Abstract
Author SummaryThe human immunodeficiency viruses HIV-1 and HIV-2 originated from cross-species transmission of simian immunodeficiency viruses (SIVs) from chimpanzees (SIVcpz) and sooty mangabeys (SIVsm), respectively. A related virus, SIVmac, causes AIDS-like pathogenesis in rhesus macaques; like HIV-2, SIVmac is the product of a cross-species jump of SIVsm from sooty mangabeys. The primate TRIM5 gene encodes a factor with potent antiviral activity when tested in the laboratory, and TRIM5 proteins are thought to play a role in restricting the movement of viruses between species in nature. In this study, we show that genetic variation in the TRIM5 gene of rhesus macaques heavily influences the outcome of cross-species transmission of SIVsm and that emergence of SIVmac in rhesus macaques in the 1970s required adaptations to circumvent the genetic barrier imposed by the rhesus macaque TRIM5 gene. Our results confirm the hypothesis that TRIM5 can influence the process of cross-species transmission and emergence of viruses related to HIV-1 and HIV-2 and serve as a striking illustration of how host genes can influence virus evolution.
Highlights
The Simian immunodeficiency viruses (SIVs) are widespread among African primates [1]
The human immunodeficiency viruses HIV-1 and HIV-2 originated from cross-species transmission of simian immunodeficiency viruses (SIVs) from chimpanzees (SIVcpz) and sooty mangabeys (SIVsm), respectively
A related virus, Simian immunodeficiency viruses of rhesus macaques (SIVmac), causes AIDS-like pathogenesis in rhesus macaques; like HIV-2, SIVmac is the product of a cross-species jump of SIV from sooty mangabeys (SIVsm) from sooty mangabeys
Summary
The Simian immunodeficiency viruses (SIVs) are widespread among African primates [1]. In a striking parallel to the emergence of HIV-1 and HIV-2, SIVsm jumped into captive Asian macaques in the United States, resulting in emergence of SIVmac and outbreaks of AIDS-like disease at several U.S National Primate Research Centers in the 1970s [3,5,6]. The exact time and means by which SIVsm was transmitted to macaques are unknown, but since isolation of the first SIV strains from captive macaques in the 1980s, experimental infection of rhesus macaques with SIV has become the primary animal model for preclinical research on AIDS vaccines and pathogenesis. Variation in susceptibility to infection and disease progression in nonhuman primate models often confounds such studies, and identifying the sources of variation will lead to more efficient use of AIDS models.
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