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Scientists Probe How HIV Infection Turns Into AIDS


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What the two scientists found surprised them. According to the new model, AIDS actually begins when a less fit variety of HIV wins the day. This strain kills immune system cells extremely widely and quickly, but, in doing so, also limits the number of copies of itself it can produce. "It basically kills its own habitat, its house," Wodarz explained.

However, because this form of HIV is very good at quickly killing large numbers of immune cells, "once these less-fit strains emerge, they can plunge the patient into AIDS," Wodarz said.

In many cases, two or more strains of the virus can co-infect the same immune system cell, he added. If a fast-killing variety is one of those strains, it kills the cell before slower -- but better-replicating -- versions can go to work making millions of new viral particles.

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"But without this ganging up on the same cell, the killer virus [that leads to AIDS] would go extinct, because evolution would select against it -- because it is less fit and replicates less," Wodarz explained.

That means that -- according to the model -- one way of keeping AIDS at bay might be to make sure that only one type of HIV invades a cell at any given time.

Specific cellular mechanisms do allow a second or third viral particle to enter a cell, and a medicine that thwarted these "party crashers" might keep the deadliest form of HIV from ever emerging, Wodarz speculated.

He pointed to wild monkeys that are infected throughout their lives with HIV-like simian immunodeficiency virus (SIV) but never get sick.

"Some of them have a lot of the virus, and it evolves a lot, but it does not cause AIDS, ever," Wodarz said. He suspects the monkey's immune cells may have evolved to block secondary viral entry and thereby keep the most dangerous strain of SIV at bay.

Not everyone is convinced by the new model, however.

Dr. Benigno Rodriguez is assistant professor of medicine at Case Western Reserve University in Cleveland, and a specialist in the evolution of HIV disease. He called Wodarz and Levy's paper "an interesting concept," but said it contained a few significant flaws.

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Copyright © 2007 ScoutNews, LLC. All rights reserved.
Last updated 8/3/2007

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SOURCES: Dominik Wodarz, Ph.D., associate professor, biology, University of California, Irvine; Benigno Rodriguez, M.D., assistant professor, medicine, Case Western Reserve University, and attending physician, infectious disease, Case Medical Center, Cleveland; July 31, 2007, Proceedings of the Royal Society B


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