The genetic adaptations in the malaria parasite, Plasmodium falciparum, which allow it to infect human hosts, have been revealed in a study published this week in Nature Communications. Plasmodium falciparum causes most human malaria deaths, having prehistorically evolved from parasites of African Great Apes.
Matthew Berriman and colleagues explore the genomic basis of P. falciparum adaptation to human hosts by fully sequencing the genome of the closely-related chimpanzee parasite species P. reichenowi for the first time.
The authors found that the genome of both species is almost entirely conserved; however there are significant differences in genes associated with the blood stages of the parasite’s life cycle. Specifically, they found changes at the host-parasite interface, both during invasion of red blood cells and in modifications to receptors on the surface of the infected cells that cause them to adhere to host endothelial cells.
In addition, they discovered a short list of genes of unknown function that may also contribute to host specificity. Further research is necessary to discover the relative contribution of each of these genes to speciation and host adaptation.