Although humans share most of their genes—and many analogous diseases—with chimpanzees, these close relatives are not likely to blame for the menace of human malaria, according to new genetic research.
Malaria kills some one million people worldwide each year and sickens another 350 million to 500 million. In recent years the origins of this disease, the most common and deadly form of which is from the protozoan parasite Plasmodium falciparum carried by the Anopheles mosquito, had been winnowed down to the chimpanzee.
But after a new molecular analysis of more than 2,500 primate droppings sampled in central Africa from primarily wild chimps (Pan troglodytes), bonobos (Pan paniscus), eastern gorillas (Gorilla beringei) and western gorillas (Gorilla gorilla), a team of researchers has concluded that the modern human P. falciparum has its closest correlates in a variety found in western gorillas, not chimpanzees.
"When we first saw it, it was a surprise," says Beatrice Hahn, a professor of medicine and microbiology at the University of Alabama at Birmingham and co-author of the new paper, which was published online September 22 in Nature. (Scientific American is part of Nature Publishing Group.)
Although the findings contradict a 2009 report published in Proceedings of the National Academy of Sciences co-written by Nathan Wolfe, a visiting professor of human biology at Stanford University, he is excited about the results.* "It's nice to have higher resolution," he says. His group had not examined gorillas as a possible point of origin, and he notes that the new work "helps to push the field forward."
The new research proposes that the human P. falciparum malaria parasite variety emerged from a single cross-species transmission event.
This single-bite theory "would suggest that there is a hurdle to go from apes to humans," Hahn says. And because in many places humans and primates live in close proximity, a more easily crossed barrier would likely have given rise to novel human infections on multiple occasions, she explains.
But the findings do not rule out the possibility that less harmful primate varieties of Plasmodium are making their way into the human blood stream from time to time. "Are there transmissions going on on a lower level that we don't recognize?" Hahn asks. She suggests that many of these infections might have avoided detection because they do not infect other humans. And with standard clinical diagnostic practices, most of which are based on laboratory slide analysis, "you wouldn't be able to identify" great ape varieties of malaria, Wolfe points out. It is likely that most Plasmodium species "would look pretty similar" under the microscope, he says, noting that scientific studies typically rely on genetic analysis that provides a much higher level of species-specific detail.
One of the big debates about the origins of malaria in recent years had been whether the parasite emerged in human populations—and then spread to great apes—or whether it had been in human and great ape lineages for eons, Wolfe says. The new paper "cements the great ape origin of human malaria," he says. But it throws a wrench in the time line of human malaria's origin.
"We really don't know how fast or slow Plasmodium parasites evolve," Hahn points out. Previous analyses of chimpanzee malaria parasite Plasmodium reichenowi had suggested the human variety P. falciparum likely split off some seven million to five million years ago. The new findings suggest that the human variety likely emerged less than 300,000 years ago (and possibly as recently as 5,000 years ago), she says.