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Chloroquine (CQ)-resistant Plasmodium vivax malaria was first reported 12 years ago, nearly 30 years after the recognition of CQ-resistant P. falciparum. Loss of CQ efficacy now poses a severe problem for the prevention and treatment of both diseases. Mutations in a digestive vacuole protein encoded by a 13-exon gene, pfcrt, were shown recently to have a central role in the CQ resistance (CQR) of P. falciparum. Whether mutations in pfcrt orthologues of other Plasmodium species are involved in CQR remains an open question. This report describes pfcrt homologues from P. vivax, P. knowlesi, P. berghei, and Dictyostelium discoideum. Synteny between the P. falciparum and P. vivax genes is demonstrated. However, a survey of patient isolates and monkey-adapted lines has shown no association between in vivo CQR and codon mutations in the P. vivax gene. This is evidence that the molecular events underlying P. vivax CQR differ from those in P. falciparum.

Original publication

DOI

10.1086/320707

Type

Journal article

Journal

J Infect Dis

Publication Date

01/06/2001

Volume

183

Pages

1653 - 1661

Keywords

Amino Acid Sequence, Animals, Chloroquine, Codon, Dictyostelium, Drug Resistance, Humans, Molecular Chaperones, Molecular Sequence Data, Mutation, Parasitic Sensitivity Tests, Plasmodium, Sequence Alignment