Timothy Ray Brown (aka, The Berlin Patient) is the first person to go from being HIV+ to HIV-. Usually, he's described as the first person to be cured of AIDS. Scientists are a bit more circumspect about the situation. Brown got a bone marrow transplant using marrow donated by a person whose body has natural resistance to HIV. That was in 2005. Now off of anti-retroviral drugs, Brown's HIV has (so far) not returned. Two other men have been through the same treatment with promising results, although they are still taking anti-retroviral drugs, so it's impossible to say yet whether they are also actually HIV-.

Even if this is a cure, it is not the world's most widely applicable cure. Yet. But it is very interesting and, obviously, an amazing story.

I've never heard Timothy Ray Brown speak before, so I wanted to post this interview video from Democracy Now. It probably won't add much to the story that you didn't already know, but it's powerful to see the guy, himself, talking about it.

PREVIOUSLY

We've talked here before about the importance of the protein CCR5 in HIV/AIDS treatment research. CCR5 is a protein on the surface of immune cells. Some people have a genetic mutation, called Delta-32, which alters how that protein works, how often it appears, or changes its structure. People with the mutation have immunity to some strains of HIV, the virus that causes AIDS.

CCR5 is the key to the Berlin Patient—Timothy Ray Brown—who, until recently, was the only person to ever be cured of AIDS. Brown received bone marrow transplants from people who had the Delta-32 mutation. His body has been HIV-free for five years. And, last week, researchers announced that two other people successfully received the same treatment.

But here's the thing, until today, I didn't totally understand how the connection between CCR5, Delta-32, and HIV worked. There's a story (and some great digital illustrations) on NPR's Shots blog that makes the situation much more clear. HIV, apparently, have little spikes all over its surface. These spikes are how the virus injects itself into cells.

When it bumps into a T cell, a finger-like projection on the cell's surface, called CCR5, pushes down on the spike. This interaction pops open the HIV and releases the infectious genes into the cell. A gene therapy could protect T cells by inactivating the CCR5 gene.

Great "A-ha!" moment for me. Read the rest of the story and look at the illustrations. It'll make some thing make a lot more sense.

Read the rest at NPR's Shots blog

PREVIOUSLY:
If AIDS Has Been Cured, Why is the Victory Party So Small?
AIDS Research Done by 17-Year-Olds

Tony Papa of the Drug Policy Alliance says:

Millions of people have died of AIDS because of bad drug policy – and millions more lives hang in the balance.

The International AIDS Conference will be held in the U. S. for the first time in 22 years this July 22-27, in Washington DC. Activists, public health professionals, and distinguished world leaders are mobilizing in Washington with a clear message: the criminalization of people who use drugs – and especially backward government policies that restrict syringe access – are driving the HIV/AIDS pandemic.

Throughout the world, research has consistently shown that drug criminalization forces people who use drugs away from public health services and into hidden environments where HIV risks become significantly elevated. Mass incarceration of nonviolent drug offenders also plays a major role in spreading the pandemic, as inhumane conditions and lack of HIV prevention or treatment measures in prison lead to HIV outbreaks and AIDS cases behind bars – and among families and communities once those imprisoned are released.

Yet in countries where addiction is treated as a health issue, the fight against HIV/AIDS is being won. New HIV infections in countries such as Australia, Germany and Switzerland have been virtually eliminated among people who use drugs, just as mother-to-child HIV transmission has been eliminated in countries that make medicines for pregnant women accessible.

In the United States, however, the federal government has resisted evidence-based HIV prevention strategies – costing us hundreds of thousands of lives and billions of dollars. Congress re-instated a longstanding ban last December that prohibits using federal funds for syringe access programs – a move that will cost thousands of more lives in years to come.

Want to know more about the drug war and AIDS? Check out the infographic and take action by urging Congress to end the syringe access funding ban.

It's that time again. Maggie is back at the largest science convention in the Western Hemisphere for four days of wall-to-wall awesomeness. Each day, she'll tell you about some of the cool things she learned watching scientists from all over the world talk about their work. Check the bottom of each post to find links to earlier posts in this series!

Fifteen years ago, Dr. Harry Kestler got a call from a colleague in Florida who had inadvertently stumbled across a very unique family. An African-American woman had brought her sick child into the hospital only to discover that the child was HIV-positive and experiencing symptoms of AIDS. Further tests showed that she, herself, had HIV. As did four of her five children. It was a family tragedy. But in the midst of that, Kestler's colleague had noticed something odd.

The woman knew how she must have been infected—her ex-husband had been an intravenous drug user. But that had been more than 20 years ago. She, and her oldest child, had had HIV for over two decades without developing any symptoms. And her second-oldest child—who shared the same father—wasn't infected with HIV at all.

I've written here before about long-term non-progressors—a rare class of people who can be infected with HIV and live for decades without the virus ever developing into anything serious. Their secret: mutations in their genes that prevent HIV from binding to cells, which means it can't invade the cells or replicate.

Yesterday at the American Association for the Advancement of Science conference, I visited the student poster session, a place where undergraduate college students present research projects they're involved in and compete against one another to earn their poster a spot in an upcoming issue of the journal Science. There, among undergrads from MIT, Harvard, and other prestigious institutions, I met some surprising entrants. Eric McCallister—a student at Ohio's Lorain County Community College—and Megan Sheldon and Conner Anderson—two teenagers who go to high school at the same community college. All three of them are working with Harry Kestler to study the mutations that protect HIV non-progressors against an otherwise deadly virus. Unique researchers studying a unique family.

If you're not from the United States, you might not realize what a big deal this is. Research like this does not normally happen at community colleges. Instead, those schools are usually treated as a second-class system—a way for people to knock out two years' worth of college courses for less money, or just earn a two-year associates' degree. Lorain has partnerships with multiple traditional universities and allows students to take all but 30 credit hours of a four-year degree at the community college. They graduate with a full bachelor's degree from the four-year university. Because of that, the school offers more advanced classes than you can usually find at a community college, and it attracts highly-credentialed, research-oriented professors like Harry Kestler.

If you've heard about HIV non-progressors much at all, you've probably heard about one specific mutation called Delta 32. It's the most commonly talked about. "Basically, if you have this deletion mutation, there are 32 base pairs that should be in your gene sequence that just aren't there," Megan Sheldon told me. (Again, take a moment to process the fact that Megan is 17.) "When you loose those, it means you don't have this specific receptor on your cells and HIV can no longer bind to them."

Delta 32 mutations have been used to cure one man of HIV. In 2007, doctors killed off all the blood cells in the body of a man named Timothy Ray Brown, replacing them with a bone marrow transplant from a donor who carried the Delta 32 mutation.

If you're homozygous for Delta 32—that is, if you carry two copies of the gene that creates this mutation—you simply can't get HIV. About 1% of caucasians are homozygous, Sheldon said. If you're heterozygous, and have one copy of the gene, then you can contract HIV, but it will move very slowly, often taking 10 or even 20 years longer to progress into full-blown AIDS than would otherwise have happened.

Now that you know that, let's go back and talk about that anonymous family in Florida. They seem like they fit the patterns we're talking about here. But they didn't have the Delta 32 mutation. Their mutations were completely different. In fact, all three of the family members studied—the mother, and her two oldest children—had different mutations from one another. They represented three different paths to protection.

Eric McCallister, the college student who getting his bachelor's degree through that Lorain/university partnership, is doing research on blood samples from the second-oldest child—the one who never contracted HIV. Right now, he's trying to prove that this particular mutation—a shift in a single base, compared to the 32 base pair deletion you see with Delta 32—is, in fact, responsible for the child's ability to fend off HIV.

If he can prove that, though, it would be a big deal. I already mentioned that scientists have used Delta 32 mutations from one person to cure HIV in another person. This is not a cheap procedure, a safe procedure, nor a widely available one. The new mutation that McCallister is studying has the potential to remove one of the many roadblocks to curing HIV this way.

As with Delta 32-based treatments, doctors would still have to kill off all the blood cells in a patient's body. But, instead of needing to find a bone marrow donor who is both a match to patient and a carrier of Delta 32, McCallister says the single-point mutation could be induced in a sample of patient's own bone marrow. You'd remove some of their bone marrow, make the change, and then, after their blood cells had been killed off, transplant the altered version of their own marrow back into them.

As McCallister tries to prove he's found a better option for HIV treatment, his teenage colleagues are trying to document Delta 32 mutations in a more diverse swath of the population. Megan Sheldon, and her 16-year-old research partner Connor Anderson, got involved because they go to high school at Lorain County Community College. Every year, the school accepts 100 high school students through an application/lottery system. Those students attend class with college students through all four years of high school, graduating with both a high school diploma and an associates' degree. They'll have two years worth of college credits already knocked out.

Right now, Sheldon said, most of the research on Delta 32 mutations has been done in caucasian populations. When we say that the homozygous mutation is present in 1% of white people, that's not the same thing as saying that it's present in other populations. The truth is that we just don't know because those populations haven't been as well documented.

Sheldon and Anderson want to get a better idea of the rates of Delta 32 mutations within different racial and ethnic groups. Their current poster is basically a proof-of-concept, showing that they are capable of doing the research necessary to reach this goal. For their first study, the teenagers took blood samples from 50 students and teachers at a local high school. The data was completely anonymized. Although they want to study demographics of the mutation in the future, Sheldon and Anderson don't know anything about the people the current samples came from.

What they do know: Out of that 50 people, five were heterozygous for Delta 32. If any of those five contract HIV, they would be long-term non-progressors, going far longer without symptoms than other infected people.

PREVIOUSLY FROM AAAS:

As important as proteins are, we know relatively little about how and why these complex chains of amino acids fold and twist the way they do and how that structure relates to function. Foldit takes advantage of the fact that, given the right rules, people can come up with possible, plausible protein structures far faster than a computer program can factor out all the possible permutations. And that's why Foldit players—citizen scientists of a sort—were so useful in this case. Ed Yong at Not Exactly Rocket Science explains:

They discovered the structure of a protein belonging to the Mason-Pfizer monkey virus (M-PMV), a close relative of HIV that causes AIDS in monkeys. These viruses create many of their proteins in one big block. They need to be cut apart, and the viruses use a scissor enzyme –a protease – to do that. Many scientists are trying to find drugs that disable the proteases. If they don’t work, the virus is hobbled – it’s like a mechanic that cannot remove any of her tools from their box.

To disable M-PMV’s protease, we need to know exactly what it looks like. Like real scissors, the proteases come in two halves that need to lock together in order to work. If we knew where the halves joined together, we could create drugs that prevent them from uniting. But until now, scientists have only been able to discern the structure of the two halves together. They have spent more than ten years trying to solve structure of a single isolated half, without any success.

The Foldit players had no such problems. They came up with several answers, one of which was almost close to perfect. In a few days, Khatib had refined their solution to deduce the protein’s final structure, and he has already spotted features that could make attractive targets for new drugs.

“This is the first instance that we are aware of in which online gamers solved a longstanding scientific problem,” writes Khatib. “These results indi­cate the potential for integrating video games into the real-world scientific process: the ingenuity of game players is a formidable force that, if properly directed, can be used to solve a wide range of scientific problems.”

Wayne Martin Belger created the blood camera, which incorporates HIV-infected blood that acts as a red filter for portraits of HIV+ people. Now he's taking the project, which is called "Untouchable," to Africa:

I'm taking the untouchable to Sierra Leona, Liberia, Uganda, Ethiopia, Calcutta and 5 locations in Cambodia to do portraits of people living with HIV. I'm working with a major international HIV Health organization to make it all happen and they are really excited about the possibility of this project creating a new view of the global HIV community. So far, I've photographed about 60 people all over the US. With the Africa/Asia photos it will give a world contrast on how your geo location makes all the difference in your well-being and how major pharmaceutical profits need are at the heart of life and death.

I have a publisher that wants to do a book on the project and two major venues that are excited about exhibiting the finale work next year.

Apparently, the South African version of the show already has a HIV+ character, as Mark reported in 2002.

"If we're writing scripts for programs in Nigeria, the writers will be Nigerian scriptwriters," explains Farouky. "We'll often look for people who already have some experience in writing, but because we're aware [of] the format that we use and the methodology that we use, we'll provide training on how to write."

According to Farouky, collaboration is at the heart of the production process. "We work with our local teams to find ways in which we take the content that's important to them, to infuse the project with the cultural values, making sure we know which the taboo issues are and which are not," she told CNN...

"Our program is hosted by two muppets, a boy and a girl," she told CNN. "And because there is an entire region in Nigeria up in the North which is very Muslim, we had to be very sensitive. Even our publicity pictures could not have the muppets hugging, which we would normally have," she explained.

Although the first adaptation to reach West Africa, "Sesame Square" will be the latest in a long line of region-specific shows around the world, which include "Sisimpur" in Bangladesh, "Ulitsa Sezam" in Russia, and "Takalani Sesame" in South Africa.