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Background Malaria is a devastating disease, transmitted by female  Anopheles  mosquitoes infected with  Plasmodium  parasites. Current insecticide-based strategies exist to control the spread of malaria by targeting vectors. However, the increase in insecticide resistance in vector populations hinder the efficacy of these methods. It is, therefore, essential to develop novel vector control methods that efficiently target transmission reducing factors such as vector density and competence. A possible vector control candidate gene, the ecdysone receptor, regulates longevity, reproduction, immunity and other physiological processes in several insects, including malaria vectors.  Anopheles funestus  is a prominent vector in sub-Saharan Africa, however, the function of the ecdysone receptor in this mosquito has not previously been studied. This study aimed to determine if the ecdysone receptor depletion impacts  An. funestus  longevity, reproduction and susceptibility to  Plasmodium falciparum  infection. Methods RNA interference was used to reduce ecdysone receptor expression levels in  An. funestus  females and investigate how the above-mentioned phenotypes are influenced. Additionally, the expression levels of the ecdysone receptor, and reproduction genes lipophorin and vitellogenin receptor as well as the immune gene, leucine rich immune molecule 9 were determined in ecdysone receptor-depleted mosquitoes using quantitative polymerase chain reaction. Results Ecdysone receptor-depleted mosquitoes had a shorter lifespan, impaired oogenesis, were less fertile, and had reduced  P. falciparum  infection intensity. Conclusions Overall, this study provides the first experimental evidence that supports ecdysone receptor as a potential target in the development of vector control measures targeting  An. funestus .

The ecdysone receptor regulates several key physiological factors in Anopheles funestus