A Novel L932F mutation in the Voltage-Gated Sodium Channel associated with Deltamethrin Resistance in Aedes aegypti (Diptera: Culicidae) from Southern Taiwan.

Aedes aegypti is a primary vector for major arboviruses such as dengue, Zika, and chikungunya, imposes a significant disease burden in tropical and subtropical regions. The widespread application of pyrethroid insecticides for vector control has led to the global dissemination of knockdown resistance (kdr) mutations, a major resistance mechanism. Continuous surveillance of kdr mutations is therefore essential to inform and optimize vector control strategies. To characterize the kdr profile, we first employed targeted capture sequencing on 12 individual mosquitoes from three field-derived strains collected in Taiwan in 2021. Subsequently, direct Sanger sequencing was performed on 99 mosquitoes field-collected in 2024. Furthermore, topical bioassay using a series of deltamethrin concentrations were conducted on 200 mosquitoes, followed by direct sequencing to link resistance phenotypes to specific genotypes. A characterized insecticide-susceptible strain (KHSM) served as a control. We identified a novel leucine to phenylalanine substitution at position 932 (L932F) in the voltage-gated sodium channel (VGSC) of Aedes aegypti in Taiwan. The emerging mutant was initially detected in a strain carrying the double kdr genotype (S989P and V1016G) and was subsequently detected in field population across Southern Taiwan, with its presence confirmed in archived samples dating from 2020-2022. The mutation was crucially associated with reduced susceptibility to deltamethrin in topical bioassays. This study provides the first report of the L932F kdr mutation in Ae. aegypti, indicating the emergence of a novel mutation in Taiwanese populations. Furthermore, the L932F mutation may contribute to reduced deltamethrin susceptibility, even in triple-mutant individuals co-harboring the well-established S989P and V1016G resistance alleles.