| Literature DB >> 18843361 |
Jane M Carlton1, John H Adams, Joana C Silva, Shelby L Bidwell, Hernan Lorenzi, Elisabet Caler, Jonathan Crabtree, Samuel V Angiuoli, Emilio F Merino, Paolo Amedeo, Qin Cheng, Richard M R Coulson, Brendan S Crabb, Hernando A Del Portillo, Kobby Essien, Tamara V Feldblyum, Carmen Fernandez-Becerra, Paul R Gilson, Amy H Gueye, Xiang Guo, Simon Kang'a, Taco W A Kooij, Michael Korsinczky, Esmeralda V-S Meyer, Vish Nene, Ian Paulsen, Owen White, Stuart A Ralph, Qinghu Ren, Tobias J Sargeant, Steven L Salzberg, Christian J Stoeckert, Steven A Sullivan, Marcio M Yamamoto, Stephen L Hoffman, Jennifer R Wortman, Malcolm J Gardner, Mary R Galinski, John W Barnwell, Claire M Fraser-Liggett.
Abstract
The human malaria parasite Plasmodium vivax is responsible for 25-40% of the approximately 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.Entities:
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Year: 2008 PMID： 18843361 PMCID： PMC2651158 DOI： 10.1038/nature07327
Source DB: PubMed Journal: Nature ISSN： 0028-0836 Impact factor: 49.962