B型流感病毒（IBV）每年以局部暴发或季节性流行的方式存在。早期研究发现IBV感染宿主细胞后可以诱导机体产生比A型流感病毒感染更早更快的天然免疫应答，进而抑制IBV病毒的复制。而在IBV复制过程中，随着抗病毒因子的逐渐增加，病毒蛋白也会不断增加。提示我们IBV在复制过程中可以逃避宿主的先天免疫反应，进而维持病毒和宿主细胞之间的相对平衡的。我们前期研究发现IBV感染多种宿主细胞均可诱导细胞自噬的产生，而抑制细胞自噬可以显著的抑制IBV在细胞中的复制，并且进一步诱导干扰素及干扰素诱导因子的产生。这提示我们在IBV复制过程中，细胞自噬对于IBV的复制及病毒复制过程中诱导的天然免疫应答网络具有重要的调控作用。本项目拟开展细胞自噬在IBV病毒感染复制过程中调控机制研究，阐明细胞自噬在IBV复制过程中所发挥的作用及IBV诱导细胞自噬的分子机制，为抗病毒药物研发及药物靶标筛选提供有效策略和理论基础。

Influenza B virus (IBV) generally causes mild epidemics and seasonal epidemics. The several lines of evidence demonstrated that the robust production of innate immune response can be induced by IBV rather than IAV in multiple cells during early infection, resulting in the decreased virus replication, to some extent. However, there is the scientific question is why IBV protein expression increases whereas host antiviral cytokines gradually increase during IBV virus infection. It gives us a clue that IBV can evade the innate immune response and keep the balance with the host cells. In our previous study, we demonstrated that the IBV can trigger the cell autophagy. Biochemical inhibition of autophagy induction with chloroquine displayed the suppressed IBV replication and enhanced interferon response. These results suggest that autophagy plays a key role in mediating the innate immune response during IBV virus replication. In this proposal, we will focus on the regulation of influenza B virus replication by autophagy, elucidate the function of autophagy during virus replication and uncover a novel evasion mechanism whereby IBV exploit host cell autophagy to thwart host defenses. The study will provide novel targets for the development of novel anti-influenza drugs.