Status of potential <it>Pf</it>ATP6 molecular markers for artemisinin resistance in Suriname

<p>Abstract</p> <p>Background</p> <p>Polymorphisms within the <it>PfATP6</it> gene have been indicated as potential molecular markers for artemisinin efficacy. Since 2004, the use of artemisinin combination therapy (ACT) was introduced as first-line treatment of the uncomplicated malaria cases in Suriname. The aim of this research was to determine changes in Suriname in the status of the polymorphic markers in the <it>PfATP6</it> gene before and after the adoption of the ACT-regimen, particularly of the S769N mutation, which was reported to be associated with <it>in vitro</it> Artemether resistance in the neighboring country French Guiana.</p> <p>Methods</p> <p>The <it>PfATP6</it> gene from <it>Plasmodium falciparum</it> parasites in Suriname was investigated in 28 samples using PCR amplification and restriction enzyme analysis, to assess and determine the prevalence of potentially interesting single nucleotide polymorphisms. The polymorphisms [L263E; A623E; S769N], which may be associated with the artemisinin resistant phenotype were characterized in parasites from three endemic regions before and after the adoption of the ACT-regimen. In addition, the status of these molecular markers was compared in paired <it>P. falciparum</it> isolates from patients with recurring malaria after controlled ACT.</p> <p>Results</p> <p>All the investigated samples exhibit the wild-type genotype at all three positions; L263, A623, S769.</p> <p>Conclusion</p> <p>All investigated isolates before and after the adoption of the ACT-regimen and independent of endemic region harbored the wild-type genotype for the three investigated polymorphisms. The study revealed that decreased artemisinin susceptibility could occur independent from <it>PfATP6</it> mutations, challenging the assumption that artemisinin resistance is associated with these mutations in the <it>PfATP6</it> gene.</p