Malaria in humans is caused by one of five different species of Plasmodium parasites. The deadliest of these is P. falciparum, especially within Africa where native resistance to P. vivax is high. Where the vivax parasites seem to have been around for at least tens of thousands of years, P. falciparum in many ways looks relatively young. Its comparative lack of genetic variation suggests either a recent origin from some other primate species, or an intense bottleneck or selective sweep affecting the parasite's demography. In either case, the falciparum history seems to indicate that its present widespread distribution is a very recent phenomenon -- possibly within the last 5000 years.
Because P. falciparum is phenotypically similar to the major chimpanzee malaria parasite, P. reichenowi, most scientists have assumed that we got falciparum malaria from chimpanzees. But in a new report, Weimin Liu and colleagues [1] have surveyed parasite variation in gorillas, bonobos and chimpanzees across Africa, finding that human falciparum parasites all group in with a single small clade of gorilla parasites. The other primates carry many varieties of parasites, with typical individuals being highly heteroplasmic -- that is, carrying several different strains.
From the discussion:
Using single-template amplification strategies and a much larger collection of ape specimens than previously analysed, we show here that wild-living chimpanzees and western gorillas are naturally infected with at least nine Plasmodium species. Among more than 1,100 SGA-derived mitochondrial, apicoplast and nuclear gene sequences from 80 chimpanzee and 55 gorilla samples, we found a total of nine sequences that were related to P. malariae, P. ovale or P. vivax (Supplementary Table 5). All others grouped within one of six chimpanzee- or gorilla-specific lineages representing distinct Plasmodium species, three of which had not previously been described. Significantly, all currently available human P. falciparum sequences constitute a single lineage nested within the G1 clade of gorilla parasites. This indicates that human P. falciparum is of gorilla origin, and not of chimpanzee9, 10, 12, bonobo11 or ancient human5 origin, and that all known human strains may have resulted from a single cross-species transmission event. What is still unclear is when gorilla P. falciparum entered the human population and whether present-day ape populations represent a source for recurring human infection. It has been suggested that the limited levels of genetic diversity seen at many loci in human P. falciparum reflect a relatively recent selective sweep8. Our data suggest that this bottleneck or ‘Eve event’ was instead the consequence of cross-species transmission of a gorilla parasite. It is difficult to date this event without having reliable dates with which to calibrate the Plasmodium phylogenetic trees.
What's interesting about the study is the sheer coverage of wild primates, and the application of multiple gene trees, which suggests that this is a recent origin of human parasites instead of introgression and selection of a single gene. I don't know if it makes any difference whether the disease came from gorillas or chimpanzees, but it certainly helps to confirm that it is new and not a long-time coevolution. That explains the burst of recent selection associated with resistance genes, especially within Africa.