Profile of pfcrt, pfmdr-1 and K13 Propeller Genes of Plasmodium falciparum Isolates from Bouaflé, Bondoukou and Séguéla, Côte d'Ivoire
ABY K. Jérôme, BLA K. Brice, GNAGNE A. Paterne, KONATE-TOURE A, KOUASSI M. Firmin, GOHOUN W.Carole Z., BEDIA A.Valérie, ASSANVO A.N. Stevenson, YAVO W
International Journal of TROPICAL DISEASE & Health · pp. 14–25 · Published 12 Aug 2025
10.9734/ijtdh/2025/v46i81679Abstract
Background: With the aim of eliminating malaria, it is necessary to therapeutic efficacy and genetic markers of antimalarial drug resistance in order to ensure treatment efficacy. In this context, this study analyzed the polymorphism variability of the pfcrt, pfmdr-1 and K13 propeller genes in three health regions, Bouaflé, Bondoukou and Séguéla. Method: A total of 292 P.falciparum-infected blood samples were collected from patients coming for consultation during the period May - November 2019. Demographic information and blood samples were collected. P.falciparum genomic DNA was extracted from blood samples and polymorphisms of pfcrt, pfmdr-1, and K13-propeller were amplified by nested PCR followed by sequencing. Data were analyzed using Word Excel version 2016 and BioEdit version 2012 software. Results: Analysis of the pfcrt gene in Bouaflé showed a prevalence of 66.66% for the wild-type CVMNK haplotype, compared with 33.33% for the CVIET, CVMET, CVMDT, CVMEK and CVMDK mutants. These results were statistically identical to those obtained in Bondoukou and Séguéla (p>0.05). Analysis of the pfmdr-1 gene yielded the wild-type haplotype N86Y184 with frequencies of 45.45%, 48.15% and 27.78% in Bouaflé, Bondoukou and Séguéla respectively. The N86F184 mutant genotype was described in proportions of 27.27% in Bouaflé, 48.15% in Bondoukou and 58.33% in Séguéla. Y86F184 was observed at a prevalence of 9.1% in Bouaflé (n=1), compared with 3.70% in Bondoukou (n=1) and 11.11% in Séguéla (n=4). Concerning the K13 propeller gene, non-synonymous SNPs of type G674Y and S681F in Bouaflé and P443S and T685P in Bondoukou were reported. Conclusion: This study revealed great genetic variability in antimalarial resistance markers from one site to another, and highlighted major haplotypes such as CVIET for pfcrt, N86F184 and Y86F184 for pfmdr-1, and non-synonymous candidate mutations for resistance such as A675D for K13 propeller. Consequently, monitoring of these markers must be stepped up to ensure the effectiveness of antimalarial treatments.
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