Environmental BPA exposure promotes flavivirus replication and extends mosquito lifespan.

Environmental exposure to endocrine-disrupting chemicals (EDCs) is widespread, yet their influence on arthropod-borne virus transmission remains poorly understood. Here, we show that bisphenol A (BPA), a common EDC, enhances the replication of Zika virus (ZIKV) and Dengue virus (DENV) in the mosquito Aedes aegypti by modulating host oxidative stress responses. Through systematic screening of nine EDCs, BPA and dichlorodiphenyltrichloroethane (DDT), significantly promoted viral replication, with BPA exhibiting the strongest effect. Chronic larval exposure to BPA led to its residual accumulation in adults and increased susceptibility to viral infection. Transcriptomic and biochemical analyses revealed that BPA upregulates antioxidant enzymes-superoxide dismutase (SOD) and catalase (CAT)-and reduces lipid peroxidation, thereby alleviating oxidative stress and creating a cellular environment conducive to viral replication. Furthermore, BPA extended the lifespan of ZIKV-infected mosquitoes, potentially extending the period during which infected mosquitoes could transmit virus, although this remains to be directly demonstrated. Our findings uncover a mechanism by which environmental BPA exposure may influence flavivirus transmission dynamics through redox modulation in mosquitoes, highlighting the need to incorporate pollutant impacts into arboviral risk assessments.