Selection for insecticide resistance can promote Plasmodium falciparum infection in Anopheles

Insecticide resistance is under strong selective pressure in Anopheles mosquitoes due to widespread usage of insecticides in vector control strategies. Resistance mechanisms cause physiological changes that may affect the mosquito competence for Plasmodium parasites and alter malaria transmission dynamics. Though fitness costs of insecticide resistance are often presumed, they have not been well characterized for most resistance mechanisms. Further, it remains poorly understood how resistance or sublethal exposure to insecticides alter the ability of mosquitoes to host and transmit a Plasmodium infection. From highly pyrethroid-resistant field-derived mosquitoes, we established a resistant (RES) colony and susceptible (SUS) colony by either selection for, or loss of, insecticide resistance. We show increased prevalence, intensity, and oocyst growth rate of Plasmodium falciparum infection in RES females compared to SUS. The increase in infection intensity is not associated with the presence of the kdrL1014F mutation, and is not impacted by inhibition of Cytochrome P450s nor by permethrin exposure. Instead, we observe upregulation of the lipid and cuticular hydrocarbon transporter, lipophorin, in RES compared to SUS, and hypothesize that increased lipid transport, possibly selected for by insecticide pressure, may be associated with increased vector competence for P. falciparum. We discuss the relevance of these results for future insecticide-based vector control strategies in the face of insecticide resistance. ### Competing Interest Statement The authors have declared no competing interest.