Detection of S989P and V1016G Knockdown Resistance (kdr) Mutations in the Voltage-Gated Sodium Channel (VGSC) Gene of Aedes aegypti Populations in West Sumatra

Aedes aegypti is the principal vector of dengue and several other arboviral diseases, and its control remains heavily dependent on chemical insecticides. However, the prolonged and widespread use of insecticides has promoted the development of resistance, including knockdown resistance associated with mutations in the voltage-gated sodium channel (VGSC) gene. This study assessed insecticide susceptibility and investigated the occurrence of the S989P and V1016G kdr mutations in Aedes aegypti populations collected from dengue-endemic areas of West Sumatra, Indonesia. Mosquitoes were sampled from six districts. Larval susceptibility to temephos and adult susceptibility to malathion, permethrin, and alpha-cypermethrin were evaluated using standard World Health Organization bioassays. VGSC genotyping was performed using tetra-primer amplification-refractory mutation system polymerase chain reaction and allele-specific polymerase chain reaction. The bioassays revealed marked geographical variation in insecticide susceptibility, with widespread resistance to malathion, permethrin, and alpha-cypermethrin across the study sites. Molecular analysis detected the S989P and V1016G substitutions, corresponding to serine-to-proline and valine-to-glycine amino acid changes, respectively. These findings demonstrate reduced susceptibility to multiple insecticides and provide region-specific molecular evidence of kdr-associated mutations in Aedes aegypti populations from West Sumatra. Although the number of genotyped specimens was limited, the results provide important baseline information for expanded resistance surveillance and the development of evidence-based insecticide resistance management and vector-control strategies.