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Lack of association between putative transporter gene polymorphisms in Plasmodium falciparum and chloroquine resistance in imported malaria isolates from Africa

DOI: 10.1186/1475-2875-5-24

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This study tried to find an association between putative transporters gene polymorphisms with in vitro response to CQ and pfcrt genotype in isolates originating from various African countries. To avoid biases of parasites adaptation in culture, fresh isolates obtained from symptomatic, malaria-infected travellers returning from Africa to France were used. Monoclonal isolates included in the study were selected using a msp-2 fragment analysis method. In vitro susceptibility to CQ, single nucleotide polymorphisms and microsatellite polymorphisms in pfcrt, pfmdr1 and six putative transporter genes were established in 27 isolates and three reference strains.Polymorphism of pfcrt at positions 76 and 220 showed a significant association with in vitro chloroquine resistance (P < .02 and P < .05 respectively). Polymorphism of pfmdr1 at position 86 showed an equally significant association with in vitro chloroquine response (P < .05). No association was found between SNPs or microsatellite polymorphisms of putative transporter genes and in vitro CQR or pfcrt genotype in imported malaria isolates from Africa.The previously described association between putative transporter gene polymorphisms and in vitro response to chloroquine (CQ) was not confirmed in the present study.Plasmodium falciparum malaria remains one of the major causes of morbidity and mortality in sub-Saharan Africa, leading each year to the death of an estimated number of 1–2.7 million individuals, mostly children [1]. Chloroquine (CQ) resistance of P. falciparum represents today a major health care problem in malaria endemic countries [2]. PfCRT, a member of the drug/metabolite transporter superfamily, was demonstrated to play a central role in the resistance of P. falciparum to CQ [3-6]. The identification of PfCRT and the discovery of its role in CQR were a step by step work. Using a genetic cross, the Wellems'group demonstrated that a 36 kb locus in chromosome 7 was linked to CQR [7,8]. Initially a first ca


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