Resistance profiles and mechanisms in pyrethroid-resistant Aedes aegypti populations: first detection of the V1016G kdr mutation in Abidjan, Côte d’Ivoire

Background Côte d’Ivoire is facing an acceleration of outbreaks of Aedes -borne arboviral diseases (e.g., dengue and yellow fever), with the highest incidence rate reported in the city of Abidjan where control responses are mostly based on insecticide space spraying (ISS). We investigated the insecticide resistance profiles and underlying mechanisms, including target site knock-down resistance ( kdr ) mutations and metabolic resistance, in wild Aedes aegypti populations across Abidjan. Methods Aedes aegypti larvae were collected from their natural breeding habitats in four study sites (Anono, Ayakro, Entente and Gbagba) and reared to adults. Adult female Ae . aegypti aged 2–5 days were tested against multiple pyrethroids (deltamethrin, alphacypermethrin and permethrin) with and without pre-exposure to the synergist piperonyl butoxide (PBO), the carbamate bendiocarb, and the organophosphate pirimiphos-methyl, using standard World Health Organization (WHO) insecticide susceptibility bioassays. Additionally, mosquito samples were screened for five kdr mutations (V410L, S989P, V1016I, V1016G, and F1534C) using an allele-specific polymerase chain reaction (AS-PCR). Results Overall, Ae. aegypti populations showed low to moderate mortality and evidence of multiple insecticide resistance mechanisms, including V1016G, a new kdr mutation. Mortality was low with all three pyrethroids (8%-33%), and moderate with bendiocarb (58%-85% mortality), and pirimiphos-methyl (60%-79% mortality) in all four study sites. Increased susceptibility to all three pyrethroids following PBO pre-exposure suggests the potential involvement of cytochrome P450 oxidase-mediated metabolic resistance. The 1534C mutation was nearing fixation at 93%, while the respective allelic frequencies for 1016I and 410L were approximately 55% and 45%, respectively. Overall, F1534C, V1016I and V410L kdr mutations were associated with phenotypic resistance, with the triple homozygous mutant CIL/CIL genotype being mostly found in alive individuals (89.2%) compared with dead individuals (10.8%). The V1016G kdr mutation, typically found in Asia, was detected in a single individual, representing the first report in Ae. aegypti in Côte d’Ivoire. Conclusions Aedes aegypti populations from Abidjan are resistant to all five insecticides across the four study sites. Pyrethroid resistance was associated with multiple kdr mutations and is also likely due to P450 oxidase-mediated metabolic resistance. In addition, the present study reports the first detection of the V1016G kdr mutation in Ae. aegypti in Côte d’Ivoire. The presence of these multiple resistance mechanisms may be compromising the effectiveness of ISS interventions. Therefore, neither insecticide is an option and alternatives ought to be looked for. Our findings are important for developing effective and sustainable control of local Aedes vectors of arboviral diseases.