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dc.contributor.authorDuangkamon Loesbanluechaien_US
dc.contributor.authorNamfon Kotananen_US
dc.contributor.authorCristina de Cozaren_US
dc.contributor.authorTheerarat Kochakarnen_US
dc.contributor.authorMegan R. Ansbroen_US
dc.contributor.authorKesinee Chotivanichen_US
dc.contributor.authorNicholas J. Whiteen_US
dc.contributor.authorPrapon Wilairaten_US
dc.contributor.authorMarcus C.S. Leeen_US
dc.contributor.authorFrancisco Javier Gamoen_US
dc.contributor.authorLaura Maria Sanzen_US
dc.contributor.authorThanat Chookajornen_US
dc.contributor.authorKrittikorn Kümpornsinen_US
dc.contributor.otherGlaxoSmithKline plc, Spainen_US
dc.contributor.otherChurchill Hospitalen_US
dc.contributor.otherNational Institute of Allergy and Infectious Diseasesen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherWellcome Sanger Instituteen_US
dc.identifier.citationInternational Journal for Parasitology: Drugs and Drug Resistance. Vol.9, (2019), 16-22en_US
dc.description.abstract© 2018 The Authors Artemisinin derivatives and their partner drugs in artemisinin combination therapies (ACTs) have played a pivotal role in global malaria mortality reduction during the last two decades. The loss of artemisinin efficacy due to evolving drug-resistant parasites could become a serious global health threat. Dihydroartemisinin-piperaquine is a well tolerated and generally highly effective ACT. The implementation of a partner drug in ACTs is critical in the control of emerging artemisinin resistance. Even though artemisinin is highly effective in parasite clearance, it is labile in the human body. A partner drug is necessary for killing the remaining parasites when the pulses of artemisinin have ceased. A population of Plasmodium falciparum parasites in Cambodia and adjacent countries has become resistant to piperaquine. Increased copy number of the genes encoding the haemoglobinases Plasmepsin II and Plasmepsin III has been linked with piperaquine resistance by genome-wide association studies and in clinical trials, leading to the use of increased plasmepsin II/plasmepsin III copy number as a molecular marker for piperaquine resistance. Here we demonstrate that overexpression of plasmepsin II and plasmepsin III in the 3D7 genetic background failed to change the susceptibility of P. falciparum to artemisinin, chloroquine and piperaquine by both a standard dose-response analysis and a piperaquine survival assay. Whilst plasmepsin copy number polymorphism is currently implemented as a molecular surveillance resistance marker, further studies to discover the molecular basis of piperaquine resistance and potential epistatic interactions are needed.en_US
dc.rightsMahidol Universityen_US
dc.subjectImmunology and Microbiologyen_US
dc.titleOverexpression of plasmepsin II and plasmepsin III does not directly cause reduction in Plasmodium falciparum sensitivity to artesunate, chloroquine and piperaquineen_US
Appears in Collections:Scopus 2019

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