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TUESDAY, April 29 (HealthDay News) -- Most drugs aimed at suppressing HIV target proteins lying on the virus itself, but new research suggests that focusing on the human host's immune cells might work even better.
That's because human cells mutate at much slower rates than does HIV, so the virus would have much less chance of mutating around the drug, scientists explained.
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The research is still in its early stages, but it "provides a very nice model that you can inhibit a cellular protein and affect HIV replication," explained co-senior author Dr. Pamela Schwartzberg, a senior investigator at the U.S. National Human Genome Research Institute.
Her team published the findings in this week's edition of the Proceedings of the National Academy of Sciences.
Almost all antiretroviral drugs work by targeting a viral protein. But HIV replicates continually, raising the odds for drug-resistant mutations. For this reason, HIV-positive patients must often take two or three different medications, so that if one drug fails, the others will still fend off the virus.
But there's another player in HIV infection: the human immune system T-cell, the virus' preferred host. T-cells carry their own surface proteins, but because humans replicate much less often than HIV, the odds of developing drug-resistant genetic mutations are much lower.
"If you are looking to affect a human protein, it's going to be much less susceptible to the process of developing resistance," explained Rowena Johnston, vice president of research at The Foundation for AIDS Research (amfAR) in New York City.
In their research, Schwartzberg and co-senior author Andrew Henderson, of Boston University, decided to focus on a T-cell protein called interleukin-2-inducible T-cell kinase (ITK). ITK is a "signaling" protein that works in a variety of ways to activate T-cells.
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