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

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, a...

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Detalles Bibliográficos
Autores principales: Otto, Thomas D., Rayner, Julian C., Böhme, Ulrike, Pain, Arnab, Spottiswoode, Natasha, Sanders, Mandy, Quail, Michael, Ollomo, Benjamin, Renaud, François, Thomas, Alan W., Prugnolle, Franck, Conway, David J., Newbold, Chris, Berriman, Matthew
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Pub. Group 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4166903/
https://www.ncbi.nlm.nih.gov/pubmed/25203297
http://dx.doi.org/10.1038/ncomms5754
Descripción
Sumario: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.