While causing an estimated 214 million cases of malaria every year, the parasite Plasmodium falciparum is thought to have killed 438,000 people in 2015. But the parasite is just one of a few different species of Plasmodium, and so identifying what makes P. falciparum particularly deadly is a little hard to discern. To try and answer this question, among others, researchers have decided to delve back into the parasite’s evolutionary history, and compare its genetics to two other species of malaria found in wild chimpanzees.
African apes are known to have at least six different Plasmodium species which infect them, three of which are found in chimps, while the other three are found in gorillas. But it was only a few years ago that scientists discovered the origin of the human malarial P. falciparum, and that it seemingly evolved from one of the species found in wild gorillas. Why it has suddenly become so deadly now it infects humans is a crucial question that the researchers want to answer.
The answer must lie in the blueprint the genome of its chimpanzee and gorilla cousins, explains Beatrice Hahn, who coauthored the study published in Nature Communications. We also want to know how and when the gorilla precursor of Plasmodium falciparum jumped into humans, and why this happened only once. To start to understand some of these things, they looked at two species of Plasmodium found in chimpanzees, P. reichenowi and P. gaboni, isolated from blood samples taken from chimps held in sanctuaries.
The parasite infects red blood cells, and if left untreated eventually leads to death.Viviane Rolfe/Flickr CC BY-SA 2.0
These two species have been found to be almost indistinguishable in appearance from P. falciparum, leading some to suspect that the parasites have been diverging along with their hosts since chimps and humans split around 5 million years ago. But what the analysis of the species genomes showed was something different. The two chimp Plasmodium species were found to be 10 times as genetically diverse as P. falciparum, which implies that the human parasite went through a bottleneck around 10,000 years ago, suggesting that this is when it was first transmitted to humans and that it actually has a very recent origin.
Not only that, but they also found differences in the number of genes that the parasite use to infect red blood cells. The parasites have an ability to alter their host red blood cells to make them less likely to be detected by the immune system. Whereas most species from this group only have one gene involved in this process, they found that those species that infect the African apes had up to 21, suggesting that this massive increase in the number of genes could aid in their infectiousness.
We also found a short region of the genome, including two essential invasion genes, where Plasmodium falciparum was much more different from its close relatives than we expected, says Lindsey Plenderleith, another of the authors. The researchers are uncertain how these findings play into the wider questions of what lead the parasite to evolve, but hope that future research in which they will decode other closely related Plasmodium species might help them understand further.
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