Gene Helps Halt HIV Species Jump

The human AIDS viruses (HIV-1 and HIV-2) originated as viruses of apes and monkeys, respectively, yet little is known about whether or how these invaders adapted to the new genetic "environment" encountered in humans. One group of host genes, collectively known as restriction factors, is thought to influence the ability of such viruses to move between different primate species.

A study conducted by Andrea Kirmaier and Welkin Johnson of Harvard Medical School, together with Vanessa Hirsch of the National Institutes of Health, provides direct evidence in apes and monkeys of a restriction factor gene called TRIM5 acting as a genetic barrier to cross-species transmission of a primate immunodeficiency virus related to HIV-2. The findings will publish next week in the online, open access journal PLoS Biology.

The primate immunodeficiency viruses include HIV-1 and HIV-2 as well as the numerous simian immunodeficiency viruses found among African apes and monkeys. The distribution of SIVs among their natural hosts reflects a long history of viruses jumping between species, including the very recent invasions of humans by SIVs from chimpanzees, giving rise to HIV-1, and sooty mangabey monkeys, giving rise to HIV-2. SIV from sooty mangabeys also jumped into Asian rhesus monkeys where, like HIV-1 and HIV-2 in humans, it causes AIDS.

Scientists believe that the movement of viral pathogens between hosts ultimately drove the evolution of certain genes, called restriction factors, as protection against such events. Expression of one such gene, TRIM5, renders cultured cells resistant to infection by retroviruses (including human retroviruses like HIV-1 and HIV-2) in the laboratory. The study by Kirmaier and colleagues now confirms the ability of TRIM5 to suppress cross-species transmission of SIV in vivo.