寨卡等虫媒病毒的广泛流行严重威胁人类健康和公共卫生。虫媒病毒通过吸血过程感染媒介昆虫，而中肠是病毒感染媒介的第一道屏障，因此，虫媒病毒必须要抑制媒介的中肠免疫。申请人的前期研究结果显示，寨卡病毒囊膜蛋白E的糖基化修饰可以特异的抑制中肠的活性氧免疫信号通路，从而促进病毒感染其媒介埃及伊蚊。而虫媒病毒的囊膜蛋白普遍有糖基化修饰，因此，本项目计划进一步研究糖基化修饰在其他蚊虫传播病毒感染蚊虫中肠过程中的作用。本研究将以乙型脑炎病毒/淡色库蚊和基孔肯亚病毒/埃及伊蚊为研究对象，他们分别代表了黄病毒属和甲病毒属两类主要的虫媒病毒，以及库蚊和伊蚊两类主要蚊虫媒介。本项目还将在前期研究结果的基础上，通过转录组学分析，揭示虫媒病毒糖基化修饰抑制蚊虫中肠活性氧信号通路的分子机制，为通过阻断病毒传播而防治虫媒病提供理论参考。

Arbovirus, such as dengue, Zika and Chikungunya virus, are threatening human healthy. Transmission of arbovirus by hematophagous insects such as mosquitoes requires acquisition of the virus during blood-feeding on the host, with midgut as the primary infection site. Certain strategies must be evolved to antagonize the immune barrier of midgut. Previously, we report that N-glycosylation on the E protein, which is conserved among most flaviviruses, is critical for the Zika virus to invade the vector midgut by inhibiting the reactive oxygens species (ROS) pathway of the mosquito immune system. Here, we propose to investigate whether this strategy was universal among different arbovirus during infection of different vectors. Furthermore, we are going to uncover the molecular mechanism underlying the regulation of ROS by N-glycosylation. The understanding of the mechanism of arbovirus/vector interaction will lead to the new strategies of blocking virus transmission at vector level.