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AIDS at 25

A blog about the 16th International AIDS Conference in Toronto, August 13-18, 2006.

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Why doesn't everyone who's HIV-positive develop AIDS?

Category: The Science of HIV/AIDS
Posted on: August 16, 2006 2:30 PM, by Tara C. Smith

Ran across this interesting article in New Scientist on natural resistance to HIV.

Researchers are launching a project to discover how certain people, dubbed "elite controllers", are successfully able to fend off the HIV virus without using drugs.

More and more cases of such people - also known as "elite suppressors" - are coming to light. Unlike the sex workers in Kenya identified a decade ago as being HIV-negative despite their constant exposure to the virus, elite controllers are infected, and do develop antibodies to the virus, but at a very, very low level.

Their immune system is naturally able to suppress the virus and they remain as healthy and symptom-free as people on antiretroviral drugs, despite not receiving this treatment.

"We have recruited over 100 elite controllers ourselves and an additional 100 through our collaborators," says Bruce Walker at the Massachusetts General Hospital in Boston, US. "We are now identifying about 10 a week through word of mouth, he told New Scientist.

We already know about one mutation, called CCR5 delta 32. This gene encodes for a protein on human cells that acts as a "dock" for HIV. If people carry one copy of the mutated gene and become HIV-infected, they generally progress to AIDS more slowly than those who carry two copies of the normal gene. If someone carries two copies of the mutated gene, it's unlikely they'll become HIV infected at all. This seems to be a bit different from the "elite controllers," though, who become infected by keep the virus in check at low levels for a long, long time.

This is an important group to study, as determining exactly what it is that's different about them may provide a key insight into ways to control the virus in people who aren't elite controllers. It could be a difference in the virus, in the host genetics, in some third cofactor, or some combination of the three; a large, systematic study (like the one that's in the works and described in the article) can help to sort this out, pinpointing just why these people, though infected, keep the virus at such a low level and don't progress to AIDS.

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Comments

One of the first projects I worked on during college was to develop a rybozyme to induce CCR5d32. While this deletion protects against HIV, it seems to make you more susceptable to West Nile Virus. Is anyone working on a small protetin to induce d32 as we were with rybozymes?

Posted by: Dior | August 17, 2006 7:43 AM

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