Diversity in the CD4 Receptor Protects Chimpanzees from Infection by AIDS-Like Viruses

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Beatrice H. Hahn, MD, a professor of Medicine and Microbiology in the Perelman School of Medicine at the University of Pennsylvania, and her colleagues have been studying the origin of HIV-1 in non-human primates for decades.

Beatrice H. Hahn, MD, a professor of Medicine and Microbiology in the Perelman School of Medicine at the University of Pennsylvania, and her colleagues have been studying the origin of HIV-1 in non-human primates for decades. They previously discovered that simian immunodeficiency viruses (SIVs) infecting wild-living chimpanzees and gorillas jumped the species barrier into humans on four occasions, one of which spawned the AIDS pandemic. Understanding how these viruses are transmitted within and between species may reveal clues for novel vaccine strategies in humans.

HIV and SIV infect and kill immune cells called CD4 T cells, a process that ultimately leads to AIDS. Publishing this week in the Proceedings of the National Academy of Sciences, Hahn’s lab and an international team of collaborators, found that the CD4 surface protein, which is used by HIV and SIV as the receptor to enter immune cells, is highly variable among wild chimpanzees. Characterizing fecal samples from over 500 chimpanzees across sub-Saharan Africa, they found, to their surprise, nine CD4 variants. They went on to demonstrate that this diversity in CD4 protects chimpanzees from their own strain of SIV, as well as potentially dangerous SIVs carried by other monkey species on which they prey.

SIVs infect over 40 primate species in sub-Saharan Africa and can be deadly. Hahn’s group showed in previous studies that SIV-infected chimpanzees in the wild have a higher mortality than uninfected chimpanzees and can develop an AIDS-like disease, like that in humans.

Read more at Perelman School of Medicine at the University of Pennsylvania

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