boiMAGazine “World AIDS Day” by boiMAGazine & boiMAG.com

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EDITORIAL

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Publisher: BOI Magazine, Inc. Editor: Mark Anthony Feature Editor: Nicole Marsh Media: Christian Conner, Jr. Graphic Design: Titanium Graphic Team

COVER

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layout & design Titanium Graphics, Inc. Layout Specialist: JR Garcia

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Chicago & Suburbs: Tag Team Delivery, Inc. World Wide Distribution: AnyFlip/Social Media Network Strut Model Brian Boyle (Interview Inside)

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"world science festival"

why is hiv so hard to kill? Humanity’s war against the HIV has been a constantly shifting battle, thanks to the wily nature of the virus. But humans, being quite wily themselves, have persevered in the search for a cure despite setback after setback. Recently scientists found a way to snip HIV’s genetic code out from the genomes of infected cells. The technique’s only been tried in cultured cells so far, but it could represent a powerful new weapon in the arsenal against AIDS.

But just what makes HIV such a formidable foe?

In most viruses, the genetic transfer of information mimics a host’s: DNA is transcribed to RNA, which is translated into a protein. But HIV is a retrovirus (in the family Retroviridae), meaning that it carries its genes around in the form of a single strand of RNA, rather than a DNA strand or doublehelix. In infected persons, HIV hacks the cells of the body with the help of an enzyme called reverse transcriptase, which allows it to create a DNA version of the viral genome after it invades the cell. The viral DNA strand becomes integrated into a host’s genome, and the cell copies out the instructions in those genes, creating new copies of the virus that can burst forth and infect other cells. In normal DNA replication, a cell employs a variety of molecular proofreaders to help avoid changes to the genetic code. But in reverse transcription, there aren’t those checks, meaning that a retrovirus’ genome can mutate very quickly. This is one reason HIV is particularly good at ducking treatments, it mutates so quickly, it’s hard to figure out what anchor a drug or vaccine can latch onto. HIV is also a member of the Lentivirus genus within the retroviruses, giving it another nasty set of armaments. Other retroviruses can only infect cells in the midst of division; lentiviruses aren’t bound by that restriction.

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The AIDS virus is also hard to destroy because it tends to infect the very cells designed to destroy it: a kind of white blood cell called a CD4 lymphocyte. These types of cells can be activated to fight pathogens, but can also lie inactive. If infected, these dormant CD4 cells can maintain a hidden reservoir of HIV that can bring the infection roaring back to life even after a successful course of treatment; most drugs can’t touch these reservoirs. As of now, there are two main strategies for a potential AIDS cure. One is a bone marrow transplant, first used by German doctors in 2008 to treat an HIV-infected man who was also suffering from leukemia. The doctors gave the patient marrow from a donor who possessed a special mutation called Delta 32, which helps resist HIV infection. Nearly two years after the treatment, the doctors could not find any trace of HIV in the patient’s blood, bone marrow, or other organs. But bone marrow transplants are too risky a procedure to become a widespread cure. One option for a “functional cure” involves patients taking antiretroviral medicines, which interfere at various stages of HIV infection and replication, very soon after infection. This approach has been shown to leave patients with very low levels of HIV in their blood, even after they stop taking the drugs. But there are limitations: a patient has to start treatment right after infection, and it’s still unclear just how long the effects can last. The “Mississippi baby,” seemingly cured of HIV after an intense antiretroviral therapy regimen lasting for 18 months shortly after her birth, has shown signs of HIV infection again. And the genome-editing techniques unveiled this week, though promising, still have to be proven in human subjects. There could be other complications as well. To edit HIV out of the genome, Temple University researchers Kamel Khalili and Wenhui Hu use a specially designed small strand of RNA that sniffs out the virus’ code. But, as mentioned before, HIV has a predilection for mutation, which could complicate creating effective code sniffers. Hopefully, further testing of Khalili and Hu’s technique won’t send them back to the drawing board once more.

WORLD AIDS DAY

FASHION SHOW Name of the show:

“STRUT”

Years in Existence:

This is the 10th year anniversary

Beneficiaries:

Project Vida and South Side Help Center Both organizations have been serving the community for over 20 years.

Date of Event"

Sunday, December 2nd, 2018 Location

The Promontory Chicago 5311 S. Lake Park Ave. Hyde Park, Illinois Produced by:

MadMan Productions Time:

Doors: 4:30pm Reception: 5pm Showtime: 6pm Designers & Models:

14 Designers 2 from NYC: Amy Verrier & HALZ NYC 25 models Tickets:

General admission: $27 Reserved: Front & Second rows: $37 Tables: $40

Cover Model:

Brian Boyle

Photographer:

Studio Meiling Productions Model Stylist:

John Fleming, Jr. boiMAG

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=INTERVIEW= Hello Brian. It is so wonderful to be able to sit down with you during the release of your first magazine cover and the buzz around STRUT’s 10 year anniversary event.

How are you feeling right about now?

I feel amazing, it’s an honor to have my first magazine cover, I am so excited for this opportunity. All the fittings for the show are finalizing and everything is just coming together wonderfully. It’s going to be such an exciting event and I can’t wait for the show.

This is your second time walking in STRUT. What brought you back? Strut was the show that really got me excited about runway. I had just started out performing in shows and didn’t really know what to expect. Strut is an upbeat, high energy, fastpaced show. There is music playing and everyone in the audience is cheering. By the end of the show I knew I had found something I was passionate about. Just seeing all the happiness and joy the show brought to the audience made me excited to come back and perform again this year.

This show is known for mixing the avant garde with the conservative. Which do you prefer and why? I enjoy modeling any type of style, it’s cool to be able to wear something that I would not normally wear in my daily life. Knowing how hard the designer has worked on any outfit makes it an honor to model it for them, but if I had to pick a preference I would go with avant garde. I like to put myself out there and love rocking the real extravagant and wild designs.

Obviously, I believe in you, and I have the upmost confidence in your talent. Does that put any pressure on you.

Your confidence in me and knowing that people are counting on me to perform well makes me motivated and excited to perform my best. I’ve been physically preparing for the show for weeks and it’s relieving to know that you’re rooting for me.

I’m sure this is just the first of many covers for you. The business side of modeling

is very different from the runway. How serious are you about the business side?

The business side is just as important as the runway side. It’s necessary to form relationships and build up a network with people businesswise to keep getting more work. As an independent contractor this is especially true. It’s crucial to stay professional, be reliable and represent anyone you’re working for at a level that wants them to keep you coming back. This is what I strive to do with any job I take.

How is your career going?

It’s going well, I’m happy with where I am. I only started modeling at the beginning of last February doing strictly print, then I moved on to walking in shows just over a year ago. So to come from not having any idea where this would lead me to where I am now, I am satisfied with how far I’ve come. But in the same sense, I plan on continuing to push myself and stay open to what other new opportunities may be presented to me.

Most of the models in STRUT have done the show for years because of some sort personal connection. Is it the same for you, and if so, in what way?

I feel a personal connection to Strut because I really believe in the cause. Over 1 million people in the US are living with HIV and it’s very important to continue raising awareness about the issue. I like to challenge STRUT models to be better..... to take risks and to seize opportunities. How do you feel about that and why? I am all for seizing new opportunities, especially with a little risk. In my modeling career so far I have come to realize that most of the reward comes with some risk. People always have preconceived beliefs about models. Let’s leave them with something surprising and interesting. I think that some people have the preconceived notion that models don’t have much else to them besides a pretty face. I haven’t found this to be true, most models I’ve had the privilege to meet and work with over the last few years are smart, intellectual people. People are often surprised to learn that I have a Mechanical Engineering degree from Purdue and work full time as a day trader.

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HIV BEFORE THE AGE OF AIDS by Mary Carmichael

HOW IT BEGAN

As soon as HIV was identified in 1983, scientists started trying to understand where it had come from, when it had arisen, and why it had spread.

Were they too late?

To answer most of their questions, they would have had to witness the virus’s evolution. Scientists can track new pathogens such as SARS and avian flu because they produce obvious symptoms almost immediately. But HIV is a stealth virus that takes as many as 10 years to present symptoms; by the time researchers knew enough to wonder about its origins, those origins were in the distant past. For the last 23 years, scientists have been trying to peer into that past. Jon Cohen, a correspondent for Science who has written extensively about the virus, compares the work to fossil hunting, using a few precious shreds of evidence to construct a possible history. “Everybody’s always looking for certainty. It doesn’t exist [in this field],” he says. “In a sense it’s all theory.” Nonetheless, the theory rests on facts, and at least a few of them are undisputed, including, most significantly, HIV’s family tree. There are two species of the virus, HIV-1 and HIV-2. The first evolved from a simian immunodeficiency virus (SIV) found in chimpanzees, while the second came from an SIV in a type of monkey called the sooty mangabey. HIV-1, which is responsible for the vast majority of AIDS cases worldwide, is divided into three groups, the “major” group M, and the much rarer “outlier” group O and “new” group N, that have diverged over years of mutation and evolution. Within the M group, which

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makes up 90 percent of all infections worldwide, there are at least nine strains, known as “clades,” of HIV-1 that are constantly mutating and merging with each other, creating yet more new varieties. “The M group epidemiologically has overwhelmed what else is out there,” says Dr. Beatrice Hahn of the University of Alabama-Birmingham, who has conducted much of the research into HIV’s origin. HIV-2, on the other hand, is not as virulent and largely confined to West Africa, where it originated. In May 2006, an international group of researchers led by Hahn answered two major questions about the origin of HIV-1 M, the deadliest and most widespread form of the virus: Where was its cradle, and what kind of chimp did it come from? Answering the questions was literally messy work, researchers collected 599 waste samples from wild chimpanzees and analyzed the viral particles they contained, but the results were immaculate. Three populations of Pan troglodytes troglodytes living in southern Cameroon provided the crucial data. Two of those populations currently carry SIVs that are molecular dead ringers for HIV-1 M, while many chimps in the third group are infected with an SIV remarkably similar to HIV-1 N. Group O’s simian sibling is probably lurking in other chimp populations in West Central Africa, says Hahn, adding that she has “a pretty good idea where it’s going to be … and we’re going to find it.” The research puts to rest decades of speculation about the birthplace of most types of HIV and their animal “reservoir” in the wild. But there are still many questions that haven’t yet been definitively settled, questions such as:

When did HIV-1 first start spreading in humans?

HIV-1 is surprisingly old, and it probably “debuted” in humans at least three separate times, one for each subtype, M, N, and O. Scientists’ best guess is that the precursor of the most common “M” virus jumped from the Cameroon chimps to humans sometime before 1931. Using samples of HIV-infected tissue harvested over the last three decades, virologist Dr. Bette Korber of Los Alamos National Laboratory has calculated that an ancestral form of HIV started spreading, slowly at first, in humans about 75 years ago. The actual jump from chimps to humans probably occurred shortly before that, says Hahn: “There’s no reason to believe this was just lingering around in people.” Korber’s model estimates a virus’ age based on how extensively different strains have mutated. HIV is an unusual virus; it changes its DNA by both mutation and, more often, recombination, when two strains merge within the body and exchange genetic material. Some scientists refer to this process as “viral sex,” and it may partially explain why it is so hard for scientists to make a treatment or vaccine. Korber’s model does not take recombination into account, but given a virus’ DNA configuration, it can roughly predict the age of that strain. Korber has tested the oldest known HIV sample, taken in 1959, and derived the 1931 estimate.

Why do scientists look at recent samples of HIV to determine the virus’ overall age? Wouldn’t it be better to use older samples that haven’t had as much time to mutate?

It would, but scientists don’t have that luxury. Other than the 1959 sample, there are very few preserved specimens of HIV-infected tissue that predate the early ‘80s, when the virus was first recognized

by health authorities. Researchers still hope there are forgotten samples in African freezers. “There has to be some serum or plasma somewhere, and given modern technology we could fish out the virus,” says Dr. David Ho, director of the Aaron Diamond AIDS Research Center and one of the world’s leading authorities on HIV. But even if those samples are found someday, they won’t necessarily yield definite answers about the virus’ age, says Korber: “Often, you can’t get anything out of samples like that.” Most African samples are made of blood serum, and serum samples contain viral RNA, which degrades much faster than the DNA found in tissue samples. In fact, says Ho, the 1959 sample, which was sequenced by his laboratory, was kept in a freezer but still didn’t survive the ravages of time. “It was completely dried up,” he says. “We were only able to get small pieces [of genetic material], and we had to stitch them together.”

So scientists have estimated when and where the most deadly type of HIV started infecting humans, but how did it do that?

Most AIDS researchers believe that the “bushmeat trade” allowed the HIV-1 virus, and separately HIV-2, to enter the human bloodstream several times. Hunters who kill and butcher chimps and monkeys are regularly exposed to animal blood teeming with SIVs. If the hunters have cuts, bites, or scratches, and given the nature of their work they almost always do, they can catch the viruses from their prey. Hunters going after chimps in Cameroon could have caught the first strains of HIV-1. Sooty mangabeys, hunted and kept as pets in West Africa, could have transmitted HIV-2 to humans.

Africans have hunted chimps and monkeys and kept them as pets for centuries; they’ve presumably been exposed to SIVs during most of that time. But the conditions Continued on a following page >>> boiMAG 13

continued

How it began needed for HIV to spread widely weren’t in place until after the continent was colonized and urbanized. The first victims would have found it easier to unwittingly spread the virus to sexual partners far and wide as roads and vehicles started connecting previously isolated villages and cities. Hospitals may have played a role, too. Strapped for cash, some of them probably re-used dirty needles, unknowingly infecting patients in the process.

Are there other theories about how the virus could have gotten into humans?

There are several competing theories, ranging from implausible conspiracies to arguments grounded in extensive research. The best-known of the latter, the “OPV/AIDS” theory, was exhaustively detailed in the 1999 book The River, by author Edward Hooper. As many as a million Africans were given oral polio vaccines (OPV) between 1957 and 1960. Hooper says witnesses have told him that a few batches of those vaccines were “grown” in chimp cells at a lab in Kisangani, a city in the Democratic Republic of the Congo and that the chimp cells, and thus the vaccines, could have contained SIVs that jumped into humans. “There are highly significant correlations between the places where this vaccine was administered and the places where AIDS first appeared on the planet four to 20 years later,” Hooper says. The majority of HIV researchers subscribe to the bushmeat theory and raise several arguments against the OPV theory. Hahn’s recent research confirming that HIV-1 M and N arose from Pan troglodytes troglodytes chimps in Cameroon presents one problem: The Kisangani lab is in the Democratic Republic of the Congo, and it’s home to a different subspecies of chimp than the one that was the source

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of HIV-1 M and N. However, it is possible that the chimps used in the Kisangani experiments were not from the area. In the spring of 2006, Hooper found a paper indicating that at least one of eight chimps at the Kisangani lab was a Pan troglodytes troglodytes. The 1959 sample also presents a problem for the OPV theory. Judging by how fast the virus mutates, it had already diverged significantly from its SIV ancestors by the time doctors extracted it from a patient. However, the African polio vaccination program had begun only two years earlier, so under the OPV theory, the virus would have had only those two years in which to evolve. Dr. Ho, who sequenced the sample, says it looks like the virus has been around a lot longer than that. Proponents of each theory have acknowledged (albeit grudgingly) that the other is scientifically possible. In the last two years researchers have found that both “simian foamy viruses” and at least two types of retroviruses can and do jump from monkeys to humans via hunting and butchery. And no one doubts that a vaccine cultured in primate cells could be contaminated with a primate virus. Some early polio vaccines contained SV40, a simian virus discovered in 1960, and the RNA virus that causes Marburg hemorrhagic fever. The question is not whether either scenario could have happened, it’s which one did. To truly disprove the OPV theory, Hahn says, researchers would have to find HIV-infected human tissue samples that predate the polio vaccine trials. To prove the OPV/AIDS theory, on the other hand, they’d have to find the ancestral SIV in batches of the vaccine that were made in Kisangani. Neither of those things has happened, and it’s possible they never will. (Mary Carmichael, is a Boston-based science writer. Additional credits: PBS.org & Frontline.)

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Event Details: Date: Wednesday - Sunday, March 20-24, 2019 Time: Wednesday-Saturday from 10am-8pm. Sunday from 10am-6pm. 26 boiMAG