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dc.contributor.authorKaslow, S.R.
dc.contributor.authorKim, A.
dc.contributor.authorSá, J.M.
dc.date.accessioned2019-10-01T15:10:14Z
dc.date.available2019-10-01T15:10:14Z
dc.date.issued2019
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85072540054&doi=10.1038%2fs41467-019-12256-9&partnerID=40&md5=5f8689e94669350e162d4e0def357f30
dc.identifier.urihttp://hdl.handle.net/10713/11038
dc.description.abstractMainstay treatment for Plasmodium vivax malaria has long relied on chloroquine (CQ) against blood-stage parasites plus primaquine against dormant liver-stage forms (hypnozoites), however drug resistance confronts this regimen and threatens malaria control programs. Understanding the basis of P. vivax chloroquine resistance (CQR) will inform drug discovery and malaria control. Here we investigate the genetics of P. vivax CQR by a cross of parasites differing in drug response. Gametocytogenesis, mosquito infection, and progeny production are performed with mixed parasite populations in nonhuman primates, as methods for P. vivax cloning and in vitro cultivation remain unavailable. Linkage mapping of progeny surviving >15 mg/kg CQ identifies a 76 kb region in chromosome 1 including pvcrt, an ortholog of the Plasmodium falciparum CQR transporter gene. Transcriptional analysis supports upregulated pvcrt expression as a mechanism of CQR.en_US
dc.description.urihttps://doi.org/10.1038/s41467-019-12256-9en_US
dc.language.isoen-USen_US
dc.publisherNature Publishing Groupen_US
dc.relation.ispartofNature communications
dc.subjectparasite geneticsen_US
dc.subject.meshDrug Resistance, Microbialen_US
dc.subject.meshAntiparasitic Agentsen_US
dc.subject.meshMalariaen_US
dc.titlePlasmodium vivax chloroquine resistance links to pvcrt transcription in a genetic crossen_US
dc.typeArticleen_US
dc.identifier.doi10.1038/s41467-019-12256-9
dc.identifier.pmid31541097


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