Richmond Afoakwah, Johnson N. Boampong, Desmond O. Acheampong and Ekene K. Nwaefuna
Antimalarial drugs will continue to be a major control tool for controlling malaria, through treatment and prophylaxis, until an effective malaria vaccine is developed. Plasmodium falciparum, the major malaria parasite, has developed resistance to most available antimalarial drugs. The last decade has seen an increase in malaria burden due to drug resistant strains of P.falciparum. Currently combination therapy has been recommended by World Health Organization (WHO) for treating uncomplicated malaria, with formulations containing an artemisinin compound as policy standard. This is aimed at improving treatment as well as delaying resistance. Research has, however, reported in vitro resistance to artemisinins a few years after implementation of Artemisinin-based Combination Therapy (ACT) policy. The objective of this review is to provide comprehensive information on the Single nucleotide polymorphisms (SNPs) of the Plasmodium falciparum adenosine triphosphatase 6 (PfATPase6) gene and also to argue the significance of PfATPase6 SNPs in malaria treatment. Articles used for this review were searched from Hinari, Pubmed and JSTOR electronic databases. So far about forty-four (44) SNPs have been identified in the PfATPase6 gene in samples collected from thirty-five (35) countries. In vitro resistance tests have not been carried out on most of the identified SNPs. Again the E431K, A623E, S769N and L263E mutations that have been shown to confer resistance to artemisinins have not been found in most analyzed samples. The identified PfATPase6 SNPs have not been shown to have arisen as a result of drug selection pressure. The prevalence of SNPs which are associated with decrease in artemisinin susceptibility may increase under the new drug selection pressure and eventually impair ACT treatment.
