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dc.contributor.authorOtto, Thomas D.
dc.contributor.authorRayner, Julian C.
dc.contributor.authorBöhme, Ulrike
dc.contributor.authorPain, Arnab
dc.contributor.authorSpottiswoode, Natasha
dc.contributor.authorSanders, Mandy
dc.contributor.authorQuail, Michael
dc.contributor.authorOllomo, Benjamin
dc.contributor.authorRenaud, François
dc.contributor.authorThomas, Alan W.
dc.contributor.authorPrugnolle, Franck
dc.contributor.authorConway, David J.
dc.contributor.authorNewbold, Chris
dc.contributor.authorBerriman, Matthew
dc.date.accessioned2014-11-25T13:59:42Z
dc.date.available2014-11-25T13:59:42Z
dc.date.issued2014-09-09
dc.identifier.citationOtto, T. D., Rayner, J. C., Böhme, U., Pain, A., Spottiswoode, N., Sanders, M., . . . Berriman, M. (2014). Genome sequencing of chimpanzee malaria parasites reveals possible pathways of adaptation to human hosts. Nat Commun, 5. doi: 10.1038/ncomms5754
dc.identifier.issn2041-1723
dc.identifier.pmid25203297
dc.identifier.doi10.1038/ncomms5754
dc.identifier.urihttp://hdl.handle.net/10754/336097
dc.description.abstractPlasmodium 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.
dc.description.sponsorshipThis 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).
dc.language.isoen
dc.publisherSpringer Nature
dc.relation.urlhttp://www.nature.com/doifinder/10.1038/ncomms5754
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/
dc.titleGenome sequencing of chimpanzee malaria parasites reveals possible pathways of adaptation to human hosts
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.contributor.departmentBioscience Program
dc.contributor.departmentComputational Bioscience Research Center (CBRC)
dc.contributor.departmentPathogen Genomics Laboratory
dc.identifier.journalNature Communications
dc.identifier.pmcidPMC4166903
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionParasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge CB10 1SA, UK
dc.contributor.institutionNational Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA
dc.contributor.institutionWeatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK
dc.contributor.institutionCentre International de Recherches Médicales de Franceville, CIRMF, BP 769 Franceville, Gabon
dc.contributor.institutionLaboratoire MIVEGEC, UMR 5290 CNRS-IRD-UMI-UMII, IRD, BP 64501, 34394 Montpellier, France
dc.contributor.institutionBiomedical Primate Research Centre, Department of Parasitology, 2280 GH Rijswijk, The Netherlands
dc.contributor.institutionDepartment of Pathogen Molecular Biology, London School of Hygiene & Tropical Medicine, London WC1E 7HT, UK
dc.contributor.affiliationKing Abdullah University of Science and Technology (KAUST)
kaust.personPain, Arnab
refterms.dateFOA2018-06-13T16:03:39Z
dc.date.published-online2014-09-09
dc.date.published-print2014-12


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