For a small percentage of the population--a very fortunate few--exposure to HIV is not a death sentence. Nature has somehow enabled these individuals to resist infection or stave off progression to AIDS. Probing their secrets could eventually lead to better vaccines and treatments. To that end, researchers at the National Institute of Allergy and Infectious Diseases (NIAID) looked at tiny variations called single nucleotide polymorphisms (SNPs) in an immune system gene dubbed RANTES in HIV-positive and HIV-resistant subjects. Their investigation revealed a variant of RANTES that leaves a person twice as susceptible to HIV infection. Yet, intriguingly, the variant also slows the rate of progression to AIDS by about 40 percent.

NIAID researcher David McDermott and his colleagues described their findings in this week's issue of the journal AIDS. "At first blush it doesn't make sense," McDermott muses, "but nothing involving HIV is simple." He does offer a speculative explanation: SNP causes the RANTES gene to make a surplus of the RANTES immune system molecule, which normally acts to cause inflammation. Because such inflammation expands spaces between cells, HIV can enter the body more easily, which explains why RANTES increases susceptibility to HIV infection. At the same time, in order to spark inflammation, RANTES must glom onto the surface receptors of the so-called T cells--the same receptors HIV uses to enter those cells. In so doing, RANTES prevents HIV from entering the T cells, thwarting the virus's ability to spread. RANTES's ability to block HIV has not escaped the attention of drug companies, several of which are attempting to develop a RANTES-based HIV drug. But McDermott cautions that although the team's findings support that endeavor, "higher RANTES levels may increase the likelihood of aquiring HIV."