Plasmodium falciparum causes most human malaria deaths, having prehistorically evolved from parasites of African Great Apes. Here we 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, and obtaining partial sequence data from a more distantly related chimpanzee parasite (P. gaboni). The close relationship between P. reichenowi and P. falciparum is emphasized by almost complete conservation of genomic synteny, but against this strikingly conserved background we observe major differences at loci involved in erythrocyte invasion. The organization of most virulence-associated multigene families, including the hypervariable var genes, is broadly conserved, but P. falciparum has a smaller subset of rif and stevor genes whose products are expressed on the infected erythrocyte surface. Genome-wide analysis identifies other loci under recent positive selection, but a limited number of changes at the host–parasite interface may have mediated host switching.
KAUST Repository Item: Exported on 2020-10-01
Acknowledgements: This work was supported by the Wellcome Trust (grant number WT 098051) with additional funding to T.D.O. from the European Community’s Seventh Framework Programme (FP7/2007-2013), under grant agreement number 242095; J.C.R., from the National Institutes of Health (R01 AI091595); B.O. from Centre International de Recherches Médicales de Franceville; F.R. and F.P., from CNRS and IRD; F.R., B.O. and F.P. from the Agence Nationale de la Recherche (grant ANR JCJC SVSE 7-2012 ORIGIN); D.J.C. from an ERC Advanced Award (grant number 294428); and C.N. from the Wellcome Trust (grant number WT 082130/Z/07/Z).