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Variation in HIV's ability to disable host defenses contributes to rapid evolution

One of the reasons HIV is so difficult to contain and treat is its rapid evolution. Understanding how host defenses and viral countermeasures contribute to that evolution is vital.

Host cells produce two proteins that mutate HIV DNA and interfere with the virus's ability to replicate. But HIV produces a protein, called Vif, that can disable the two defensive proteins.

Vif is full of variation, both in sequence and in function, according to a new study in PLoS Pathogens, and this could in turn potentially accelerate the evolution of HIV.

Within a single patient, some versions of Vif don't work at all; others counteract only one of the host's defensive proteins. "It's a leaky system," according to Paul D. Bieniasz, senior author of the study and associate professor at The Rockefeller University's Aaron Diamond AIDS Research Center.

Some variations in Vif only partially inactivate the defensive proteins that cause HIV to mutate, and might even promote further variation in the virus within patients. "This work elucidates new pathways which shape the evolution of the virus," says Viviana Simon, lead author of the study.


Citation: Simon V, Zennou V, Murray D, Huang Y, Ho DD, et al. (2005) Natural variation in Vif function can differentially impact APOBEC3G/3F neutralization: A potential role in HIV-1 diversification. PLoS Pathogens 1(1): e6



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