Absence of Artemisinin Resistance-Associated Mutations in the Plasmodium Falciparum Kelch 13 (K13) Propeller Domain Gene Following Widespread Use of Artemisinin-Based Combination Therapy in Iran.

PURPOSE: Continuous surveillance of Plasmodium falciparum Kelch 13 (pfk13) mutations associated with artemisinin resistance is essential for monitoring the emergence of drug-resistant parasites in malaria-endemic regions. Herein, we have assessed the prevalence of point mutations in the pfk13 gene linked to artemisinin resistance in Iranian P. falciparum isolates, 18 years following the nationwide introduction of artemisinin-based combination therapies (ACTs).

METHODS

A total of 60 finger-prick blood samples were obtained from Iranian patients with symptomatic, uncomplicated P. falciparum malaria during the period of 2022 to 2023. A nested polymerase chain reaction (PCR) assay was employed to verify infections by amplifying the 18 S small subunit ribosomal RNA (18 S ssrRNA) gene. Nested PCR was utilized to amplify the pfk13 gene, followed by sequencing of the amplicons to identify both previously reported and novel mutations.

RESULTS

Of the successfully sequenced samples (n = 50), 98% (49/50) carried the wild-type allele. One sample harbored a novel nonsynonymous mutation, R513C, corresponding to a C1537T nucleotide change.

CONCLUSION

No validated pfk13 mutations indicative of artemisinin resistance were detected in the study population. These findings suggest that artemisinin remains effective for treating P. falciparum malaria in this region. Continued molecular surveillance is warranted to ensure early detection of emerging resistance.