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FRIDAY, Aug. 3 (HealthDay News) -- The common scientific wisdom on how HIV infection proceeds to full-blown AIDS might be wrong, two U.S. researchers say.
They hope that their new insights, if proven, will lead to exciting new treatment targets down the line.
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Working from a complex mathematical model of viral replication and immune cell death, the researchers now suspect that AIDS begins when one especially fast-killing strain of HIV gains the upper hand over a less-lethal, but more prolific, strain.
"This throws into question a lot of the notions that have been accepted about the evolution of the virus" within a typical infected human, explained study co-author Dominik Wodarz, associate professor of biology at the University of California, Irvine.
He and another researcher, David Levy, of New York University, published their findings in the July 31 issue of the Proceedings of the Royal Society B.
Since its first recorded appearance nearly three decades ago, HIV infection has followed the same deadly path: a short, weeks-long period of acute flu-like symptoms followed by years of asymptomatic dormancy, and then symptoms of immune system breakdown that herald the emergence of AIDS.
But what is it that tips asymptomatic, low-level infection into AIDS?
The common dogma among scientists has long been that various strains of HIV battle a silent war within the body over time until the fittest -- defined as the strain that reproduces itself the most -- wins. That strain then goes on to overwhelm the body's immune cells and destroy the host's defenses against disease.
To test that theory, Wodarz and Levy constructed a complex mathematical model that took into account two factors about HIV: how fast the various strains replicate and how fast they kill cells (not always the same thing, the researchers noted). They also factored in human immune system responses to HIV.
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