock scabs into the nose. e) Exposure of young children to people with an active smallpox infection. Answer: d
3) Which of the following groups of organisms are the primary hosts for poxviruses? a) Humans b) Insects c) Plants d) Plants and insects. e) Birds, mammals and insects. Answer: e
4) Which of the following describes the structure of the vaccinia virus genome? a) Linear DNA with covalently closed ends.
b) Linear DNA with free ends. c) Linear DNA with protein-bound ends. d) Multiple linear DNA segments e) Covalently closed circle of DNA. Answer: a
5) The mRNAs of poxviruses do not undergo splicing. Which of the following explains why? a) Poxvirus genomes are small and they need to conserve genome space. b) Poxviruses replicate in the cytoplasm of infected cells. c) They do not need to regulate gene expression through alternative splicing. d) They do not encode the proteins that carry out mRNA splicing. e) Poxvirus mRNAs do not contain exons. Answer: b
6) Poxviruses produced two distinct types of virions. Which of the following describes the primary role of the extracellular virus particle? a) They regulate the host cell antiviral defenses. b) They are transmitted via an insect vector. c) They infect new cells and tissues within a single host. d) They are transmitted between hosts. e) They can survive harsh environmental conditions. Answer: c
7) Which of the following describes the major distinguishing feature of poxviruses when compared to other DNA containing viruses that replicate in eukaryotic cells? a) They encode their own DNA polymerase. b) They have large complex genomes that encode over 100 different proteins. c) They have large complex virions. d) They replicate exclusively in the cytoplasm of infected cells. e) They encode a wide-variety of regulatory proteins. Answer: d
8) Because poxviruses replicate exclusively in the cytoplasm of the host cell, they must encode which of the following enzymes?
a) DNA-dependent RNA polymerase. b) DNA-dependent DNA polymerase. c) mRNA processing enzymes. d) Enzymes to produce deoxoynucleotides. e) All of the above are encoded. Answer: e
9) During infection with poxviruses, all of the following proteins are produced from early genes EXCEPT: a) mRNA processing enzymes. b) Viral Intermediate Transcription Factor. c) Viral Early Transcription Factor. d) Viral DNA-dependent DNA polymerase. e) Viral DNA-dependent RNA polymerase. Answer: c 10) The gene regulation cascade of poxviruses is controlled by virus produced transcription factors. At what point in the virus replication cycle is the viral early transcription factor synthesized? a) Early b) Delayed Early c) Intermediate d) Late e) All of the above. Answer: d
11) If viral DNA replication is inhibited in poxviruses, which of the following genes will not be expressed? a) Gene encoding the mRNA processing enzymes. b) Genes encoding virion structural proteins. c) Genes encoding DNA replication enzymes. d) Gene encoding the RNA polymerase subunits. e) Genes encoding the nucleotide metabolism enzymes. Answer: b
12) If a purified poxvirus genome was heated to melt the hydrogen bonds holding the two strands of DNA together, which of the following would describe the structure of the genome? a) Multiple pieces of single-stranded DNA b) Two linear pieces of single-stranded DNA c) A covalently closed circle of double-stranded DNA. d) Two single-strand circles entwined together. e) A circle of single-stranded DNA. Answer: e 13) DNA replication in poxviruses uses a “rolling hairpin” model, similar to the method used by viruses in which of the following families? a) Parvoviruses b) Polyomaviruses c) Adenoviruses d) Herpesviruses e) Baculoviruses Answer: a 14) Intermediate and late transcripts from poxviruses have a unique “poly(A) head” near the 5’ end of the mRNA. What is the proposed function for this structure? a) It binds to the poly(A) tails at the 3’ end of the mRNA. b) It stabilizes and protects the 5’ end of the genome. c) It aids in recognition of the AUG start codon by ribosomes. d) It helps the nascent transcript bind to the viral RNA polymerase during transcription. e) It associates with the cap binding complex. Answer: c
15) Which of the following cellular components is used to help extracellular virus particles of poxviruses reach and infect neighboring host cells? a) Export vesicles. b) Actin containing microvilli. c) Microtubules. d) Golgi-derived cisternae e) Viroplasm. Answer: b
16) Poxviruses express viral proteins that interfere with all of the following host-defense systems EXCEPT: a) Interferon induced PKR kinase system. b) Complement system. c) Interleukin-1 cytokine activation. d) Production of antibodies by B lymphocytes. e) Tumor-necrosis factor activity. Answer: d
17) One of the strategies used by poxviruses to inhibit host defenses involves the synthesis of a viral serpin. What is the function of the serpin? a) It inhibits components of the complement system. b) It prevent the presentation of peptides on MHC-I. c) It is a soluble receptor for the tumor necrosis factor. d) It binds to the PKR kinase and inhibits its activity. e) It inhibits a serine protease that activates interleukin-1. Answer: e Question Type: True/False 18) Smallpox was named in 15th century France to distinguish it from “large pox” or syphilis. Answer: True 19) Smallpox was eliminated from the human population through the use of antiviral drugs. Answer: False. 20) We no longer vaccinate people for smallpox because there are no stocks of smallpox anywhere on the planet. Answer: False
21) Vaccinia virus virions do not need any host proteins to carry out transcription and processing of the early gene mRNAs. Answer: True 22) Intermediate and late gene transcription of poxviruses does NOT require any host cell proteins. Answer: False 23) Vaccinia virus has been developed to express foreign proteins from bacteriophage T7 promoters. Answer: True Question type: Essay 24) Describe the observations that Edward Jenner made and the experiment that he carried out to show that the “cowpox” virus could protect people from smallpox. Answer: Edward Jenner in the late 1700’s knew the following pieces of information which helped him carry out the first vaccination experiment: 1) introduction of smallpox virus into the skin produced lifelong immunity to smallpox, 2) milkmaids had beautiful facial complexion because they did not suffer the scars left by smallpox, and 3) and milkmaids often acquired a pock-like lesions on their hands from a disease called cowpox. He used the pus from a lesion on the hand of milkmaid to inoculate a young boy, who got a limited and non-debilitating infection with the cowpox. Several weeks later he purposefully infected the boy with smallpox from an infected individual. The boy did not get any signs of smallpox infection, demonstrating that he was immune to the more deadly virus. 25) Describe the unique structure of the genome of poxviruses and how this genome is replicated to solve the problem with replicating the ends of linear DNA. Answer: The genomes of poxviruses are linear but have covalently closed ends where the 5’ phosphate of one DNA strand is attached to the 3’ OH group of the opposite strand. This means that intact poxvirus genomes do not have any free ends in their genomes. In addition, the ends of the genome form hairpin structures that are used during DNA replication of the genome. DNA replication is initiated from a site-specific nick, which produces a 3’OH group on which DNA replication can initiate. DNA replication continues to produce complete viral genomes linked tail to tail. These genomes are then resolved into two separate genomes by a viral endonuclease.
Since there is no RNA primer used in replication of the poxvirus genomes, there is no gap at the 5’ end when the RNA primer is removed, and therefore no “end problem”.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 27
Question type: Multiple Choice
1) Which of the following represents the group of organisms infected by phycodnaviruses? a) Insects. b) Plants. c) Prokaryotic cyanobacteria. d) Eukaryotic algae. e) Amoeba. Answer: d
2) All of the following virus families are members of the superfamily of Nucleo-Cytoplasmic Large DNA viruses EXCEPT... a) Phycodnaviridae b) Adenoviridae c) Mimiviridae d) Poxviridae e) Asfarviridae Answer: b
3) All of the following characteristics are common to the virions of all of the phycodnaviruses EXCEPT: a) They have a core which contains the double-stranded DNA genome. b) The DNA containing core is surrounded a lipid bilayer. c) The internal lipid membrane is surrounded by an icosahedral capsid. d) The presence of an outer membrane acquired by budding from the host cell. e) All of the above are found in the virions of all phycodnaviruses. Answer: d
4) There is a 1788bp sequence in the middle of the genome of PBCV-1, a phycodnavirus, that does not code for any proteins. What is the function of this region of the genome?
a) It contains 11 tRNA genes. b) It is the origin of DNA replication. c) It is an enhancer involved in regulating gene expression. d) It is a packaging sequence involved in insertion of the viral genome into the capsid. e) None of the above. Answer: a
5) The primary capsid protein of the phycodnavirus PBCV-1, Vp54, is glycosylated. Which of the following describes how the viral protein is thought to acquire its sugar residues? a) The sugars are added to the protein inside the lumen of the rough ER. b) Cellular enzymes in the cytoplasm add the sugars to the capsid protein. c) Viral enzymes add the sugars directly to the capsid protein. d) The sugars are added to the protein in the Golgi of the host cell. e) The sugars are added by viral enzymes after release of the virion from the host cell. Answer: c
6) The virion of the chlorovirus PBCV-1 has a spike located at one of the 12 pentameric vertices. Which of the following describes the function of this spike? a) It represents the point in the capsid where the DNA is packaged into the virion. b) It attaches to the host cell and initiates entry of the virion. c) It contains enzymes at its outer tip that degrade the cell wall of the host. d) It is an important intermediate in the assembly of the capsid. e) It is the point of attachment between the internal lipid envelope and the outer capsid. Answer: b
7) Which of the following statements describes a characteristic of the late genes of the phycodnavirus PBCV-1? a) They are only transcribed after DNA synthesis has begun. b) They are transcribed by the host cell RNA polymerase. c) They encode structural proteins. d) They were detected by hybridizing RNA to probes of each viral gene. e) All of the above are characteristics of late genes. Answer: e
8) Which of the following characteristics distinguishes the coccolithoviruses from the chloroviruses, which are both member of the phycodnavirus family? a) Only the coccolithoviruses have a virion with an internal envelope. b) Only the coccolithoviruses are predicted to encode over 300 proteins. c) Only the coccolithoviruses replicate entirely in the nucleus of the host cell. d) Only the coccolithoviruses encode their own DNA polymerase. e) Only the coccolithoviruses encode their own RNA polymerase. Answer: e
9) The coccolithoviruses encode enzymes that produce the sphingolipid ceramide. What is the proposed function of this lipid in infected cells? a) It enhances the production of cellular membranes, which the virus requires for replication. b) It modifies cellular membranes, which enhances binding and entry of virions. c) It activates apoptosis, causing host cells to lyse and release virus particles. d) It inhibits apoptosis, allowing host cells to stay alive longer. e) It induces signaling pathways in the host cell that increase viral replication. Answer: d
10) Upon infection with a coccolithovirus, the microalgal host cell may switch from the usual diploid life stage to a haploid cell. Which of the following describes the advantage this has for the host cell? a) The haploid cell can not replicate the viral genome, so no new viruses are produced. b) The haploid cell produces a barrier that prevents virus particles from entering. c) The haploid cell can swim away from virus infested waters. d) The haploid cell can fuse with other haploid cells, producing virus resistant strains. e) The haploid cell does not produce the host cell receptor for virus entry. Answer: b
11) Which of the following describes the primary distinguishing feature of the prasinoviruses? a) They have the largest virions of any known virus. b) They have the largest genome of any known virus. c) They produce more virions per round of replication than any known virus. d) They infect the smallest free-living eukaryotic cell. e) They only replicate inside the nucleus of their host cell. Answer: d
12) The prasinovirus which infects the green alga Ostreococcus only produces 6-15 virus particles per infectious cycle. Which of the following explains why the burst size is so small? a) The host cell is not big enough to hold any more virus particles without lysing. b) The host cell has a hard outer coating that makes it difficult for virus particles to leave the cell. c) The host cell dies too quickly to allow more virus particles to be produced. d) The cell does not contain enough raw materials to allow production of any more virions. e) The host cell produces an inhibitor that halts viral DNA replication after the first few virus genomes are produced. Answer: a 13) What does the name “mimivirus” refer to? a) The name of the person who discovered the virus. b) A shortened version of “microbe-mimicking” virus. c) Abbreviation of “mega informational monstrous infectious” virus d) The name of the host species that the virus infects. e) The name of the location where the virus was discovered. Answer: b
14) Which of the following statements about the phaeoviruses, members of the phycodnavirus family, is FALSE? a) They infect the multicellular brown algae. b) They integrate their viral genome into the host cell genome. c) They are found in both marine and freshwater environments. d) They only infect the free-swimming gametes of their host. e) Productive replication of the virus makes the host sterile. Answer: c
15) Which of the following mechanisms is thought to have caused the mimivirus genome to become so large? a) Insertion of the genome of another virus into the mimivirus genome. b) The insertion of a large transposon into the genome. c) Acquisition of new genes from the genome of its host. d) Acquisition of large segments of non-coding DNA. e) Self-duplication of regions of the genome.
Answer: e
16) What does mimivirus have in common with poxviruses? a) They both have genomes of over 1 million base-pairs. b) Their virions are both large enough to be easily seen with a light microscope. c) They both have a brick shaped virion. d) They both replicate in the cytoplasm of their host cell. e) The both cause severe and deadly diseases in humans. Answer: d
17) While mimiviruses encode more of the components of the protein synthesis machinery than other viruses, they still do not produce which of the following? a) Aminoacyl-tRNA synthetases. b) Ribosomes c) tRNA methyltransferases d) tRNAs e) Translation initiation factors Answer: b
18) Which of the following may explain why mimiviruses encode a high number of DNA repair enzymes? a) Their host produces a large number of nucleases. b) The method used to replicate the viral genome introduces many mutations. c) During long periods between infections, they are exposed to UV light. d) During entry, the genome would be exposed to oxidizing conditions. e) Both “c” and “d” are correct. Answer: e Question Type: True/False 19) One of the reasons why the phcyodnaviruses are so diverse is that their hosts are ancient and equally as diverse. Answer: True
20) Like most other eukaryotic viruses, the entire virion of the chlorovirus PBCV-1, a phycodnavirus, enters the host cell and releases the viral genome into the nucleus. Answer: False 21) Chloroviruses, like PBCV-1, encode enzymes which can produce hyaluronan and chitin, two different saccharide polymers. Answer: True 22) The famous white cliffs of Dover were formed by shells of a marine organism killed by coccolithoviruses. Answer: True 23) The enzymes encoded by the phycodnavirus PBCV-1 are notable because they are the largest known enzymes of their type found in a viral genome. Answer: False 24) The genome of the giant mimivirus contains more non-coding and “junk” DNA than most other DNA viruses. Answer: False Question type: Essay 25) Describe how the viruses that infect the marine coccolithophore Emiliania huxleyi can change local weather patterns. Answer: When the coccolithoviruses infect the E. huxleyi host, they cause the precursor dimethyl sulfoniopropionate (DMSP) to be converted to dimethyl sulfide (DMS). DMS is a gas which is released into the atmosphere where is has several effects, such as making the virus infected cells more appealing to grazers and preventing further infection of E. huxleyi with coccolithoviruses. The DMS released into the atmosphere is oxidized into acidic particles that form cloud condensation. This causes the sun to be reflected back out to space and causes the earth to cool down. This also causes a reduction of sun hitting the surface of the ocean, which would slow the growth of the phytoplankton, thereby acting as a self-correcting mechanism to prevent the increase of large marine blooms.
26) Discuss the evidence that mimiviruses may have transferred a gene from a bacterium to a eukaryote. Why would amoebae, the host cell of the mimivirus, be hypothesized to be sources of this type of horizontal gene transfer? Answer: The mimivirus genome contains a copy of the MutS gene, which encodes is component of the DNA mismatch repair enzyme system. The mimivirus MutS gene is most closely related to homologues in the bacterium Nitratiruptor, which is found in deep-sea hydrothermal vents, and the eukaryote Octocorallia, a marine soft coral. The Octocorallia homologue is found on the mitochondrial genome and is not present in any of the closely related species. It has then been suggested that an ancestral mimivirus transferred the MutS gene from the bacterium to the eukaryotic genome. This has suggested a hypothesis that scavengers like the amoebae, which are the hosts of the mimiviruses, could facilitate horizontal gene transfer between species in the different domains of life since they ingest many different types of organisms, which allows them to interact and exchange DNA with each other.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 28
Question type: Multiple Choice
1) Important discoveries about retroviruses were responsible for Nobel Prizes awarded to all of the following scientists EXCEPT: a) Robert Gallo b) Peyton Rous c) Howard Temin d) David Baltimore e) Michael Bishop Answer: a
2) Retroviruses use which of the following cellular molecules as the primer for genome replication? a) The TATA-box binding protein. b) The 5S ribosomal RNA. c) A specific transfer RNA. d) A spliceosome snRNA. e) A specific spliceosome protein. Answer: c
3) All of the following features are associated with the incoming RNA genomes of retroviruses EXCEPT: a) 5’ cap structures b) 3’ poly(A) tails c) Repeated (R) sequence at each end of the genome. d) A single open reading frame. e) Unique sequences at each end of the genome. Answer: d
4) Which of the following primarily determines the species and type of cell infected by a specific retrovirus?
a) The tRNAs found in the cytoplasm. b) The host cell receptor found on the cell. c) The types of transcription factors in the nucleus. d) The level of deoxynucleotide triphosphates in the cytoplasm of the cell. e) All of the above. Answer: b
5) Which of the following describes the first step in the replication cycle of retroviruses? a) Replication of the host genome into daughter DNA molecules. b) Integration of the viral genome into the host cell DNA. c) Translation of the viral genome into protein. d) Transcription of the viral genome into mRNA. e) Reverse transcription of the viral genome into dsDNA. Answer: e
6) What is the enzymatic function of the RNaseH activity of reverse transcriptase? a) It converts RNA sequence to DNA sequence. b) It converts RNA sequence to RNA sequence. c) It degrades single-stranded RNA. d) It degrades RNA in an RNA:DNA hybrid. e) It degrades RNA in an RNA:RNA hybrid. Answer: d
7) All of the following are distinct features of the reverse transcription process, used by retroviruses to convert their ssRNA genome into a dsDNA provirus, EXCEPT… a) A significant number of cellular enzymes are required to carry out reverse transcription. b) The viral reverse transcriptase uses a cellular tRNA molecule as a primer. c) The R sequence present at both ends of the viral genome is critical in the reverse transcription process. d) There are two separate strand transfer events where the nascent DNA strand is moved to the other end of the template. e) Degradation of segments of the viral RNA, when bound to a complementary strand of DNA, is important for the process. Answer: a
8) The reverse transcriptase enzyme of retroviruses includes between 1 and 10 mistakes when it copies the viral genome into DNA. Which of the following explains why? a) It lacks the 3’-to-5’ exonuclease activity found in the cellular DNA polymerase. b) It lacks the 5’-to-3’ exonuclease activity found in the cellular DNA polymerase. c) It doesn’t bind to the cellular proteins involved in proofreading. d) The virus doesn’t produce the proteins involved in proofreading. e) The production of RNA is inherently more mistake prone than the production of DNA. Answer: a
9) Most retroviruses, with the exception of lentiviruses, can only infect cells that are actively dividing. Which of the following explains the primary reason for this? a) The viral genome is amplified by replicating cells. b) They need actively replicating cells to spread the virus throughout the body. c) They need the cell to undergo mitosis so the viral genome can enter the nucleus. d) They need the cell to produce high levels of nucleotide triphosphates. e) They need the cell to produce DNA polymerase to replicate the viral genome. Answer: c
10) Which of the following statements about the integration of the retrovirus provirus into the host genome is FALSE? a) The viral integrase makes a staggered cut in the host cell DNA at the site of integration. b) During integration, two bases are lost from each end of the viral provirus. c) Integration results in a 4-6bp direct repeat of the host cell DNA on either side of the provirus. d) Retroviruses produce an enzyme that can remove the provirus from the cellular genome. e) Cellular host DNA repair enzymes are involved in the integration process. Answer: d
11) Which of the following is a description of the long terminal repeats found in retroviruses? a) They consist of direct repeats found at the ends of the incoming viral genome. b) They consist of direct repeats found at the ends of the provirus. c) They consist of inverted repeats found at the ends of the incoming viral genome. d) They consist of inverted repeats found at the ends of the provirus. e) They are the repeats found in the host cell genome on either side of the integrated viral provirus.
Answer: b
12) Which of the following determines the level of viral mRNAs produced from the integrated provirus in retrovirus infected cells? a) The level of mRNA splicing and polyadenylation that occurs. b) The amount of reverse transcriptase packaged into the virion. c) The site in the host cell genome where the provirus integrates. d) Binding of specific transcription factors to the U5 region. e) Binding of specific transcription factors to the U3 region. Answer: e
13) Which of the following describes the phenomenon of promoter occlusion seen in retroviruses? a) Transcription from the left-hand LTR inhibits transcription from the right-hand LTR. b) Cellular RNA polymerase can only recognize the factors bound to the left-hand LTR. c) The inability of the LTR to be transcribed because it has integrated into heterochromatin in the host cell genome. d) Deletion of the left-hand LTR inhibits transcription from the right-hand LTR. e) Transcription from both LTRs can occur simultaneously. Answer: a
14) The viruses in the gammaretrovirus genus use which of the following mechanisms to synthesize the proteins from the pol gene? a) Alternative mRNA splicing. b) RNA editing. c) Read through of a translational stop codon. d) Ribosomal frameshifting. e) Initiation of translation at a downstream start codon. Answer: c
15) The Gag and Pol proteins are coded for in two different reading frames in the avian retroviruses. Which of the following mechanisms is used to produce the Pol proteins? a) Alternative mRNA splicing. b) RNA editing. c) Read through of a translational stop codon.
d) Ribosomal frameshifting. e) Initiation of translation at a downstream start codon. Answer: d
16) Which of the following ensures that the Pol protein is packaged into the virions of retroviruses during assembly? a) The Pol protein is bound to a fatty acid. b) The Pol protein is packaged as a Gag-Pol fusion protein. c) The Pol protein binds to the packaging sequence on the viral genome. d) The Pol protein is translated into the lumen of the endoplasmic reticulum. e) The Pol protein binds to the reverse transciptase enzyme during assembly. Answer: b
17) Which of the following statements about acute transforming retroviruses is TRUE? a) They produce viral enzymes that lead to cellular transformation. b) They cause tumors because of where they integrate into the host genome. c) They carry a mutated or deleted version of a cellular gene. d) They are usually competent to replicate and produce virions. e) They only transform cells in which the provirus has not been integrated. Answer: c
18) Nontransforming retroviruses can cause an infected cell to become tumorigenic by doing which of the following? a) The virus inactivates the cellular pRb protein. b) Integrating into and disrupting a cellular oncogene. c) Inducing the host cell to enter S phase and begin DNA replication. d) Integrating into and disrupting a tumor suppressor gene. e) Integrating the LTR adjacent to a proto-oncogene. Answer: e Question Type: True/False 18) Retroviruses package a positive ssRNA genome, which resembles an mRNA and is immediately translated upon entry into the host cell.
Answer: False 19) Most retroviruses cause cancers in their animal hosts. Answer: True 20) Unlike most other viruses, retroviruses package two identical copies of their genome in the virion. Answer: True 21) Retroviruses only integrate into a few very sequence specific sites within the host cell genome. Answer: False 22) The envelope protein is translated from the unspliced mRNAs produced during retrovirus infections. Answer: False 23) When retroviruses integrate their provirus into germ line cells they can be vertically transmitted. Answer: True Question type: Essay 24) The double-stranded proviral genome of retroviruses is longer than the incoming singlestranded RNA genome. What is the function of this extra DNA sequence and where did it come from? Answer: The 5’ end of the incoming retrovirus RNA genome contains a copy of the R-U5 sequence. The 3’ end of the incoming viral genome contains a copy of the U3-R. When the ssRNA genome is reversed transcribed to produce the dsDNA provirus, the ends of the genome are copied to make a complete long terminal repeat (LTR) at each end of the provirus. The LTR consists of U3-R-U5. Since the U3 sequences contains the enhancer and promoter sequences that allow the viral RNAs to be transcribed from the integrated provirus, it is critical that a copy of
this sequence be added to the 5’ end of the provirus. Likewise the U5 sequence contains the polyadenlyation sequences that allow the poly(A) tail to be added to the 3’ end of the viral RNAs, so a copy must be added to the 3’ end of the provirus. Because the 5’ copy of U3 and the 3’ copy of U5 are not part of the transcribed viral RNA, they must be added back during reverse transcription. 25) Explain the different mechanisms used by acute transforming viruses and nontransforming retroviruses to cause tumor formation. Why does transforming by the acute transforming viruses take less time than the nontransforming retroviruses? Answer: The acute transforming viruses cause cells to become cancerous because they carry a copy of an oncogene. An oncogene is a truncated or mutated copy of a cellular proto-oncogene, which is involved in stimulating growth or division of cells. The normal proto-oncogene is regulated and only functions when the cell needs to divide. The oncogene or viral version of the gene has become truncated or mutated in the process of being acquired by the retrovirus and is no longer under its proper regulation. By bringing in the oncogene and expressing the protein in the cells, the virus causes the cell to divide in an uncontrolled manner. The nontransforming retroviruses do not carry a copy of an oncogene. Instead, they randomly integrate next to a protooncogene. Because of the strong LTR, the proto-oncogene is over expressed. The increased amounts of this protein then cause the cell to divide in an uncontrolled manner, which leads to tumor formation.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 29
Question type: Multiple Choice
1) HIV-1 is a member of which of the following subgroups of retroviruses? a) Acute transforming retroviruses b) Nontransforming retroviruses c) Alpharetroviruses d) Lentiviruses e) Spumaviruses Answer: d
2) Which of the following viruses was thought to have been transmitted to humans and became the source of the HIV-1 pandemic? a) Sooty-mangaby SIV b) Chimpanzee SIV c) African Green monkey SIV d) Equine infectious anemia virus e) Feline immunodeficiency virus Answer: b
3) Which of the following is NOT a mode of transmission for HIV? a) Sexual contact. b) Breast milk. c) Aerosoled particles. d) Blood transfusions. e) Contaminated needles. Answer: c
4) Which of the following cell types facilitates the initial infection with HIV and helps to transmit the virus across mucosal membranes? a) Dendritic cells
b) CD4-positive T lymphocytes c) CD8-positive T lymphocytes d) B lymphocytes e) Monocytes Answer: a
5) Which of the following lymphoid tissues is the first to be depleted by infection with HIV-1? a) Thymus gland b) Spleen c) Lymph nodes d) Tonsils e) Gut associated lymphoid tissue Answer: e
6) All of the following affect the clinical outcome of an infection with HIV EXCEPT: a) The level of viral RNA maintained in the person’s blood. b) The route of infection with the virus. c) The nature of the immune response to the virus. d) The diversity of epitopes recognized by the immune system. e) The strain of HIV the person was infected with. Answer: b
7) Which of the following is the primary host cell receptor for most of the cell types infected with HIV? a) DC-SIGN b) CD8 c) CCR5 d) CD4 e) CXCR4 Answer: d
8) HIV, unlike most other retroviruses, can infect nondividing cells. Which of the following explains why?
a) The HIV reverse transcriptase enzyme can function with a lower concentration of nucleotide triphosophates. b) The HIV integrase enzyme can work without the help of cellular enzymes. c) The HIV matrix protein can direct the nuclear import of the HIV preintegration complex. d) The HIV Vpr protein can interact with cellular microtubules to bring the virion close to the nucleus. e) All of the above are correct. Answer: c
9) What is unusual about how the tat protein from HIV activates transcription from the LTR? a) It binds to the tat response element as RNA but not as DNA. b) It binds directly to the cellular RNA polymerase II. c) It binds to the reverse transcriptase enzyme and enhances its processivity. d) It binds next to the TATA box and enhances binding of TBP to the LTR. e) It inactivates the repressor of NF-B so that this protein can bind to the LTR. Answer: a
10) The Rev protein from HIV has which of the following functions? a) It can enter the nucleus of the host cell via the nuclear pore. b) It binds to a specific RNA sequence in the viral genome. c) It enhances transport of unspliced viral RNAs to the cytoplasm. d) It indirectly enhances the translation of the viral mRNAs. e) Rev has all of the above functions. Answer: e
11) The doubly splice mRNAs produced by HIV do not contain the Rev Response Element (RRE). Which of the following explains why they are transported out of the nucleus without the help of the Rev protein? a) They interact with the small subunit of the ribosome, which transport them out of the nuceus b) They lack the cis-acting repressive sequences. c) The exportin protein binds directly to the mRNAs to transport them. d) The inportin protein binds directly to the mRNAs to transport them. e) The HIV Rev protein is still required for their export, but it binds to the poly(A) tail instead of the RRE. Answer: b
12) Which of the following proteins from HIV are synthesized first in an infected cell? a) Vpr and Vpu b) Gag and Pol c) Rev d) Tat Answer: e
13)Which of the following describes the function of the HIV protein Vif (viral infectivity factor). a) It enhances the packaging of viral genomes into new virions. b) It enhances the synthesis of unspliced viral RNA genomes by the cellular RNA polymerase II. c) It causes the cellular protein APOBEC3G to be degraded in infected cells. d) It allows the unspliced viral genomic RNA to be transported out of the nucleus. e) It increases the levels of the gp120/gp41 proteins on the surface of infected cells. Answer: c
14) The Vpr from HIV can cause the infected cell to stall in the G2 stage of the cell cycle. What purpose does this serve for the virus? a) This is when there are the highest number of ribosomes in the cell. b) This is when c) This is when membrane synthesis is at its highest level. d) This is when transcription levels from the LTR are the highest. e) This is when the host cell replicates the cellular genomic DNA. Answer: d
15) The Vpu protein from HIV increases the release of newly synthesized virus particles from the surface of infected cells. Which of the following describes the mechanism by which Vpu does this? a) It degrades the sialic acid residues on the surface of the cell, which the virions can bind to. b) It induces the degradation of the protein tetherin, which keeps the virions attached to the cell surface. c) It increases the number of CD4 proteins to be exported to the cell surface. d) It causes the plasma membrane to become flexible and fold around the budding virion. e) It increases the export of gp120 and gp41 to the cell surface. Answer: b
16) The Nef protein from HIV causes a reduction in the amount of the MHC 1 protein on the surface of infected CD4 positive T cells. Which of the following is the result of this process? a) It prevents antibodies from binding to the viral proteins on the cell surface. b) It increases the amount of infectious virus released from the T cells. c) It increases the amount of virus that can bind and infect the T cells. d) It prevents the immune system from detecting that the T cells are infected. e) It causes the cytotoxic T cells to attack and kill the HIV infected T cells. Answer: d
17) The loss of CD4 positive T cells as a result of infection with HIV eventually causes which of the following to happen in an HIV infected person? a) Loss of immune competency and an increase in other infections. b) An increase in the number of T cells leading to leukemia. c) An over activation of the immune system and autoimmune diseases. d) An increase in the production of cytokines, leading to a “cytokine storm”. e) B cell lymphomas as a direct result of infection of B cells with HIV. Answer: a
Question Type: True/False
18) While most old world monkeys do not appear to suffer any disease when they are infected with SIV, chimpanzees suffer from significant disease when infected with SIV-cpz. Answer: True
19) During the first two to six weeks after infection with HIV, most people do not have any symptoms of infection. Answer: False
20) The majority of individuals infected with HIV develop AIDS 8-10 years after the initial infection. Answer: True
21) During the clinical latency period of an HIV infection, the virus is not replicating and no virus particles are produced. Answer: False
22) After treatment for ten years with highly active anti-retroviral drugs, most HIV infected patients can stop taking the medications and are considered cured. Answer: False
23) People who have a natural mutation in the gene encoding the CCR5 protein are resistant to infection with HIV. Answer: True
24) Monkeys infected with a mutant of SIV that lacks the Nef coding sequence have reduced virus titers and less severe disease. Answer: True
Question type: Essay 25) Describe three unique aspects of HIV’s biology that make it an extremely difficult virus for the human immune system to eliminate. Answer: 1) Because HIV is a retrovirus it integrates its genome into the genome of the host cell. This means that the cell can never be “cured” of the virus. Every time this cell replicates, it passes a copy of the HIV provirus on to the daughter cells, allowing the virus to spread passively. 2) HIV has an extremely high mutation rate. Because reverse transcriptase does not have a proofreading function like other DNA polymerases, it makes approximately one mutation per genome replication cycle. Because of the large number of particles produced in an untreated patient, this means that a huge number of virus genome sequences are produced. This allows for a high degree of variability in the amino acid sequence of the surface proteins, which allows the virus to evade immune detection. 3) The virus infects and kills critical cells in the immune system. Because HIV infects CD4 positive T lymphocytes, which are critical regulators of the immune system, the virus actually destroys the body’s main defense against the virus. As the number of CD4 positive T cells drops, the ability of the immune system to keep the virus in check decreases and the patient eventually succumbs to opportunistic infections or cancers.
26) Describe the clinical progress of an HIV infection in a typical patient who has not been treated with anti-HIV drug therapy. What are the other two potential disease courses, which occur in a minority of individuals, that could result from infection with HIV? Answer: In the majority of HIV infected patients, the time from initial infection with HIV to death is approximately 8-10 years. During the first few weeks after infection, patients will experience flu-like symptoms. At this point the virus is replicating rapidly and spreading to many tissues in the body. As the immune system begins to control the virus, the levels of HIV in the blood decrease and the symptoms disappear. Over the next 8-10 years, termed clinical latency, the immune system maintains a set level of virions in the blood, the patient experience few or no symptoms, and the numbers of CD4 positive cells slowly decline. When the number of CD4 positive T cells drops below a critical level, the individual begins to experience symptoms and suffer opportunistic infections. The patient is now suffering from AIDS and will succumb to the infection. There are two other populations of HIV infected individuals, rapid progressors who develop AIDS within 2-3 years of initial infection and long-term nonprogressors, who show not decline in their CD4 positive T cells over long periods of time.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 30
Question Type: Multiple Choice
1) Like retroviruses, hepatitis B virus (HBV) uses a reverse transcription step. Which of the following distinguishes HBV from the retroviruses? a) HBV has an enveloped virion. b) HBV packages a DNA genome in the virion. c) HBV packages reverse transcriptase enzyme in the virion. d) HBV fuses its envelope with the cellular plasma membrane. e) All of the above distinguish HBV from retroviruses. Answer: b
2) Which of the following is a likely purpose for the noninfectious particles produced by hepatitis B virus? a) They bind to antibodies allowing the virus to evade the immune system. b) They bind to the host cell receptor, improving entry of virus particles. c) They stimulate cytotoxic T lymphocytes. d) They bind to liver cells and stimulate them to replicate. e) They are just packaging mistakes that occur in some cells and they serve no purpose. Answer: a
3) The copy of the hepatitis B virus genome that is inside of the virion has unusual structures as the 5’ and 3’ ends. Which of the following describes the genome ends? a) The 5’ end has a cap structure and the 3’ end has a poly(A) tail. b) The 5’ end has a triphosphate and the 3’ end has a hydroxyl group. c) The 5’ end has a fragment of RNA and the 3’ end has a protein attached. d) The 5’ end has a protein attached and the 3’ end has a fragment of RNA. e) There are no ends, the genome is a covalently closed circle. Answer: d
4) The early steps of hepatitis B virus replication in an infected cell are poorly understood. Which of the following explains why?
a) It is difficult to get hepatitis B virions to enter the host cell. b) Hepatitis B virus kills the infected cells too quickly. c) There are no cultured cells that can be productively infected with the virus. d) There are no antibodies available that can bind to the envelope proteins. e) There is not a good animal model that mimics the hepatitis B virus infection. Answer: c
5) The hepatitis B genome as it is found inside the virion has an unusual structure. Which of the following is NOT a characteristic of the virion genome? a) It has a gap of single-stranded DNA. b) It has an inverted repeat at each end of the genome. c) It has a piece of RNA attached to the 3’ end of the genome. d) The plus strand is shorter than the minus strand. e) It has a protein covalently attached to the 5’ end of the genome. Answer: b
6) Which of the following occurs immediately after entry of the hepatitis B virus genome into the host cell? a) Translation of the viral genome into proteins. b) Integration of the viral genome into the host genome. c) Reverse transcription of the genome into double-stranded DNA. d) Transcription of the viral genome to make mRNAs. e) Conversion of the genome to a covalently closed circular form. Answer: e
7) Which of the following describes the control sequences that hepatitis B viruses uses to direct transcription and processing of the viral mRNAs? a) There are 5 promoters and 1 polyadenylation site. b) There are 3 promoters and 2 polyadenylation sites. c) There are 2 promoters and 2 polyadenylation sites. d) There is only 1 promoter and 1 polyadenylation site. Different mRNAs are produced via alternative mRNA splicing. e) The virus only produces a single mRNA which is the pregenomic mRNA. Answer: a
8) Which of the following describes an interesting feature of the preC and pregenomic mRNAs produced by the hepatitis B virus? a) They are extensively spliced to produce a set of nested mRNAs. b) They are transcribed by the cellular RNA polymerase III enzyme. c) They are produced by the reverse transcriptase enzyme. d) They are transcribed past a polyadenylation site near the promoter. e) They each code for several proteins due to the use of alternative start codons. Answer: d
9) Scientists have generated mice that synthesize the X protein from hepatitis B virus in all of the liver cells. Which of the following describes the effect of the X protein on mice? a) When infected with hepatitis B, they have a greater amount of liver damage. b) When infected with hepatitis B, they develop a less severe liver disease. c) They are predisposed to developing liver cancer. d) They are resistant to infection with hepatitis B. e) The X protein by itself can induce a hepatitis-like disease. Answer: c
10) The membrane binding domain for all three surface antigens from hepatitis B virus is located at which of the following locations? a) It is in the common N terminal domain, which is the large surface protein region. b) It is in the common C terminal domain, which is the small surface protein domain. c) The surface antigens have a myristate attached to the large protein domain. d) The transmembrane alpha helices are found in the middle antigen region of the protein. e) It is located in a beta-barrel structure found in the large surface antigen. Answer: b
11) The longest open reading frame in the genome of hepatitis B virus genome encodes which of the proteins? a) The E protein. b) The X protein. c) The largest surface antigen. d) The capsid protein. e) The reverse transcriptase enzyme.
Answer: e
12) Which of the following mechanisms is used by hepatitis B to get the viral genome packaged into the virion? a) The polymerase interacts with both the pregenomic mRNA and the capsid protein. b) The capsid protein interacts with the completed DNA genome. c) The capsid is assembled around the completed DNA genome. d) The large surface antigen interacts with the completed DNA genome. e) The large surface antigen interacts with both the pregenomic mRNA and the capsid protein. Answer: a
13) Which of the following mechanisms prevents packaging of the preC mRNA into the virion of hepatitis B virus? a) Binding of the P protein to the packaging site prevents the C protein from binding. b) Binding of the C protein to the packaging site prevents the P protein from binding. c) Translation of the C open reading frame blocks the packaging site. d) Translation of the preC reading frame blocks the packaging site. e) Translation of the P open reading frame blocks the packaging site.
Answer: d
14) All of the following describe similarities between the reverse transcription process in retroviruses and hepadnaviruses EXCEPT: a) They both use a virally encoded reverse transcriptase enzyme. b) They both use a protein primer to begin DNA synthesis. c) They both produce a double-stranded DNA product. d) They both require the presence of repeat sequences in the viral RNA. e) They both use a ribonuclease H enzyme activity during reverse transcription. Answer: b
15) Which of the following explains why there is a gap in the DNA genome of hepatitis B virus? a) There is a segment of RNA that can’t be removed from this region of the genome. b) There are proteins bound to the template that block the polymerase. c) The polymerase enzyme runs out of deoxynucleotide triphosphates. d) The complementary strand can’t base pair in this region of the genome.
e) This is where the genome integrates into the host chromosome. Answer: c
16) Hepatitis B virus produces both infectious and noninfectious particles. Only the infectious particles contain the large surface antigen. Which of the following explains why? a) The small and medium surface antigens are sequestered in the ER. b) The small and medium surface antigens are sequestered in the noninfectious particles. c) Only the large surface antigen is retained in the endoplasmic reticulum. d) Only the large surface antigen is found on the plasma membrane. e) Only the large surface antigen interacts with the core protein. Answer: e
17) It is recommended that people in certain professions or with certain disease should receive the hepatitis B vaccine. For which of the following individuals would it NOT be critical for them to be vaccinated against hepatitis B? a) Zoo keeper b) Nurse c) Tattoo-parlor worker d) Barber e) Hemophiliac Answer: a
18) The drug Lamivudine (3TC) has been shown to inhibit which step in the infectious cycle of hepatitis B virus? a) Binding and entry into the host cell. b) Reverse transcription of the viral genome. c) Transcription of the viral genome. d) Translation of the viral mRNAs. e) Assembly of new virions. Answer: b
19) A new method of preventing transmission of hepatitis B virus, called immunoprophylaxis, is described by which of the following statements? a) Stimulation of the production of anti-hepatitis B antibody production using a vaccine.
b) Use of anti-hepatitis antibodies to bind to virus present in blood donations. c) Injection of cytotoxic T cells into a chronically infected patient. d) Injection of anti-hepatitis B antibodies into newborns. e) Stimulation of immune response against hepatitis B using interferon. Answer: d
Question Type: True/False
20) Hepatitis B is usually transmitted via the oral-fecal route. Answer: False
21) Hepatitis B replication is completely limited to hepatocytes. Answer: False
22) The unusual structure of the of the hepatitis B virus genome found in the virion is a result of the mechanism used to replicate the genome. Answer: True
23) Like retroviruses, the genome of hepatitis B virus is integrated into the genome of the host cell. Answer: False
24) The X protein from hepatitis B virus is thought to activate gene transcription because it is found in the nucleus of infected cells. Answer: False
25) The polymerase protein from hepatitis B virus binds to the epsiolog () stem-loop on the pregenomic mRNA, which is important for packaging of the genome into the capsid. Answer: True
26) Scientists are currently testing an edible vaccine for hepatitis B virus by engineering the antigens into bananas. Answer: True
Question type: Essay
27) Compare and contrast the genome replication cycles of retroviruses and hepadnaviruses, like hepatitis B virus. Answer: The major difference between the genome replication cycles of hepadnaviruses, like hepatitis B virus, and retroviruses is the nature of the incoming viral genome and the timing of the reverse transcription process. In retroviruses, the incoming genome is single-stranded positive sense RNA that is reverse transcribed into double-stranded DNA that is then integrated into the genome of the host cell. The integrated genome is then transcribed back into mRNA, which is packaged into the virion. In hepadnaviruses, the incoming genome is a partially doublestranded molecule of DNA. The DNA genome of hepadnaviruses is never integrated into the host genome like the retroviruses. This DNA is transcribed into viral mRNAs, one of which is the pregenomic mRNA. The pregenomic mRNA is packaged and then reverse transcribed into DNA while inside the virion.
28) Describe the methods used to both prevent and treat hepatitis B virus (HBV) infections. Answer: Public health measures can be used to teach people how to avoid infection with HBV. These include avoiding injection drug use and unprotected sexual intercourse with multiple partners. The primary method to prevent infection with hepatitis B virus is through vaccination with the recombinant vaccine that contains the surface antigens, which is effective at inducing immunity in over 90% of the people who receive the full vaccination series. Unfortunately the vaccine is not widely available in many developing countries, leaving large populations at risk of infection. Immunoprophylaxis, which is the injection of antibodies against HBV, has been used to prevent infection of babies born to mothers infected with HBV. Current drug regimens used to treat HBV infections take many months of treatment and are not 100% effective. These include using drugs, like 3TC that inhibit the replication of HBV, as well as treatment with interferon, which has serious side effects.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 31
Question Type: Multiple Choice
1) Which of the following is NOT a type of infectious RNA that can cause disease? a) Viroid b) Prion c) Hepatitis delta virus d) Satellite RNA e) Viroid-like plant satellite RNA Answer: b
2) Which of the following groups of organisms do viroids cause disease in? a) Plants b) Insects c) Mammals d) Algae e) Paramecia Answer: a
3) Which of the following is a major difference between the group A and the group B viroids? a) Whether they affect the RNAi pathway or not. b) Whether they infect animals or plants. c) Whether they produce a protein or not. d) Whether they have a self-cleaving RNA or not. e) Whether they replicate in the endoplasmic reticulum or not. Answer: d
4) The typical structure of the genome of a viroid is described as? a) Circular double-stranded DNA of 3000-4000bp. b) Linear double-stranded RNA segment of 500-1000bps. c) Circular singled-stranded RNA of 250-400nts.
d) Linear single-stranded RNA of 500-1000nts. e) Circular double-stranded RNA of 400-800bp. Answer: c
5) How do we differentiate between the positive and negative strands of a viroid genome? a) The positive strand produces the viral protein. b) The positive strand is transcribed to make the viral mRNA. c) The positive strand is packaged into the viroid particle. d) The positive strand is the only strand copied by a cellular RNA polymerase. e) The positive strand is the most abundant RNA produced. Answer: e
6) What is surprising about the observation that a cellular RNA polymerase copies the viroid genome? a) RNA polymerases usually require a pre-existing RNA primer. b) RNA polymerases usually transcribe from a DNA template. c) RNA polymerases don’t usually synthesize DNA. d) RNA polymerases don’t usually initiate synthesis from a protein primer. e) RNA polymerases are not found in the cytoplasm of the host cell. Answer: b
7) When the ribozyme activity in the avocado sunblotch viroid cleaves the RNA genome, which of the following describes the structure of the nucleotide on the 5’ side of the cleavage? a) It contains a 5’ phosphate group b) It contains a 3’ phosphate group c) It contains a 3’-OH group d) It contains a 2’, 3’-cyclic phosphate e) It contains a 3’ hydrogen Answer: d
8) Which of the following is NOT thought to be a mechanism by which viroids cause disease in their plant hosts? a) By basepairing to an important cellular RNA, preventing its function. b) By activating the dsRNA induced protein kinase.
c) By causing the degradation of cellular mRNAs via the RNAi pathway. d) By interfering with mRNA splicing because they resemble a cellular snRNA. e) By inhibiting the machinery that exports mRNAs out of the nucleus. Answer: e
9) Which of the following statements about the plant satellite RNAs is FALSE? a) Satellite RNAs encode their own capsid protein. b) Satellite RNAs are transmitted to new hosts via a virion. c) Satellite RNAs require a helper virus in order to be replicated. d) Satellite RNA genomes are composed of small circular RNA molecules that contain a high degree of base pairing. e) Satellite RNAs contain a ribozyme function that can cleave longer RNA molecules into single genomes. Answer: a
10) Which of the following describes the major difference between hepatitis delta virus (HDV) and the plant viroids and satellite RNAs? a) Only the HDV genome contains a ribozyme activity. b) Only HDV requires a helper virus. c) Only the HDV genome encodes a protein. d) Only HDV replicates using a rolling circle mechanism. e) Only HDV requires RNA polymerase II during its replication cycle. Answer: c
11) When studying the replication of viroids and hepatitis delta virus, which of the following allows scientists to distinguish which of the three cellular RNA polymerases is required? a) The sub-cellular location of each RNA polymerase. b) Whether the polymerase requires an RNA primer or not. c) Whether the polymerase can synthesize mRNAs or not. d) Whether the polymerase will use an RNA molecule as a template. e) The sensitivity of the RNA polymerase to the toxin -amanitin. Answer: e
12) The formation of the antigenome template of hepatitis delta virus requires which of the following cellular enzymes?
a) DNA polymerase b) RNA-dependent RNA polymerase c) RNA polymerase I d) RNA polymerase II e) RNA polymerase III Answer: d 13) How is the 3’ end of the hepatitis delta virus mRNA formed? a) It is cleaved by the viral ribozyme activity. b) It is cleaved and polyadenylated by cellular enzymes. c) It folds into a distinct stem-loop structure. d) The polymerase stutters at a poly(U) region in the genome. e) The delta antigen is covalently attached to the 3’ end. Answer: b
14) The ribozyme function found in virioids and hepatitis delta virus can be used to cleave exogenous RNA molecules. Which of the following is a requirement for the ribozyme to be recycled and cleave more than one substrate? a) The entire length of the substrate must not be too long. b) The structure of the ribozyme RNA must be very stable. c) Only a short region of complementarity between the target and the ribozyme. d) The level of magnesium ions must be low enough. e) The temperature of the reaction must be high enough. Answer: c
15) The deamination of an adenine residue in the genome of the hepatitis delta virus causes which of the following to occur? a) A stop codon to be converted to a tryptophan codon. b) A stop codon to be converted to a start codon. c) A 5’ splicing signal to be added. d) A 3’ splicing signal to be added. e) It creates a polyadenylation signal. Answer: a
16) Which of the following mechanisms is used to produce the two different forms of the delta antigen from the hepatitis delta virus? a) RNA editing by the insertion of an extra base into the mRNA. b) RNA editing by deamination of a specific base in the genome. c) Alternative mRNA splicing. d) Translational readthrough of a stop codon. e) Ribosomal frameshifting. Answer: b
17) Which of the following describes the function of the large delta antigen, produced by hepatitis delta virus? a) It stimulates the binding of the host cell RNA polymerase for genome replication. b) It carries out the cleavage of the genome multimers into monomers. c) It is required to package the genome into the hepatitis B virions. d) It forms capsids to package the hepatitis delta virus genome. e) It ligates the ends of the RNA genomes together. Answer: c
Question Type: True/False
18) Viroid RNA molecules have a high degree of base pairing throughout the molecule. Answer: True
19) Viroids encode a single protein which is used to package the RNA for transmission between hosts. Answer: False
20) The RNA polymerase that copies the genome of the avocado sunblotch viroid is highly sensitive to the toxin -amanitin. Answer: False
21) The enzymatic function that cleaves the avocado sunblotch viroid genome is called a ribozyme and does not require any proteins to function.
Answer: True
22) Hepatitis delta virus is transmitted through the same pathways as hepatitis B virus. Answer: True
23) Coinfection with both hepatitis B and delta virus together makes the resulting liver disease less severe. Answer: False
Question Type: Essay
24) There is some controversy about whether the replication of the hepatitis delta virus (HDV) genome is performed by the cellular RNA polymerase I or RNA polymerase II. Describe the evidence that supports each model. Answer: There are two observations that support the model where RNA polymerase I carries out replication of the HDV genome. The replication of the HDV genome is not sensitive to amanitin while mRNA transcription is. This suggests that transcription of the HDV mRNA is performed by RNA polymerase II, which is sensitive to -amanitin, while replication is carried out by RNA polymerase I, which is insensitive to -amanitin. Another observation that supports that replication may be carried out by RNA polymerase I is that the cleavage and polyadenylations site in the viral genome is not recognized during replication. Since RNA polymerase I does not bind to the mRNA cleavage and polyadenylation factors, this supports the model where RNA polymerase I carries out replication of the HDV genome. Alternatively some scientists suggest that RNA polymerase II could carry out replication of the HDV genome by sometimes ignoring the polyadenylation site. However, this still does not explain why HDV genome replication is sensitive to the inhibitory effects of -amanitin.
25) Describe how the ribozyme activity found in the plant virioids and hepatitis delta virus can be used as therapeutic agents to treat infections with other viruses. Answer: Ribozymes are molecules of RNA that can fold up into a conformation that has enzymatic activity. The enzymatic activity found in the ribozyme of viroids is to cleave a molecule of RNA into two pieces. Normally the ribozyme of viroids and hepatitis delta virus cleaves the genomic RNA into monomeric segments, which is termed self cleavage. But a ribozyme can also be engineered to cleave other molecules of RNA. If the ribozyme was designed to be complementary to a substrate RNA, such as the genome of an RNA virus, then
the ribozyme would bind and cleave the viral RNA, thereby inactivating it and halting the infection. While there are limitations to this technology, it holds promise for future development.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 32
Question type: Multiple Choice
1) What is the nature of the infectious agent that causes the human disease kuru? a) A positive-strand RNA virus. b) A small RNA molecule similar to a viroid. c) Kuru is only seen as an inherited genetic disease. d) A single species of protein called a prion. e) A small DNA molecule that does not code for a protein. Answer: d
2) Which of the following is the general term used to describe the type of disease caused by prions? a) Transmissible neurodegeneration b) Transmissible spongiform encephalopathy c) Chronic inflammatory neuropathy d) Creutzfeldt-Jakob disease e) Huntington’s disease Answer: b
3) What is the proposed mechanism by which humans acquired the new variant form of Creutzfeldt-Jakob disease? a) Humans who received blood from CJD infected donors. b) Humans who received corneas from CJD infected donors. c) Humans who participated in ritualistic cannibalism. d) Humans who ate sheep infected with the scrapie agent. e) Humans who ate cows infected with the BSE agent. Answer: e
4) All of the following demonstrate that prions do not appear to contain a nucleic acid EXCEPT: a) Infectivity is resistant to phenol.
b) Infectivity is resistant to UV radiation. c) Infectivity is resistant to nucleases. d) Infectivity is resistant to high concentrations of zinc ions. e) Infectivity is resistant to ammonium hydroxide. Answer: a 5) All of the following are examples of human diseases caused by prions EXCEPT….. a) Kuru b) Creutzfeldt-Jakob disease c) Fatal familial insomnia d) Scrapie e) Gerstmann-Straussler-Scheinker syndrome Answer: d
6) When it was discovered, what was surprising about the gene that codes for the prion infectious agent? a) It is easily transmitted as naked nucleic acid. b) It is coded for by RNA not DNA. c) It is found in the genome of the host. d) It has a high degree of secondary structure. e) There is no gene that codes for the prion protein. Answer: c 7) Which of the following describes the primary difference between the normal PrPC protein and the disease version of the protein (PrPSc). a) PrPSc contains additional octapeptide repeats at the N-terminus. b) PrPSc contains more beta sheet structure than PrPC. c) PrPSc lacks the sugar residues that are attached to PrPC. d) PrPSc is not exposed on the surface of the cell. e) PrPSc does not bind to copper like PrPC does. Answer: b 8) Which of the following observations about the PrPSc protein could explain how this protein causes damage to the neurons of the brain?
a) The PrPSc protein causes glycosylation of membrane proteins to become disregulated. b) The PrPSc protein causes copper to be sequestered in neurons. c) The PrPSc protein is more resistant to protease digestion than the cellular form. d) The PrPSc protein alters the signaling pathways in neurons. e) The PrPSc protein aggregates to form fibrils. Answer: e
9) All prion associated diseases are confined to which of the following organ systems of the body? a) Immune system. b) Muscular system. c) Central nervous system. d) Digestive system. e) Endocrine system. Answer: c
10) All of the following diseases have been demonstrated to be caused by protein misfolding EXCEPT: a) Alzheimers disease b) Autism c) Huntington’s disease d) Parkinson’s disease e) Cystic fibrosis Answer: b
11) Heterozygosity at codon 129 in the prion gene is present in the human population at an unexpectedly high level. Which of the following may explain why? a) It is associated with resistance to acquired CJD. b) It is associated with resistance to sproadic CJD. c) It is associated with resistance to variant CJD. d) It is associated with resistance to kuru. e) All of the above are correct. Answer: e
12) Prions from one species do not easily cause prion diseases in animals of a different species. Which of the following may explain why? a) The host cell needs to have the correct receptor for entry of the PrpSc protein. b) The host needs to have the correct proteases for the proper processing of the PrPSc protein. c) The host cell needs to provide the correct glycosylation pattern on the PrpSc protein. d) The PrpSc protein needs to interact with a PrPC protein with the same amino acid sequence. e) There are other host related proteins involved in the development of a prion disease. Answer: d
13)All of the following describe the attributes that distinguish different strains of prions EXCEPT: a) The amino acid sequence of the prion protein. b) The size of the protease resistant portion of the prion protein. c) The disease symptoms they cause. d) The pattern of glycosylation on the prion protein. e) The incubation time for the disease that they cause. Answer: a
14) Which of the following tests would be most useful to diagnose a prion disease in a patient? a) MRI of the brain to detect damage. b) CAT scan of the brain to detect damage. c) Test for the presence of PrPSc protein in the tonsils. d) Microscopically examine a brain biopsy. e) Sequencing of the patient’s prion gene. Answer: c 15) Which of the following experiments demonstrates that PrPC is required for prion disease transmission? a) Mice with the hamster PrP gene are susceptible to hamster prions. b) Mice lacking the Prp gene are resistant to prion infections. c) Yeast have proteins that can form self-propagating states like prion proteins. d) The PrPSc protein has the same amino acid sequence as the PrPC protein. e) Injection of brain extracts from kuru patients into monkeys causes the monkeys to get a similar disease.
Answer: b 16) Which of the following is NOT a characteristic of the PrPC form of the prion protein? a) It is bound to a phospholipid anchor. b) It is synthesized in the rough ER. c) It is glycosylated. d) It binds to copper ions. e) All of the above are characteristics of the PrPC protein. Answer: e
17)The genetic forms of prion diseases result from mutations in the prion gene. What is the proposed mechanism for how these mutations cause the prion disease? a) They cause the prion protein to become degraded in the cell. b) They stabilize the structure of the PrPC form of the protein. c) They lead to overexpression of the prion protein in the brain. d) They cause the prion protein to misfold more easily into the PrPSc form. e) They cause the prion protein to interact with the microtubules in the neuron. Answer: d Question Type: True/False 18) The prion hypothesis has been deemed too controversial to be eligible for a Nobel Prize. Answer: False 19) The normal cellular version of the prion protein is a cytosolic copper-binding protein involved in cell signaling. Answer: False 20) The PrPSc protein is more resistant to proteases than the PrPC protein. Answer: True 21) Mice that lack the gene encoding the normal prion protein have severe neurological defects.
Answer: False 22) Sheep that are homozygous for a specific amino acid at codon 171 of the prion gene are completely resistant to infection with scrapie. Answer: rue 23) The high proportion of people who are heterozygous at codon 129 of the prion protein gene suggests that ancient humans may have participated in ritualistic cannibalism. Answer: True Question Type: Essay 24) Explain the nucleation-polymerization model for the propagation of the PrPSc form of the prion protein. How does this differ from the alternative model? Answer: This model states that the conformational change that causes PrPC to fold into PrPSc is a spontaneous and reversible reaction. This model also states that monomers of the PrPSc protein are less stable than PrpC, so that very little of the scrapie conformation would accumulate. If a person were “infected” with some of the PrPSc form of the protein, this would act as a “seed” to bind to the unstable PrPSc proteins and stabilize its conformation. These would also cause the PrPSc proteins to aggregate with each other and form fibrils, which would foster even more conversion of PrPC to PrPSc. In the genetic form of the disease, mutations in the prion protein would increase the stability of the PrPSc form or enhance its ability for form aggregates, which would also stabilize the scrapie conformation. The alternative model suggests that the PrPSc form of the protein is more stable, but unlikely to occur. Here the exogenous PrPSc protein would act as a chaperone to induce folding of PrPC into PrPSc. Mutations are predicted to increase the rate of refolding of the normal protein into the scrapie conformation. 25) Explain the observations that link new variant CJD with BSE. Answer: New variant CJD has a different pathology, presents at an earlier age, and presents with different initial symptoms than sporadic CJD. This suggests that its is a distinct disease process. Inoculation of brain tissue from cows suffering from BSE into monkeys causes the monkeys to come down with a disease that resembles the new variant form of CJD. In addition, prion proteins isolated from the brains of new variant CJD patients show different characateristics than the prions isolated from sporadic CJD patients, including protease cleavage products and glycosylation patterns. These patterns are more similar to those seen with the prions isolated
from the brains of BSE cows, suggesting this was the original source of the new variant CJD cases. 26) Describe how the prion hypothesis explains how there can be both an acquired and a genetic form of Creutzfeldt-Jakob disease. Answer: The prion hypothesis states that diseases like Creutzfeld-Jakob disease are the result of a protein, which is normally found in the brain, to adopt a different protein conformation that is associated with the disease. Because ingestion of some of the disease protein can cause the normal protein in the brain to misfold into the disease conformation, there can be an acquired or infectious form of the disease, like kuru, which is transmitted between individuals. But since the protein is normally produced in the brain, there can also be genetic variants that cause the protein to become misfolded spontaneously. These genetic variants may also make the individual more susceptible to the acquired or infectious form of the disease as well.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 33
Question Type: Multiple Choice
1) Which of the following is NOT a characteristic of the intrinsic cellular defenses against virus infections? a) They act rapidly after infection with the virus. b) They can act locally at the site of the infection. c) They involve pathogen detection receptors. d) They involve the release of cytokines and interferon. e) They are specific for a certain type of virus. Answer: e
2) Which of the following is found on the surface of the host cell or on endosomal membranes and can recognize viral nucleic acids? a) Toll-like receptor b) 2’-5’-oligo(A) synthetase c) Jak-Stat receptor d) RNA-induced silencing complex e) Interferon receptor Answer: a
3) Besides their subcellular locations, which of the following distinguishes TLR-2 from TLR-3? a) Only TLR-2 can recognize viral capsid proteins. b) Only TLR-2 can recognize viral glycoproteins. c) Only TLR-2 can recognize viral ssRNA. d) Only TLR-2 can recognize CpG motifs on viral DNA. e) Only TLR-2 can recognize viral dsRNA. Answer: b
4) Which of the following is an accurate description of autophagy? a) Engulfment of one cell by another cell.
b) Engulfment of an extracellular virus particle. c) Degradation of cellular components in a phagosome. d) Degradation of cellular DNA by nucleases. e) Degradation of cellular proteins by proteases. Answer: c
5) What is the role of the enzyme IKK in cellular antiviral defenses? a) It phosphorylates the Stat protein during interferon signaling. b) It phosphorylates IRF-3 transcription factor and activates it. c) It phosphorylates the NF-B protein and activates it. d) It phosphorylates the IkB protein and inactivates it. e) It phosphorylates the IkB protein and activates it. Answer: d
6) Which of the following is NOT a transcription factor that regulates cellular antiviral defenses? a) TBK-1 b) IRF-3 c) IRF-7 d) NF-B e) All of the above are transcription factors. Answer: a
7) Which of the following is NOT a type of antiviral cytokine? a) Interferon (alpha) b) Interferon (delta) c) Interleukin-6 d) Tumor necrosis factor (alpha) e) NF-B Answer: e
8) Which of the following can induce the extrinsic apoptosis pathway? a) Direct damage to cellular DNA. b) Binding of TNF to the a cell surface receptor. c) Increased activity of the p53 protein.
d) Release of cytochrome c from the mitochondria. e) Activation of the cytoplasmic caspase enzymes. Answer: b 9) Interferon is a protein that…. a) binds to a cell surface receptor and induces the expression of new cellular genes. b) binds to a viral peptide and presents it to the cytotoxic T lymphocytes. c) degrades viral and cellular mRNAs after it has been activated by dsRNA. d) binds to the surface of a virion and prevents it from attaching to the host cell. e) phosphorylates proteins, like eIF2, and inhibits translation of mRNAs. Answer: a 10) When interferon binds to its receptor it stimulates an intracellular signaling pathway. Which of the following proteins is part of this signaling pathway? a) NF-B and HMG1 proteins b) Caspase proteins c) Jak and Stat proteins d) IRF-3 and IRF-7 proteins e) Death inducing signaling complex Answer: c 11) When interferon binds to its receptor, which of the following events does NOT occur? a) Two interferon receptors associate with each other. b) One Jak kinase phosphorylates another Jak kinase. c) Stat1 and Stat2 proteins bind to a phosphorylated receptor. d) Two Stat proteins bind to each other and form a dimer. e) The Stat dimer activates the MAP kinase in the cytoplasm. Answer: e
12) Which of the following interferon induced proteins has the ability to hydrolyze GTP? a) 2’, 5’-oligo(A) snythetase b) Jak-Stat c) PKR d) Mx
e) Ribonuclease A Answer: d
13) Which of the following molecules is the activator for ribonuclease L, which is part of the interferon induced antiviral pathway? a) GTP b) 2’ 5’-oligo(A) c) dsRNA d) ssRNA e) DNA with unmethylated CpG Answer: b
14) Which of the following is the best-known substrate of the interferon induced PKR? a) Jak kinase b) Ribonuclease L c) Translation factor eIF2 d) IRF-3 e) Large ribosomal subunit Answer: c
15) Human herpesvirus 8 produces a viral homologue of the v-IRF protein. Which of the following describes how this viral homologue inhibits the interferon pathway? a) It binds to the interferon promoter and inhibits transcription. b) It stimulates the expression of the Mx protein. c) It blocks the activation of the PKR enzymes by double-stranded RNA. d) It prevents binding of interferon to its receptor. e) It inactivates the caspase enzymes. Answer: a
16) Which of the following is NOT an example of viral gene product used to avoid the antiviral effects of the PKR enzymes? a) Adenovirus VA I RNAs b) Vaccinia SK-1 protein c) Reovirus 3 capsid protein
d) HIV tat transactivator e) These are all examples of anti-PKR proteins. Answer: e
17) Dicer cleaves double-stranded viral RNA into which of the following? a) small interfering RNAs b) micro interfering RNAs c) RNA induced silencing complex d) small regulatory RNAs e) VA RNAs Answer: a Question Type: True/False 18) Toll-like receptors (TLRs) 2 and 4 are found on the surface of host cells while TLR 3 and 9 are found on the endosomal membranes. Answer: True 19) Both RIG-1 and TLR-7 are membrane bound proteins that can bind to single-stranded viral RNA. Answer: False 20) The presence of double-stranded DNA in the cytoplasm is recognized by cellular receptors and initiates antiviral defenses. Answer: True 21) Many of the symptoms that accompany a virus infection, including fever, lethargy and muscle pain, are the result of the pro-inflammatory cytokines produced by infected cells. Answer: True 22) Interferon can only induce an antiviral state in a cell if it enters the nucleus and binds to the promoters of interferon inducible genes.
Answer: False 23) Interferon is an excellent treatment for certain viral infections, like those caused by heptatitis B and C, because it has very few side effects. Answer: False 24) Plants, invertebrates and fungi rely on RNA interference to protect against virus infection since they do not produce interferon. Answer: True Question type: Essay 25) Why is double-stranded RNA such a potent inducer of a cell’s antiviral defenses? Describe one antiviral defense system that requires double-stranded RNA in order to be activated. Answer: Eukaryotic cells do not normally produce double-stranded RNA. Viruses on the other hand, even DNA viruses, often produce large amounts of double-stranded RNA. For example, reoviruses enter the cell with a dsRNA genome. All ssRNA viruses produce transient dsRNA during genome replication, when the RNA genome is bound to its complementary RNA strand. Even DNA viruses produce dsRNA when mRNA transcripts are transcribed from opposite strands of DNA. If the mRNAs overlap at their 3’ ends, then they will form dsRNA. Eukaryotic cells use the presence of dsRNA as a signal that there is a virus infection. There are at least two components of the intrinsic cellular defenses that are activated by dsRNA; the PKR enzyme and 2’, 5’-oligo(A) synthetase (2’-5’ OAS). Both PKR and 2’, 5’ OAS are synthesized in inactive forms after the cell is stimulated by interferon. In the case of PKR, the presence of dsRNA causes two copies of the PKR enzyme to bind to each other and allows cross phosphorylation. This activates PKR so that it phosphorylate other proteins in the cell, like eIF2 which inhibits cellular processes like translation. After dsRNA activates the 2’, 5’ OAS enzyme, it eventually leads to the destruction of all of the RNA within the cell. 26) The interferon system induces the expression of two inactive enzymes. Name these two enzymes, explain how are they activated, and describe the advantage of producing them as inactive proteins? Answer: The goal of the interferon system is to set up an antiviral state in an uninfected cell. When interferon binds to its receptors it initiates a signaling pathway that turns on expression of many new proteins. Two of these proteins, 2’, 5’-oligo(A) synthetase and PKR are initially produced as inactive enzymes. Double-stranded RNA is the inducer that causes both enzymes to
be activated. This double-stranded RNA is usually the result of a virus infection. When the 2’, 5’-oligo(A) synthetase becomes activated, it produces an unusual nucleic acid that activates another interferon induced enzyme, RNase L. This enzyme then degrades all of the RNA in the cell, including cellular and viral RNA. Double-stranded RNA also activates the PKR enzyme, which then phosphorylates the translation initiation factor eIF2a. This halts translation of both viral and cellular mRNAs. Because both of these effects will shut down normal cell metabolism and likely cause the cell to die, there needs to be a tight control on both their production and activation. If these cells were synthesized in an active form, they would harm the cell in the absence of a viral infection, which would be more devastating the virus infection alone.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 34
Question type: Multiple Choice
1) Which of the following is NOT a component of the innate immune response system? a) Cytotoxic T lymphocytes b) Complement system c) Natural killer cells d) Polymorphonuclear leukocytes e) Macrophages Answer: a
2) Which of the following is NOT a component of the adaptive immune response system? a) B lymphocytes b) Helper T lymphocytes c) Cytotoxic T lymphocytes d) Complement system e) Antibodies Answer: d
3) The binding of an antibody to a virus particle allows it to be phagocytosed by a macrophage. Which of the following describes the mechanism by which this occurs? a) The antibody makes the virus particle large enough to be detected by the macrophage. b) The macrophage has a receptor that binds to the constant region of the antibody. c) The antibody activates the complement system. d) The antibody causes the virus particle to be lysed in the endosome. e) The antibody causes the virus particle to bind to MHC-I Answer: b
4) Which of the following describes the process of antibody-dependent cellular cytotoxicity? a) An antibody activates the Fas receptor on the infected cell and causes it to enter apoptosis. b) An antibody causes the virus to be killed by a cytotoxic T lymphocyte.
c) An antibody binds to a virus particle and it is engulfed by a macrophage. d) An antibody binds to a virally infected cell and it is attacked by a macrophage. e) Both “c” and “d” are correct Answer: e
5) Which of the following is a situation where an NK cell can recognize a virally infected cell and kill it? a) The plasma membrane contains viral glycoproteins. b) The NK cell recognizes the MHC-I complex on the surface. c) The infected cell displays peptides on MHC-I complexes on its surface d) The infected cell has a reduced amount of MHC proteins on its surface. e) The NK cell recognizes the virus host cell receptor on the surface of the cell. Answer: d
6) Many viruses reduce the amount of MHC-I complex on the surface of the infected cell. How does the immune system recognize cells that lack MHC-I? a) Cytotoxic T lymphocytes will recognize the lack of MHC-I on the surface and kill the cell b) Macrophages will recognize an antibody bound to MHC-I and engulf the cell. c) Natural killer cells will kill cells that lack MHC-I on their surface. d) Cells that don’t have enough MHC-I on their surface will enter apoptosis and die. e) Cytotoxic T lymphocytes will recognized the altered MHC-I on the cell surface. Answer: c
7) Which of the following is NOT an antigen presenting cell? a) Cytotoxic T lymphocyte b) Macrophage c) Dendritic cell d) B lymphocyte e) All of the above are antigen presenting cells. Answer: a
8) Which of the following events causes a naïve T lymphocyte to become activated and differentiate into an effector T cell? a) The T cell receptor recognizes its epitope on a peptide presented on MHC-I.
b) The T cell receptor recognizes its epitope on a peptide presented on MHC-II c) A T helper cell releases IL-12 and causes it to differentiate. d) A macrophage releases IL-4 and causes it to differentiate. e) The T cell interacts with a B cell that recognizes the same epitope. Answer: b
9) Which of the following describes the primary role of Th1 cells in modulating the immune response? a) They present foreign antigens to B and T cells. b) They engulf virus particles and present peptides on MHC-II. c) They release cytokines that stimulate differentiation of cytotoxic T cells. d) They release cytokines that stimulate a B cell to differentiate into a plasma cell. e) They recognize and kill virus infected cells. Answer: d
10) Which of the following statements about MHC class I molecules is FALSE? a) They are located on the surface of all cells in the body. b) They are used to identify the cells as belonging to the host (self-identification). c) They are recognized by natural killer cells. d) They present cytoplasmic peptides to cytotoxic T lymphocytes. e) They are recognized by B lymphocytes. Answer: e
11) Which of the following describes the structure of the B-cell receptor? a) It is a type I trans-membrane protein. b) It is a type II trans-membrane protein. c) It is a membrane bound form of an antibody molecule. d) It is composed of two polypeptides, one of which has a trans-membrane domain. e) It is composed of two polypeptides, both of which contain trans-membrane domains. Answer: c
12) Which of the following is NOT a peripheral or secondary lymphoid organ? a) Tonsils b) Thymus
c) Lymph node d) Spleen e) Peyer’s patches Answer: b
13) Which of the following types of immunoglobulin molecules is the first to be made during an immune response to a virus infection? a) IgA b) IgD c) IgE d) IgG e) IgM Answer: e
14) Which of the following is the receptor that differentiates a cytotoxic T lymphocyte from a helper T lymphocyte? a) CD8 receptor b) CD4 receptor c) MHC class I d) T cell receptor e) B cell receptor Answer: a
15) What happens when the T cell receptor on a CD8 positive T cell recognizes the peptide displayed in the MHC-I complex on an infected cell? a) It attracts natural killer cells, which kill the infected cell. b) It releases interferon which stimulates macrophages to engulf the cell. c) It releases IL-4 to stimulate the B cells to release antibodies. d) It releases proteins that kill the infected cell. e) It releases IL-12 which stimulates the production of Th1 cells. Answer: d 16) Which of the following is NOT an activity associated with interferon ? a) Induces the expression of MHC class II proteins.
b) Enhances the processing of viral proteins into peptides. c) Induces the differentiation of natural killer cells. d) Stimulates development of Th1 cells. e) Stimulates activation of macrophages. Answer: c
17) Myxoma virus, a rabbit poxvirus, produces a viroceptor that is a homologue of the interferon- receptor. What purpose does this serve the virus? a) It sequesters the interferon-. b) It stimulates the host cells to divide. c) It enhances the release of virus particles from the infected cell. d) It increases virus replication. e) It prevents the MHC-I protein from displaying viral peptides. Answer: a Question Type: True/False 18) The complement system is only effective at attacking bacterial infections but has no role in fighting off viral infections. Answer: False 19) Pathogen specific B and T lymphocytes are mostly localized in specialized organs of the lymphatic system. Answer: True 20) Antibodies are produced by CD4 positive T lymphocytes. Answer: False 21) Antigen presenting cells, like dendritic cells, interact with naïve T and B lymphocytes in the lymph nodes. Answer: True
22) The IgG molecule is the most abundant immunoglobulin produced during an immune response. Answer: True 23) A single plasma cell can secrete two different antibodies that recognize different epitopes. Answer: False 24) Antigenic drift allows viruses to evade both humoral and cellular immune defenses. Answer: True 25) The constant region of an antibody molecule is only located on the light chain. Answer: False Question type: Essay 26) Explain how B and T lymphocytes produced a variety of cell surface receptors that can bind a wide variety of epitopes on antigens. How is this related to the clonal selection theory? Answer: There are two polypeptides that compose the antibody molecules – a heavy and a light chain. These proteins contain both a constant region and a variable region. The variable regions are what make up the antigen binding domain of the antibody. The human genome contains a large library of exons that code for the variable regions of the antibody proteins. These exons are randomly selected in each B or T cell and recombined to produce a gene that encodes a unique variable region on the antibody molecule. The clone selection theory states that once each B and T cell has produced a unique receptor on the cell surface, it is the interaction with the receptor and its corresponding antigen that selects that cell for expansion. This interactions causes the cell to undergo significant cell division to produce a clone of identical cells that can secrete that same antibody, in the case of B cells, or has the same T cell receptor. 27) Explain why it is more difficult for the immune system to detect and destroy viruses than bacteria. Describe the primary mechanism used by the adaptive immune response to overcome this obstacle. Answer: Most bacterial pathogens do not enter cells during an infection, but instead stay in extracellular spaces, such as in the blood or lymphatic system. Outside of a host cell, these bacterial cells are susceptible to being bound by antibodies, attacked by complement or engulfed
by macrophages. Viruses, on the other hand, replicate entirely inside of host cells. They are only present in the blood and lymph when they are moving between host cells. When they are inside of the host cell, the are protected from recognition by antibodies, complement and macrophage. Therefore, the immune system must have a different way of recognizing and destroying viruses. The ability of the MHC-I complex to display peptides from cytoplasmic proteins is the mechanism used to detect viruses inside of a host cell. When a virus is replicating, some of the peptides are viral and can be recognized by a cytotoxic T lymphocytes. When a cytotoxic T lymphocyte recognizes a viral peptide presented on MHC-I then the T cell will release proteins that will induce the death of the infected cell. The death of the infected cell will prevent it from releasing new virus particles into the body and will shut down the infection.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 35
Question type: Multiple Choice
1) Pasteur developed a vaccine to rabies by injecting which of the following into patients? a) Purified antibodies against rabies virus. b) Purified rabies virus. c) Brain from a rabid human. d) Spinal cord from a rabid rabbit. e) Muscle from a rabid dog. Answer: d
2) Which of the following was a major development in 1931 that helped in the production of antiviral vaccines? a) The invention of the Petri dish. b) The ability to grow viruses in chicken eggs. c) The development of the agar based culture system. d) The invention of the electron microscope. e) The development of primary cell culture systems. Answer: b
3) Which of the following has been a major technological problem with producing a vaccine to the H5N1 avian influenza? a) It was difficult to produce a reassortant virus strain. b) It was difficult to identify the most antigenic regions of the virus. c) The virus can not be grown in cultured cells. d) It was difficult to produce enough of the vaccine strain in chicken eggs. e) The virus replicates to very low titers. Answer: a
4) Which of the following is an example of a vaccine that is composed of a live wild-type virus? a) Influenza virus vaccine
b) Measles virus vaccine c) Vaccinia virus d) Chickenpox virus vaccine e) Polio virus vaccine Answer: c
5) What is the advantage of using a cold-adapted strain of influenza A as a vaccine? a) It spreads between people better than the wild-type. b) It does not replicate well in the lung tissue. c) It does not stimulate the release of interferon. d) It does not cause as much cell damage as the wild-type virus. e) It is more immunogenic than the wild-type.
Answer: b
6) Recombinant vaccines could consist of which of the following? a) Recombinant vaccinia virus that can express a viral structural protein. b) A recombinant adenovirus that contains a gene for a virus protein. c) Naked DNA that expresses a viral protein. d) A single viral structural protein that forms virus-like particles. e) All of the above are correct. Answer: e 7) One advantage of a live virus vaccine, attenuated or wild-type, is that …. a) there is no possibility of it reverting to a pathogenic virus. b) it only infects the person to whom it was administered. c) it is easy to produce and store. d) it can be amplified due to viral replication in the patient. e) All of the above are advantages. Answer: d
8) Which of the following is NOT an advantage of a killed virus vaccine? a) They are less sensitive to storage conditions. b) Any contaminating viruses will be killed too.
c) They provide the best immune response. d) They are safer to use in immunocompromised individuals. e) They are incapable of causing disease. Answer: c
9) Why must adjuvants be used when administering a killed or recombinant virus vaccine? a) These vaccines must be given as injections. b) These vaccines are less efficient at stimulating the immune system. c) These vaccines are not as safe as live attenuated vaccines. d) These vaccines are less stable than live attenuated vaccines. e) These vaccines must be given in several doses. Answer: b
10) Which of the following is a disadvantage of using aluminum salts as an adjuvant for vaccines? a) They do not stimulate Th1 cells which are involved in the cellular immune response. b) They do not stimulate Th2 cells which are involved in the humoral immune response. c) They do not enhance the release of interferons. d) They do not interact with the viral antigens properly. e) They do not stimulate the cytotoxic T lymphocytes. Answer: a
11) For which of the following viruses would a vaccine that stimulates the cellular immune system be most useful? a) Herpesviruses b) Dengue virus c) HIV d) Hepatitis C virus e) All of the above. Answer: e
12) Which of the following describes the chimeric rotavirus vaccine? a) A plasmid that expresses the surface glycoprotein from rotavirus. b) A single capsid protein from human rotavirus that forms virus-like particles.
c) A chimpanzee rotavirus that has been shown to be non-pathogenic in humans. d) The surface glycoprotein gene of the human virus inserted into the bovine virus. e) The surface glycoprotein gene of the bovine virus inserted into the human virus.
Answer: d
13) For which of the following viruses is a vaccine NOT being currently developed? a) Human rhinovirus. b) Hepatitis C virus. c) Dengue virus. d) Respiratory syncytial virus. e) Human immunodeficiency virus Answer: a
14) Which of the following is NOT an improvement that is in the process of being developed for use in vaccines? a) Adjuvants that stimulate toll-like receptors. b) Injecting pulsed dendritic cells back into the patient. c) Introducing virus genes into the human genome. d) Using a gene gun to deliver the vaccine. e) Injection of plasmid DNA that expresses a viral antigen. Answer: c
15) Which of the following is NOT an example of a currently available vaccine type? a) Chimeric virus b) Plasmid DNA c) Virus-like particles d) Subunit vaccine e) Whole inactivated virus Answer: b
16) The current vaccines that are marketed for human papillomavirus and hepatitis B are examples of what type of vaccine? a) Subunit vaccine
b) Chimeric virus c) Whole inactivated vaccine d) Live attenuated vaccine e) Multivalent peptide vaccine Answer: a
17) Which of the following is the primary reason that live attenuated vaccines so difficult to develop? a) Viruses do not mutate very quickly. b) Viruses replicate very quickly. c) The mutations that determine attenuation can not be predicted. d) Not all pathogenic viruses can be grown in culture. e) It is difficult to maintain the stability of attenuated viruses. Answer: c Question Type: True/False 18) Only live wild-type or attenuated vaccines can be delivered orally or nasally. Answer: True 19) Most of the currently available attenuated virus vaccines were produced by creating known mutations in the viral genome. Answer: False 20) Passaging human viruses in non-human cells is one method used to produce an attenuated virus strain. Answer: True 21) For a vaccine to be effective, it is more important that it stimulate a humoral immune response to a virus rather than a cellular immune response. Answer: False
22) Vaccines will never be able to treat patients chronically infected with hepatitis B virus because they can not break immunological tolerance. Answer: False 23) Early vaccines for rabies virus that contained rabbit spinal chord proteins caused autoimmune reactions in some people. Answer: True Question type: Essay 24) Explain the differences between the Salk and Sabin polio vaccines. Why have most wealthy countries switched from using the Sabin vaccine to using the older Salk vaccine? Answer: The killed Salk vaccine was developed slightly earlier than the Sabin vaccine. It consists of the pathogenic strains of poliovirus which have been treated with chemicals, like formaldehyde, that render the virus non-infectious. This vaccine must be given by injection and more than one injection may be required to provide protective immunity. The Sabin vaccine consists of attenuated versions of all three poliovirus strains. Because this is a live attenuated vaccine, it can be delivered orally and will replicate in the patient providing protective immunity with a single dose. The vaccinated person will also shed the vaccine virus, potentially vaccinating other people in the same household or community. The Sabin vaccine is ideal for developing nations with low vaccination rates since it is much easier to deliver and will spread to others in the community. However, the attenuated Sabin poliovirus strains contain anywhere from 6 to 57 mutations. These strains can sometimes revert to wild-type, causing polio in the recipients. While this is rare, most developed nations have gone back to using the killed Salk vaccine, which has a very low possibility of causing disease. 25) Describe the benefits of using subunit vaccines rather than live or inactivated virus vaccines. What are some of the new techniques being investigated to produce recombinant vaccines that would improve the effectiveness of these types of vaccines? Answer: One of the major benefits of a subunit vaccine is that it involves expressing only one or a few proteins from the pathogenic virus, so there is absolutely no possibility of the vaccine causing the viral disease. They are potentially the simplest and least expensive vaccines to produce. There are several new variations on the subunit vaccine, termed recombinant vaccines, that are being studied to improve the effectiveness of this approach. Chimeric vaccines would create recombinant bacteria or viruses that express viral proteins. These would allow the viral protein to be expressed and delivered to the immune system to stimulate a response. A DNA vaccine involves producing a plasmid that expresses a single viral protein. Injection of the plasmid DNA causes it to be taken up by cells. The expression and release of the protein
stimulates an immune response. Finally, purified recombinant proteins can be used to form viruslike particles. These interact with the immune system to stimulate a response to the viral particles. Because all of these approaches will require that adjuvant be given at the same time, adjuvants that will stimulate the cellular immune system as well as the humoral are being developed. These include adjuvants that can stimulate the Th1 cells as well as the toll-like receptors.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 36
Question Type: Multiple Choice
1) What was the first successful antiviral drug developed and which virus does it inhibit? a) AZT; HIV. b) 3TC; hepatitis B virus. c) Acyclovir; herpes simplex I. d) Amantadine; influenza. e) Nevirapine; HIV. Answer: c
2) Which of the following is a characteristic of a good target protein to be used in high throughput screening for potential antiviral compounds? a) It is an essential protein for virus replication. b) It is sufficiently different from cellular proteins. c) It can be expressed and purified easily. d) It’s activity can be assayed for quickly and easily. e) All of these are characteristics of a good viral target. Answer: e
3) What is the advantage of designing an antiviral drug that inhibits the very early or very late steps of viral replication? a) The antiviral drug will be in higher concentrations in the body. b) The antiviral drug does not need to enter the cell to work. c) The antiviral drug will have a higher binding affinity for the viral protein. d) The antiviral drug has a higher chance of inhibiting the virus infection. e) The antiviral drug will be more easily eliminated from the body. Answer: b
4) Which of the following is NOT a reason why viral enzymes make good targets for the development of antiviral drugs?
a) Enzymes inhibitors bind more tightly to their targets than inhibitors of other proteins. b) Drug companies have experience designing enzyme inhibitors. c) Enzymes normally interact with small molecules. d) Enzymes are usually well understood mechanistically. e) Enzymes are present in low concentrations within the infected cell. Answer: a
5) How does the capsid-binding drug pleconaril inhibit entry of picornavirus particles? a) It causes antibodies to bind to the capsid and blocks entry. b) It causes the capsid to become degraded by proteases. c) It binds to the same location on the capsid as the host cell receptor. d) It displaces a lipid normally bound to a pocket on the capsid. e) It binds to the envelope of the virus and prevents it from fusing with the plasma membrane. Answer: d
6) How does the antiviral drug maraviroc, which was developed to inhibit entry of HIV, function? a) It binds to the gp120 protein on the surface of the HIV virion. b) It binds to the gp41 protein in the envelope of HIV. c) It binds to the host protein CCR5. d) It binds to the host protein CD4. e) It binds to the lipids in the envelope of HIV and prevents membrane fusion. Answer: c
7) How does the antiviral drug amantadine inhibit the replication of influenza? a) It binds to the M2 ion channel and blocks the uncoating of the RNPs. b) It binds to sialic acid on the host cell and prevents binding of the virion. c) It binds to the HA protein on the virion and prevents binding to the host cell. d) It binds to the polymerase protein and halts genome replication. e) It binds to the nucleocapsid protein and prevents packaging of the viral RNA. Answer: a
8) What is the definition of a therapeutic index when discussing an antiviral drug? a) The amount of the drug that inhibits the virus replication.
b) The amount of the drug that is toxic to the host cell. c) The amount of the drug that is inhibits viral replication divided by the amount of the drug that is toxic. d) The dose that exerts 50% toxic effect divided by the does that exerts a 50% antiviral effect. e) The amount of the drug that kills 50% of the hosts.
Answer: d
9) Which of the following enzymes from herpes simplex virus is required to activate the antiviral drug acyclovir? a) Ribonucleotide reductase. b) Thymidine kinase. c) DNA polymerase. d) Nucleoside diphosphate kinase. e) Guanine kinase. Answer: b
10) The antiviral drug ganciclovir was approved to be used as a treatment for which of the following viruses? a) HIV b) Herpes simplex virus c) Varicella-zoster virus d) Cytomegalovirus e) Vaccinia virus Answer: d
11) Which of the following viral enzymes encoded by cytomegalovirus is responsible for phosphorylating and activating the antiviral drug ganciclovir? a) Guanine kinase b) Cellular nucleotide kinase. c) UL97, a serine-threonine protein kinase d) Thymidine kinase e) Thymidylate kinase Answer: c
12) Many antiviral drugs, like AZT and acyclovir, belong to which of the following groups of compounds? a) Nucleotide analogues b) Nucleoside analogues c) Nonnucleoside inhibitors d) Neuraminidase inhibitors e) Protease inhibitors Answer: b 13) The HIV1 protease is a good target for inhibiting virus replication because….. a) it cleaves the gag-pol polyprotein during virus assembly. b) it is required for the maturation of HIV1 virus particles. c) it has an unusual cleavage sequence on its substrate. d) the crystal structure for the enzyme is available. e) All of the above answers are correct. Answer: e
14) The neuraminidase inhibitors zanamivir and oseltamivir have been shown to have the highest effectiveness in reducing…. a) the number of deaths caused by the H5N1 bird influenza. b) the number of missed school days by children with influenza. c) the number of children who die from chicken pox. d) the number of people who get the common cold each year. e) the number of people who need to be vaccinated for influenza. Answer: a
15) The FDA approved the drug raltegravir in 2007 to treat infection with HIV. Which of the HIV enzymes does raltegravir inhibit? a) DNA polymerase b) gp120 c) Reverse transcriptase d) Integrase e) Protease Answer: d
16) Which of the following describes how the nonnucleoside inhibitors of the HIV reverse transcriptase are different than the nucleoside inhibitors? a) The nonnucleoside inhibitors prevent addition of the next nucleotide. b) The nonnucleoside inhibitors do not bind to the active site of the enzyme. c) The nonnucleoside inhibitors must be activated by the cellular thymidine kinase. d) The nonnucleoside inhibitors prevent synthesis of the reverse transcriptase. e) The nonnucleoside inhibitors lack a 3’ OH group. Answer: b
17) The antiviral drug AZT inhibits which enzyme from which virus? a) Protease from HIV b) Reverse transcriptase from HIV c) Integrase from HIV d) Neuraminidase from influenza e) DNA polymerase from herpes simplex virus Answer: b Question Type: True/False 18) Drugs that can treat viral infections were discovered about the same time as antibiotics, which are used to treat bacterial infections. Answer: False 19) In addition to treating virus infections in patients, some antiviral drugs have been useful tools in the research lab to dissect the function of viral proteins. Answer: True 20) The anti-influenza drug amantadine blocks entry of the virion by raising the pH of the endosome. Answer: False 21) Most of the currently available antiviral drugs target viral genome replication.
Answer: True 22) Like other antiviral drugs that inhibit the HIV1 reverse transcriptase, nevirapine is a nucleoside analogue. Answer: False 23) The chemical structure of ritonavir, an inhibitor of the HIV protease, resembles both the original substrate and the transition state intermediate of the enzyme. Answer: True
Question type: Essay 24) Describe some of the factors that make drugs to inhibit virus infections harder to develop than the drugs used to fight bacterial infections. Answer: Antibiotics that inhibit the replication of prokaryotic bacteria are easier to develop than drugs that inhibit viral replication for several reasons. First, bacteria are free living organisms that usually do not enter the cells of their host. This means that they must encode all of their own enzymes and translational machinery. Since they are prokaryotic, their enzymes and ribosomes are different than the eukaryotic enzymes and ribosomes of humans. This means that an antibiotic will probably not inhibit a similar enzyme in a human cell. In addition, bacteria are more similar to each other than viruses are, so a compound that inhibits one kind of bacteria will most likely inhibit another bacteria as well, which allows for the production of wide-spectrum antibiotics. Viruses on the other hand enter the host cell and use the enzymes and ribosomes of their host cell. Any drug that inhibits the cellular enzymes or ribosomes will be toxic to the patient. That means that a drug must be designed to inhibit a specific viral enzyme in order to be effective. Finally, viruses are more diverse, so it unlikely that a drug that inhibits one virus will also inhibit the replication of another virus. 25) Explain the targeted-based high throughput screen approach to the discovery of new antiviral drugs. What makes a good viral target for this approach? Answer: This approach starts with the identification of a viral gene product or enzyme which would make good drug target. The best targets are those proteins or enzymes that are essential for virus replication and that are sufficiently different from their cellular counterpart so that there can be selective inhibition of the viral enzyme. Once a target protein has been identified, it is then expressed and purified so that an easily measured activity assay can be developed. This activity assay is then used to screen thousands of chemicals to identify potential inhibitors. These
inhibitors are then used as a starting point to develop new compounds that inhibit the target even more yet have reduced toxicity and high bioavailability. 26) Describe the two factors that determine how the antiviral drug acyclovir is specifically targeted to inhibit the replication of herpes simplex virus. Answer: Acyclovir is a potent inhibitor of herpes simplex DNA replication. There are two steps where selectivity allows acyclovir to target herpes simplex replication over cellular DNA replication. The first step involves the activation of acyclovir, which requires phosphorylation into a monophosphate. The is carried out by the herpes simplex thymidine kinase, which has a much higher affinity for acyclovir than the cellular thymidine kinase. In fact, no mammalian thymidine kinase can phosphorylate acyclovir as efficiently as the herpes enzyme. This results in a much higher concentration of the activated drug in the herpesvirus-infected cells. The second step involves the herpes simplex DNA polymerase, which has a higher affinity for the activated acyclovir and is more easily inhibited by the drug than the cellular DNA polymerases are. Taken together, these two levels of selectivity mean that herpesviral DNA replication will be inhibited more than cellular DNA replication.
Package Title: Testbank Course Title: Acheson 2nd edition Chapter Number: 37
Question type: Multiple Choice
1) Which of the following is NOT an objective for which virus vectors have been designed? a) As anticancer agents that specifically kill tumor cells. b) To create genetically modified animals. c) To vaccinate animals and humans against specific diseases. d) To produce specific proteins in cultured cells. e) To provide functional genes in people with genetic diseases. Answer: b
2) SV40 was the first virus used to express a foreign protein in a cultured cell. But SV40 has which of the following limitations? a) The small genome can only accommodate a small gene. b) It can only infect monkey cells. c) It does not integrate its genome into the host cell genome. d) It replicates very slowly. e) It does not have a strong promoter/enhancer for gene expression. Answer: a
3) Which of the following viruses has been used to express large proteins in cultured cells? a) Adenovirus. b) Baculovirus c) Herpes simplex virus d) Both adenovirus and baculovirus e) Both adenovirus and herpes simplex virus Answer: d
4) What is the purpose of gene replacement therapy? a) To change the frequency of genes in the human population. b) To give animals useful traits.
c) To treat diseases caused by an inherited mutation. d) To produce adult stem cells for medical treatments. e) To produce proteins to be used as drug treatments. Answer: c
5) A mammalian expression cassette used to produce an exogenous gene in a virus vector must have which of the following components? a) Splicing signals. b) Strong enhancer. c) Polyadenylation signal d) Translational leader sequence e) All of the above are correct. Answer: e
6) Which of the following can be used to express a second transgene from a single mRNA? a) Downstream AUG. b) IRES c) Alternative mRNA splicing signals. d) RNA editing sequences e) All of the above. Answer: b
7) Which of the following viruses has been used to produce the best characterized and mostly commonly used virus vectors? a) Lentivirus b) Herpes simplex virus c) Adeno-associated virus d) Adenovirus e) Retrovirus Answer: d
8) In the first generation of adenovirus vectors the E3 gene was deleted. How could the virus replicate in the absence of the E3 gene products? a) A plasmid containing the E3 gene is transfected along with the viral DNA.
b) The cell line that the recombinant viruses are grown in carries the E3 gene. c) The E3 gene products are not required for adenovirus replication. d) The transgene inserted into the virus complements for the E3 gene. e) The E3 gene products are packaged into the virions. Answer: c
9) Which of the following describes the primary benefit of the third generation adenovirus vectors that lack all of the viral genes? a) They can not replicate and kill the cell. b) They do not produce any toxic viral gene products. c) They have more room for a large transgene. d) They do not stimulate an immune response to the virus. e) All of the above are correct. Answer: e
10) Adenoviruses that lack which of the following genes can replicate poorly in normal cells but well in many tumor cells? a) E1A b) E1B c) E2 d) E3 e) E4 Answer: b
11) A recombinant adenovirus, called Gendicine, has been approved to treat cancer in China. Which of the following proteins does this virus express? a) p53 b) pRb c) p300 d) Cre recombinase e) E1A Answer: a
12) Which of the following viral proteins controls the types of cells that a retrovirus can infect?
a) Capsid protein b) Gag proteins c) Protease d) Envelope protein e) Reverse transcriptase Answer: d
13) Which of the following is the primary reason why it is difficult to produce packaging cell lines for both retrovirus and adenovirus vectors? a) The proteins are degraded by the proteasome in the cell. b) It is difficult to express high levels of the proteins. c) Many of the required viral proteins are toxic to the cell. d) The immune system recognizes the proteins and kills the cell. e) The proteins stimulate the RNAi defenses in the cell. Answer: c
14) Which of the following is a major disadvantage of using a vector based on adeno-associated virus (AAV) rather than an adenovirus or a retrovirus? a) The DNA of the AAV vectors integrates into specific location in the genome. b) The virus is toxic to human cells. c) It infects cells of the immune system, causing a strong immune response. d) The immune system reacts very strongly to the AAV proteins. e) The small genome can only tolerate an insert of 4.5kb. Answer: e
15) Production of adeno-associated virus (AAV) vectors requires several of the proteins from adenovirus. What is the major advantage of expressing these proteins from plasmids rather than infecting the packaging cells with live adenovirus? a) There will be no immune response against the infected cells. b) There will be no adenovirus particles in the AAV virus preparations. c) There will be no release of interferon from the infected cells. d) The packaging cells will not become transformed. e) The packaging cells will produce a higher amount of recombinant AAV particles. Answer: b
16) The EBNA-1 protein from the Epstein-Barr virus is being developed to help improve virus vectors. Which of the following describes how this protein could be used? a) It allows a vector that contains oriP to be maintained as an episome. b) It stimulates transcription of the transgene incorporated in the vector. c) It inhibits the intrinsic cellular defenses against the vector. d) It allows the cell to tolerate the toxic viral proteins. e) It stimulates cellular DNA replication. Answer: a
17) Zinc finger nucleases could be used to solve one major disadvantage of using retrovirus vectors in gene therapy treatments. Which of the following disadvantages could they solve? a) The low levels of transgene expression. b) The stimulation of the immune system by the virus vector. c) The random integration into the host genome. d) The ability to only insert small transgenes in the vector. e) The toxicity of the viral proteins to the transduced cell. Answer: c Question Type: True/False 18) Viruses make good gene therapy vectors because they are highly efficient at delivering nucleic acids to a particular kind of cell. Answer: True 19) Virus vectors that contain large transgenes do not require a helper virus to be propagated. Answer: False 20) RNA virus vectors do not require the same enhancer/promoter sequences as DNA virus vectors. Answer: True 21) The plasmids that are used to express the retroviral proteins in the packaging cell lines contain the packaging signal ().
Answer: False 22) Adeno-associated virus can infect dividing as well as nondividing cells. Answer: True 23) The genes to treat most of the severe genetic diseases could fit in the AAV genome. Answer: False 24) Since vectors based on lentiviruses can infect nondividing cells, they have an advantage over vectors based on the genomes of other retroviruses. Answer: True Question type: Essay 25) Retrovirus vectors have been used to treat children who have the genetic disease severe combined immunodeficiency, which results from a mutated T cell receptor gene. What is the advantage of using a retrovirus vector over an adenovirus vector in this situation? Some of the children got T leukemia years after their treatment. How did the treatment cause their cancer? Answer: Retroviruses integrate the DNA provirus randomly into the genome of the host cell. A good copy of the T-cell receptor gene was inserted into the retrovirus vector. When the T-cells of the children were infected with the recombinant retrovirus, a good copy of the T-cell receptor gene was integrated into the cell genome. This means that every daughter cell that results from cell division will carry a copy of the good receptor gene. Adenovirus vectors do not integrate into the host chromosome, so the good gene is not propagated in the same way. One disadvantage of the fact that retroviruses integrate is that they integrate into a random location in the genome. This means that the strong LTR of the virus may end up near a proto-oncogene. The LTR can cause the over expression of this gene which then leads to a cancer of the T-cells that were infected with the recombinant retrovirus. 26) Describe two advantages that the third generation adenoviral vectors have over the original first-generation vectors. Explain the methods used to produce a recombinant adenovirus using these third generation vectors. Answer: The third generation adenoviral vectors, sometimes referred to as high capacity or “gutless” vectors, have had all of the adenovirus genes removed. This gives the vector more
space to accommodate larger or multiple transgenes. It also eliminates all of the viral proteins, which could stimulate an immune response to the vector and eliminate the transduced cells. Because the proteins are toxic to the cell, it is difficult to produce a cell line that expresses all of the viral proteins required for viral replication and production of the recombinant virions. In this case, the cell is infected with a helper virus, usually derived from a first-generation adenoviral vector, that produces all of the adenovirus proteins required for DNA replication and virion production. To prevent the contamination of the recombinant virus with the helper virus, the packaging signal in the helper virus genome is put between two loxP sites and the virus expresses the Cre recombinase. This removes the packaging signal from the genome of the helper virus and prevents those genomes from being packaged into virions. So all of the resulting virus preparation only contains the recombinant genome with the transgene.