@article{fdi:010062602,
  title = {{G}enome sequencing of chimpanzee malaria parasites reveals possible pathways of adaptation to human hosts},
  author = {{O}tto, {T}. {D}. and {R}ayner, {J}. {C}. and {B}ohme, {U}. and {P}ain, {A}. and {S}pottiswoode, {N}. and {S}anders, {M}. and {Q}uail, {M}. and {O}llomo, {B}. and {R}enaud, {F}. and {T}homas, {A}. {W}. and {P}rugnolle, {F}ranck and {C}onway, {D}. {J}. and {N}ewbold, {C}. and {B}erriman, {M}.},
  editor = {},
  language = {{ENG}},
  abstract = {{P}lasmodium falciparum causes most human malaria deaths, having prehistorically evolved from parasites of {A}frican {G}reat {A}pes. {H}ere 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). {T}he 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. {T}he 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. {G}enome-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.},
  keywords = {{AFRIQUE}},
  booktitle = {},
  journal = {{N}ature {C}ommunications},
  volume = {5},
  numero = {},
  pages = {art. 4754 [9 ]},
  ISSN = {2041-1723},
  year = {2014},
  DOI = {10.1038/ncomms5754},
  URL = {https://www.documentation.ird.fr/hor/fdi:010062602},
}