Genome sequencing of chimpanzee malaria parasites reveals possible pathways of adaptation to human hosts

Thomas D. Otto, Julian C. Rayner, Ulrike Böhme, Arnab Pain, Natasha Spottiswoode, Mandy Sanders, Michael Quail, Benjamin Ollomo, François Renaud, Alan W. Thomas, Franck Prugnolle, David J. Conway, Chris Newbold () and Matthew Berriman ()
Additional contact information
Thomas D. Otto: Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
Julian C. Rayner: Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
Ulrike Böhme: Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
Arnab Pain: Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
Natasha Spottiswoode: National Institute of Allergy and Infectious Diseases, National Institutes of Health
Mandy Sanders: Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
Michael Quail: Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
Benjamin Ollomo: Centre International de Recherches Médicales de Franceville, CIRMF
François Renaud: Laboratoire MIVEGEC, UMR 5290 CNRS-IRD-UMI-UMII, IRD
Alan W. Thomas: Biomedical Primate Research Centre
Franck Prugnolle: Centre International de Recherches Médicales de Franceville, CIRMF
David J. Conway: London School of Hygiene & Tropical Medicine
Chris Newbold: Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
Matthew Berriman: Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus

Nature Communications, 2014, vol. 5, issue 1, 1-9

Abstract: Abstract 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.

Date: 2014
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DOI: 10.1038/ncomms5754

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