Non-Synonymous Mutations Associated with Plasmodium falciparum Artemisinin Resistant Gene (Pfkelch13) in Malaria Cases, Jos Nigeria
Joel Paul, Nelson J. Nwankwo, Mercy O. Simon, Shangshikmwa K. Gaknung, Timloh Fakdul, Dinci T. Davou, Mary M. Mankilik, Richard J. Kutshik, Bitrus Yakubu, Ishaya Y. Longdet
Journal of Advances in Biology & Biotechnology · pp. 28–38 · Published 2 Dec 2023
10.9734/jabb/2023/v26i10661Abstract
Aim: The aim of this study was to explore the Plasmodium falciparum Artemisinin Resistant Gene (Pfkelch13) in malaria cases in Jos and profile the nature of the mutations. The Plasmodium falciparum kelch13 gene is a potential molecular marker for tracking artemisinin-resistant malaria parasites. Study Design: The Study Design was Experimental Place and Duration of Study: The study was conducted within Jos, Nigeria between October 2019 and January 2021. Methodology: Thirty-six clinically screened 2 plus (++) and above positive malarial whole blood samples were collected from a Hospital in Jos, Plateau State, Nigeria in EDTA bottles after being granted ethical approval. The DNA extraction was done using Zymo Research extraction kits according to the manufacturer’s instructions. Detection of the Plasmodium genus, Plasmodium falciparum and Pfkelch13 gene in the samples was done using PCR technique and gel electrophoresis. PCR amplicons were sequenced and bioinformatics software was used to analyze the sequences for mutations. Results: Only 41.67% of the samples collected were confirmed positive for the Plasmodium genus. Out of these, 93.33% were positive for Plasmodium falciparum. The PfKelch13 (Pfk13) gene was detected in 78.57% of the Plasmodium falciparum. Non-synonymous mutations (S695C, C696M, C696H, H697S, H697V, F698I, 699L and 699S were observed at the amino acids level, but didn’t affect the structural conformation of the proteins. Conclusion: The classical method of detecting malaria is not reliable compared to the PCR technique. Non-synonymous mutations on the PfKelch13 gene have the potential to cause resistance to artemisinin drugs in the Jos human population.
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Cited by 4
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