Plasmodium vivax is the leading cause of human malaria in Asia and Latin America but is absent from most of central Africa due to the near fixation of a mutation that inhibits the expression of its receptor, the Duffy antigen, on human erythrocytes. The emergence of this protective allele is not understood because P. vivax is believed to have originated in Asia. Here we show, using a non-invasive approach, that wild chimpanzees and gorillas throughout central Africa are endemically infected with parasites that are closely related to human P. vivax. Sequence analyses reveal that ape parasites lack host specificity and are much more diverse than human parasites, which form a monophyletic lineage within the ape parasite radiation. These findings indicate that human P. vivax is of African origin and likely selected for the Duffy-negative mutation. All extant human P. vivax parasites are derived from a single ancestor that escaped out of Africa.

Comparative data on the diets of extant primates inform hypotheses about hominin resource use. Historically, data describing chimpanzee diets stem primarily from forest-dwelling communities, and we lack comparative data from chimpanzees that live in mosaic habitats that more closely resemble those reconstructed for Plio-Pleistocene hominins. We present data on the diet of a partially-habituated community of open habitat chimpanzees (Pan troglodytes schweinfurthii) from the Issa valley, western Tanzania, collected over a four-year period. Based mostly on macroscopic faecal analysis, Issa chimpanzees consumed a minimum of 69 plant species. There was no relationship between plant consumption and either fruit availability or feeding tree density; the most frequently consumed plant species were found in riverine forests, with woodland species consumed more frequently during the late dry season. We conclude by contextualising these findings with those of other open-habitat chimpanzee sites, and also by discussing how our results contribute towards reconstructions of early hominin exploitation of mosaic landscapes.

Simian immunodeficiency virus of chimpanzees (SIVcpz) has a significant negative impact on the health, reproduction, and life span of chimpanzees, yet the prevalence and distribution of this virus in wild-living populations are still only poorly understood. Here, we show that savanna chimpanzees, who live in ecologically marginal habitats at 10-to 50-fold lower population densities than forest chimpanzees, can be infected with SIVcpz at high prevalence rates. Fecal samples were collected from nonhabituated eastern chimpanzees (Pan troglodytes schweinfurthii) in the Issa Valley (n ‫؍‬ 375) and Shangwa River (n ‫؍‬ 6) areas of the Masito-Ugalla region in western Tanzania, genotyped to determine the number of sampled individuals, and tested for SIVcpz-specific antibodies and nucleic acids. None of 5 Shangwa River apes tested positive for SIVcpz; however, 21 of 67 Issa Valley chimpanzees were SIVcpz infected, indicating a prevalence rate of 31% (95% confidence interval, 21% to 44%). Two individuals became infected during the 14-month observation period, documenting continuing virus spread in this community. To characterize the newly identified SIVcpz strains, partial and full-length viral sequences were amplified from fecal RNA of 10 infected chimpanzees. Phylogenetic analyses showed that the Ugalla viruses formed a monophyletic lineage most closely related to viruses endemic in Gombe National Park, also located in Tanzania, indicating a connection between these now separated communities at some time in the past. These findings document that SIVcpz is more widespread in Tanzania than previously thought and that even very low-density chimpanzee populations can be infected with SIVcpz at high prevalence rates. Determining whether savanna chimpanzees, who face much more extreme environmental conditions than forest chimpanzees, are more susceptible to SIVcpz-associated morbidity and mortality will have important scientific and conservation implications.Among the many lentiviruses known to infect Old World primates in sub-Saharan Africa, simian immunodeficiency virus of chimpanzees (SIVcpz) is of particular interest because it is the immediate precursor of human immunodeficiency virus type 1 (HIV-1), the causative agent of AIDS (8, 16). However, SIVcpz is also an important pathogen in its own right, since it causes significant morbidity and mortality in its chimpanzee host (6, 15, 37). Recent natural history studies in Gombe National Park in western Tanzania showed that infected chimpanzees have a 10-to 16-fold increased risk of death compared to uninfected chimpanzees (15). SIVcpz-infected females were less likely to give birth and their infants had a much higher mortality rate than those of uninfected females (15). Most importantly, postmortem analyses showed that SIVcpz can cause CD4 ϩ T lymphocyte depletion and histopathological findings consistent with end-stage AIDS (15). These results demonstrated that SIVcpz has a substantial negative impact on the health, reproduction, and life span of chimpanzees, a conclusion ...

Human and simian immunodeficiency viruses (HIV/SIVs) use CD4 as the primary receptor to enter target cells. Here, we show that the chimpanzee CD4 is highly polymorphic, with nine coding variants present in wild populations, and that this diversity interferes with SIV envelope (Env)–CD4 interactions. Testing the replication fitness of SIVcpz strains in CD4+ T cells from captive chimpanzees, we found that certain viruses were unable to infect cells from certain hosts. These differences were recapitulated in CD4 transfection assays, which revealed a strong association between CD4 genotypes and SIVcpz infection phenotypes. The most striking differences were observed for three substitutions (Q25R, Q40R, and P68T), with P68T generating a second N-linked glycosylation site (N66) in addition to an invariant N32 encoded by all chimpanzee CD4 alleles. In silico modeling and site-directed mutagenesis identified charged residues at the CD4–Env interface and clashes between CD4- and Env-encoded glycans as mechanisms of inhibition. CD4 polymorphisms also reduced Env-mediated cell entry of monkey SIVs, which was dependent on at least one D1 domain glycan. CD4 allele frequencies varied among wild chimpanzees, with high diversity in all but the western subspecies, which appeared to have undergone a selective sweep. One allele was associated with lower SIVcpz prevalence rates in the wild. These results indicate that substitutions in the D1 domain of the chimpanzee CD4 can prevent SIV cell entry. Although some SIVcpz strains have adapted to utilize these variants, CD4 diversity is maintained, protecting chimpanzees against infection with SIVcpz and other SIVs to which they are exposed.