Like human immunodeficiency virus type 1 (HIV-1), simian immunodeficiency virus of chimpanzees (SIVcpz) can cause CD4+ T cell loss and premature death. Here, we used molecular surveillance tools and mathematical modeling to estimate the impact of SIVcpz infection on chimpanzee population dynamics. Habituated (Mitumba and Kasekela) and non-habituated (Kalande) chimpanzees were studied in Gombe National Park, Tanzania. Ape population sizes were determined from demographic records (Mitumba and Kasekela) or individual sightings and genotyping (Kalande), while SIVcpz prevalence rates were monitored using non-invasive methods. Between 2002–2009, the Mitumba and Kasekela communities experienced mean annual growth rates of 1.9% and 2.4%, respectively, while Kalande chimpanzees suffered a significant decline, with a mean growth rate of −6.5% to −7.4%, depending on population estimates. A rapid decline in Kalande was first noted in the 1990s and originally attributed to poaching and reduced food sources. However, between 2002–2009, we found a mean SIVcpz prevalence in Kalande of 46.1%, which was almost four times higher than the prevalence in Mitumba (12.7%) and Kasekela (12.1%). To explore whether SIVcpz contributed to the Kalande decline, we used empirically determined SIVcpz transmission probabilities as well as chimpanzee mortality, mating and migration data to model the effect of viral pathogenicity on chimpanzee population growth. Deterministic calculations indicated that a prevalence of greater than 3.4% would result in negative growth and eventual population extinction, even using conservative mortality estimates. However, stochastic models revealed that in representative populations, SIVcpz, and not its host species, frequently went extinct. High SIVcpz transmission probability and excess mortality reduced population persistence, while intercommunity migration often rescued infected communities, even when immigrating females had a chance of being SIVcpz infected. Together, these results suggest that the decline of the Kalande community was caused, at least in part, by high levels of SIVcpz infection. However, population extinction is not an inevitable consequence of SIVcpz infection, but depends on additional variables, such as migration, that promote survival. These findings are consistent with the uneven distribution of SIVcpz throughout central Africa and explain how chimpanzees in Gombe and elsewhere can be at equipoise with this pathogen.
It is now well established that human immunodeficiency virus type 1 (HIV-1), which causes acquired immune deficiency syndrome (AIDS), emerged following cross-species transmission of a simian immunodeficiency virus that infects chimpanzees (SIVcpz). Although SIVcpz was originally believed not to be pathogenic, a recent study conducted in Gombe National Park, Tanzania, found that infected chimpanzees can develop AIDS-like symptoms and have a high mortality. To examine the impact of SIVcpz on chimpanzee survival, we examined and then modeled the effect of virus infection on chimpanzee population growth. We studied three communities, including the little-studied Kalande community, located in the south of the park. We found that 46% of Kalande apes were infected with SIVcpz, compared to less than 13% of the other communities. Interestingly, the communities with lower infection rates grew, while Kalande suffered a catastrophic decline. Mathematical modeling indicated that chimpanzee populations infected with SIVcpz are likely to decline, although intercommunity migration counteracted this negative effect, allowing many simulated populations to persist. These results suggest that SIVcpz infection, together with other variables, contributed to the Kalande population decline. However, population extinction is not a necessary consequence of SIVcpz infection, but can be counteracted by other factors, such as migration, that promote population survival. These findings are consistent with the uneven distribution of SIVcpz across Africa and may explain how chimpanzees as a species have survived this pathogen.