Mitochondrial phylogeography and insecticide resistance of Aedes aegypti in Kenya.

Aedes aegypti is the primary vector of arboviruses such as dengue, yellow fever, Zika, and chikungunya. Here, we investigate the mitochondrial DNA (mtDNA) structure and insecticide resistance of Ae. aegypti populations across Kenya. Using 175 newly sequenced Kenyan COI mtDNA fragments, along with global reference sequences, we assess maternal ancestry and phylogeographic structure. Genetic structure across Kenya was not well explained by isolation-by-distance alone, with several populations deviating from this pattern. Nairobi and Mombasa, separated by >400 km, showed greater maternal genetic similarity than expected under isolation-by-distance, a pattern that may reflect gene flow along transportation corridors. Conversely, Ukunda, around 30 km from Mombasa, was comparatively divergent, and populations in Western Kenya were genetically distinct. We found no evidence of non-African ancestry in mtDNA from Rabai or Mombasa despite its previous detection in the nuclear genomes of these populations. Instead, a subset of samples from Marigat and Ukunda showed the closest maternal affinity to West African and non-African lineages. Insecticide assays revealed high susceptibility to bendiocarb, deltamethrin, and fenitrothion across populations, but substantial resistance to permethrin, particularly at coastal sites. Genotyping of the kdr 1534C allele showed the highest resistance allele frequencies in coastal populations, broadly consistent with the phenotypic patterns. This variation in resistance was not associated with mitochondrial ancestry, suggesting that local selection pressures rather than shared maternal ancestry may be shaping resistance. Together, these findings describe the maternal genetic structure of Ae. aegypti in Kenya and show that localised resistance evolution, in the absence of organised Ae. aegypti-targeted control, underscores the need to monitor resistance mechanisms.