Plasmodium vivax-like genome sequences shed new insights into Plasmodium vivax biology and evolution.
Aude Gilabert, Thomas D Otto, Gavin G Rutledge, Blaise Franzon, Benjamin Ollomo, Céline Arnathau, Patrick Durand, Nancy D Moukodoum, Alain-Prince Okouga, Barthélémy Ngoubangoye, Boris Makanga, Larson Boundenga, Christophe Paupy, François Renaud, Franck Prugnolle, Virginie Rougeron
Author Information
Aude Gilabert: MIVEGEC, IRD, CNRS, University of Montpellier, Montpellier, France.
Thomas D Otto: Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge, United Kingdom.
Gavin G Rutledge: Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge, United Kingdom.
Blaise Franzon: MIVEGEC, IRD, CNRS, University of Montpellier, Montpellier, France.
Benjamin Ollomo: Centre International de Recherches Médicales de Franceville, Franceville, Gabon.
Céline Arnathau: MIVEGEC, IRD, CNRS, University of Montpellier, Montpellier, France.
Patrick Durand: MIVEGEC, IRD, CNRS, University of Montpellier, Montpellier, France.
Nancy D Moukodoum: Centre International de Recherches Médicales de Franceville, Franceville, Gabon.
Alain-Prince Okouga: Centre International de Recherches Médicales de Franceville, Franceville, Gabon.
Barthélémy Ngoubangoye: Centre International de Recherches Médicales de Franceville, Franceville, Gabon.
Boris Makanga: Centre International de Recherches Médicales de Franceville, Franceville, Gabon.
Larson Boundenga: Centre International de Recherches Médicales de Franceville, Franceville, Gabon.
Christophe Paupy: MIVEGEC, IRD, CNRS, University of Montpellier, Montpellier, France.
François Renaud: MIVEGEC, IRD, CNRS, University of Montpellier, Montpellier, France.
Franck Prugnolle: MIVEGEC, IRD, CNRS, University of Montpellier, Montpellier, France.
Virginie Rougeron: MIVEGEC, IRD, CNRS, University of Montpellier, Montpellier, France. ORCID
Although Plasmodium vivax is responsible for the majority of malaria infections outside Africa, little is known about its evolution and pathway to humans. Its closest genetic relative, P. vivax-like, was discovered in African great apes and is hypothesized to have given rise to P. vivax in humans. To unravel the evolutionary history and adaptation of P. vivax to different host environments, we generated using long- and short-read sequence technologies 2 new P. vivax-like reference genomes and 9 additional P. vivax-like genotypes. Analyses show that the genomes of P. vivax and P. vivax-like are highly similar and colinear within the core regions. Phylogenetic analyses clearly show that P. vivax-like parasites form a genetically distinct clade from P. vivax. Concerning the relative divergence dating, we show that the evolution of P. vivax in humans did not occur at the same time as the other agents of human malaria, thus suggesting that the transfer of Plasmodium parasites to humans happened several times independently over the history of the Homo genus. We further identify several key genes that exhibit signatures of positive selection exclusively in the human P. vivax parasites. Two of these genes have been identified to also be under positive selection in the other main human malaria agent, P. falciparum, thus suggesting their key role in the evolution of the ability of these parasites to infect humans or their anthropophilic vectors. Finally, we demonstrate that some gene families important for red blood cell (RBC) invasion (a key step of the life cycle of these parasites) have undergone lineage-specific evolution in the human parasite (e.g., reticulocyte-binding proteins [RBPs]).
