Comparative genomics of the neglected human malaria parasite Plasmodium vivax
- Carlton, JM; Adams, JH; Silva, JC; Bidwell, SL; Lorenzi, H; Caler, E; Crabtree, J; Angiuoli, SV; Merino, EF; Amedeo, P; Cheng, Q; Coulson, RMR; Crabb, BS; del Portillo, HA; Essien, K; Feldblyum, TV; Fernandez-Becerra, C; Gilson, PR; Gueye, AH; Guo, X; Kang'a, S; Kooij, TWA; Korsinczky, M; Meyer, EVS; Nene, V; Paulsen, I; White, O; Ralph, SA; Ren, QH; Sargeant, TJ; Salzberg, SL; Stoeckert, CJ; Sullivan, SA; Yamamoto, MM; Hoffman, SL; Wortman, JR; Gardner, MJ; Galinski, MR; Barnwell, JW; Fraser-Liggett, CM;
Publication Year 2008-10-09, Volume 455, Issue #7214, Page 757-763
- Journal Title
- Publication Type
- Journal Article
- The human malaria parasite Plasmodium vivax is responsible for 25 - 40% of the similar to 515 million annual cases of malaria worldwide. Although seldom fatal, the parasite elicits severe and incapacitating clinical symptoms and often causes relapses months after a primary infection has cleared. Despite its importance as a major human pathogen, P. vivax is little studied because it cannot be propagated continuously in the laboratory except in non- human primates. We sequenced the genome of P. vivax to shed light on its distinctive biological features, and as a means to drive development of new drugs and vaccines. Here we describe the synteny and isochore structure of P. vivax chromosomes, and show that the parasite resembles other malaria parasites in gene content and metabolic potential, but possesses novel gene families and potential alternative invasion pathways not recognized previously. Completion of the P. vivax genome provides the scientific community with a valuable resource that can be used to advance investigation into this neglected species.
- NATURE PUBLISHING GROUP
- RED-BLOOD-CELLS; PHENOTYPIC VARIATION; RODENT MALARIA; FALCIPARUM; PROTEINS; BINDING; IDENTIFICATION; SUPERFAMILY; EXPRESSION; RESISTANCE
- Publisher's Version
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Creation Date: 2008-10-09 12:00:00Last Modified: 0001-01-01 12:00:00