Increased mortality and AIDS-like immunopathology in wild chimpanzees infected with SIVcpz

Abstract

African primates are naturally infected with over 40 different simian immunodeficiency viruses (SIVs), two of which have crossed the species barrier and generated human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2)1,2. Unlike the human viruses, however, SIVs do not generally cause acquired immunodeficiency syndrome (AIDS) in their natural hosts3. Here we show that SIVcpz, the immediate precursor of HIV-1, is pathogenic in free-ranging chimpanzees. By following 94 members of two habituated chimpanzee communities in Gombe National Park, Tanzania, for over 9 years, we found a 10- to 16-fold higher age-corrected death hazard for SIVcpz-infected (n = 17) compared to uninfected (n = 77) chimpanzees. We also found that SIVcpz-infected females were less likely to give birth and had a higher infant mortality rate than uninfected females. Immunohistochemistry and in situ hybridization of post-mortem spleen and lymph node samples from three infected and two uninfected chimpanzees revealed significant CD4+ T-cell depletion in all infected individuals, with evidence of high viral replication and extensive follicular dendritic cell virus trapping in one of them. One female, who died within 3 years of acquiring SIVcpz, had histopathological findings consistent with end-stage AIDS. These results indicate that SIVcpz, like HIV-1, is associated with progressive CD4+ T-cell loss, lymphatic tissue destruction and premature death. These findings challenge the prevailing view that all natural SIV infections are non-pathogenic and suggest that SIVcpz has a substantial negative impact on the health, reproduction and lifespan of chimpanzees in the wild.

Community structure and the spread of infectious disease in primate social networks

“…Our study suggests that grooming networks do impact patterns of parasitism. Future studies could investigate this hypothesis more directly, for instance by combining genetic data on parasites with social network analysis of their hosts (e.g., Keele et al 2009). If parasites tend to spread within social modules before spreading to other modules, then parasites found within modules should be more closely related to one another than parasites in different modules.…”

Origin of the HIV-1 group O epidemic in western lowland gorillas

“…Over recent decades, the number of wild-living gorilla populations, some of which may have harbored SIVgor, has declined rapidly because of increased human presence, hunting, and habitat loss due to deforestation, as well as infectious disease outbreaks, including Ebola (24,25). It is also possible that SIVgor is pathogenic in gorillas, because SIVcpz infection is in chimpanzees (23,26). Thus, SIVgor could have once been present across a larger geographic area but may have led to the extinction of certain gorilla populations.…”

How Samhd1 changes our view of viral restriction

“…There is a correlation between the 'time of presence' of lentiviral strains in hosts and pathogenicity: despite high viral titers and lack of immune control, infection by SIVsm in Sooty mangabeys and by SIVagm in African green monkeys fail to cause simian AIDS (reviewed in [76,77]). Recent exposition to SIV, as for SIVcpz in chimpanzees, causes symptoms close to AIDS.…”