Studies on the mechanisms of insecticide resistance in chikungunya mosquito vectors

为了构建更合理的蚊媒控制策略，降低基孔肯雅热的风险，我们对埃及伊蚊拟除虫菊酯类杀虫剂的抗药性机制进行了研究。我们主要从（1）靶标敏感性的改变，（2）杀虫剂渗透性的降低和（3）代谢活性的增强来阐明抗性的机制。我们发现，由于氨基酸取代而降低的靶位点（Vssc）的敏感性赋予了抗性。细胞色素P450代谢活性的增强也是抗性产生的主要原因之一。此外，我们确定了CYP9M6和CYP6BB2都能够代谢氯菊酯，并且在SP菌株中过量产生。

In order to construct more appropriate strategies for controlling mosquito vectors to reduce the risk of Chikungunya fever, we studied on the mechanisms of pyrethroid-insecticide resistance of Aedes aegypti. We focused on (1)Altered target site sensitivity, (2)Reduced penetration of insecticide, and (3)Enhanced metabolic activity, to elucidate the mechanism of the resistance. We found that reduced sensitivity of target site (Vssc) due to amino acid substitutions conferred resistance. Enhanced activity of pyrethroid metabolism by cytochrome P450s was also one of the major factors of the resistance. Further, we identified that both CYP9M6 and CYP6BB2 were capable of metabolizing permethrin and are over produced in SP strain.