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Proc Natl Acad Sci U S A DOI:10.1073/pnas.1507142112

Adaptive evolution of malaria parasites in French Guiana: Reversal of chloroquine resistance by acquisition of a mutation in pfcrt.

Publication TypeJournal Article
Year of Publication2015
AuthorsPelleau, S, Moss, EL, Dhingra, SK, Volney, B, Casteras, J, Gabryszewski, SJ, Volkman, SK, Wirth, DF, Legrand, E, Fidock, DA, Neafsey, DE, Musset, L
JournalProc Natl Acad Sci U S A
Date Published2015 Sep 15
KeywordsAlleles, Chloroquine, Drug Resistance, Evolution, Molecular, French Guiana, Genetic Markers, Genome, Genotype, Haplotypes, Humans, Inhibitory Concentration 50, Malaria, Membrane Transport Proteins, Mutation, Phenotype, Plasmodium falciparum, Prevalence, Principal Component Analysis, Protozoan Proteins, Quinolines, Retrospective Studies

In regions with high malaria endemicity, the withdrawal of chloroquine (CQ) as first-line treatment of Plasmodium falciparum infections has typically led to the restoration of CQ susceptibility through the reexpansion of the wild-type (WT) allele K76 of the chloroquine resistance transporter gene (pfcrt) at the expense of less fit mutant alleles carrying the CQ resistance (CQR) marker K76T. In low-transmission settings, such as South America, drug resistance mutations can attain 100% prevalence, thereby precluding the return of WT parasites after the complete removal of drug pressure. In French Guiana, despite the fixation of the K76T allele, the prevalence of CQR isolates progressively dropped from >90% to


Alternate JournalProc. Natl. Acad. Sci. U.S.A.
PubMed ID26261345
PubMed Central IDPMC4577156
Grant ListHHSN272200900018C / AI / NIAID NIH HHS / United States
R01 AI050234 / AI / NIAID NIH HHS / United States
F30 AI114070 / AI / NIAID NIH HHS / United States
T32 GM007367 / GM / NIGMS NIH HHS / United States
R01 AI109023 / AI / NIAID NIH HHS / United States
HHSN272200900018C / / PHS HHS / United States
R01AI50234 / AI / NIAID NIH HHS / United States
R01AI109023 / AI / NIAID NIH HHS / United States