Evaluates beta-cypermethrin resistance in Aedes aegypti, indicating critical resistance mechanisms.
Aedes aegypti is a major invasive vector in China, where prolonged pyrethroid use has induced resistance, complicating dengue control. This study evaluated the resistance levels of Ae. aegypti to the pyrethroid beta-cypermethrin in Yunnan and explored the underlying mechanisms to inform control strategies. Mosquitoes were collected from five regions of Yunnan in 2015–2016. Larval bioassays, adult diagnostic dose determination, and adult bioassays were conducted to assess resistance to beta-cypermethrin. Mixed-function oxidase (MFO) amount was measured in larvae, and PCR amplification was used to detect mutations in the voltage-gated sodium channel (VGSC) gene. Correlations between enzyme activity, mutations, and phenotypic resistance were analyzed. Larval bioassays indicated that all five populations exhibited resistance to beta-cypermethrin, with resistance ratios ranging from 11.31 to 41.56. The adult diagnostic dose was determined as 0.74668 g/L, with mortality rates ranging from 8.89% to 58.89%, confirming resistance. A significant negative correlation was found between adult mortality and larval LC50 values. MFO amount was closely correlated with resistance levels. The F1534C mutation was the only VGSC mutation detected, and its frequency showed a significant positive correlation with beta-cypermethrin resistance. Our data were collected in 2015–2016; resistance levels may have changed since then, and no confirmatory bioassays were performed by us after 2020. The findings demonstrate that the F1534C mutation and increased MFO amount contribute to enhanced beta-cypermethrin resistance of Ae. aegypti in Yunnan. By linking phenotype resistance to key molecular and biochemical mechanisms, these findings support the continued monitoring of resistance and provide a basis for the evidence-based optimization of dengue vector control strategies.
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