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Discovery of the origin of the Simian Immunodeficiency Virus (SIV) in the chimpanzee

June 16, 2003

The origin of HIV-1 (human immunodeficiency virus-1), responsible for the global Aids pandemic, has been a live issue in the scientific community for many years. It is now recognized that HIV-1 in the human population results from cross-species transmission of SIVcpz, from chimpanzees (Pan troglodytes troglodytes) to humans, most likely through hunting and handling of infected primate bushmeat. However, the occurrence and ancestry of this virus in the chimpanzee itself still raises many questions. Sivs are a large family of viruses, carried by many species of monkeys in africa, but chimpanzees are the only apes known to be naturally infected. Furthermore, the prevalence of SIV infection in wild chimpanzees is much lower than in monkey species.

Recent research conducted in partnership between the University of Nottingham (UK), the UniversitY OF Alabama (USA), the primatology centER at Tulane (USA) and IRD's research unit 036 has just shed new light on the origin of SIV in the chimpanzee.

The results were obtained following a large sero-epidemiological study conducted by the IRD on bushmeat sold on the markets in Cameroon. This investigation showed that the human population is indeed in contact with a large diversity of SIVs2. Complete genome sequences of SIVs identified in this primate bushmeat were characterized. in this way the researchers discovered for the first time that SIVgsn, from greater spot-nosed monkeys (Cercopithecus nictitans), a small monkey common in Cameroon, possesses the regulatory gene vpu, which up to now had only been identified in HIV-1 and SIVcpz from chimpanzees. Furthermore, they also showed that the envelope of SIVgsn is closeley related to the hiv-1/sivcpz envelope. Similarly, a previously characterized virus, SIVrcm from red capped mangabeys, has been shown to be closely related to SIVcpz in an other part of the genome, more precisely pol.

Extensive phylogenetic analyses subsequently performed on these viruses provided clear evidence that the chimpanzee virus (SIVcpz) is the result from a recombination between these two viruses - SIVgsn from greater spot-nosed monkeys and SIVrcm from red-capped mangabeyS. This recombinant virus spread through the chimpanzee species and was later transmitted to humans to become HIV-1.

These results indicate that chimpanzees acquired SIV more recently compared to other monkeys in Africa. However, SIVcpz infected chimpanzees do not develop any disease, suggesting that the chimpanzee host co-evolved with this recombinat virus for a long time.
The question remains on how chimpanzees became infected. These primates are known to hunt and eat other monkey species. It is therefore highly probable that they picked up viruses from greater spot nosed monkeys and red capped mangabeys. Similarly as humans, chimpanzees acquired their virus through cross-species transmission.

The findings on the hybrid origin of siv inchimpanzees has important implications. It will be important now to determine to what extent chimpanzees might be infected by other types of SIV which could be transmitted more easily to humans after adaptation in the chimpanzee. Actually there is not yet evidence that other SIVs have been transmitted to humans. However, it is known that several types of SIV can replicate in human lymphocytes suggesting that human contamination, and the appearance of an HIV 3, could be possible. The fact that distant HIVs and SIVs can recombine begs the question whether distantly related SIVs and HIV can potentially recombine, particularly in individuals who are HIV-positive and exposed to SIV by cross-species transmission. If this occurs, distantly related SIVs can then spread more efficiently into the human population and could contribute to widen the already extensive range of aids viruses which are currently circulating in Africa.

1. This research was sponsored by ANRS and the National Institute for Health (USA).
2. See FAS N°150 March 2002, www.ird.fr/fr/actualites/fiches/2002/fiche150.htm

Institut de Recherche pour le Développement, Paris (IRD)