流感病毒感染能引起严重的传染性呼吸道疾病，对人类健康和公共卫生存在重大威胁。因此，研究流感病毒致病机制以及病毒-宿主相互作用对开发有效的抗病毒策略具有重要意义。细胞自噬作为细胞内降解机制能有效的抑制病毒感染，然而流感病毒感染阻碍自噬溶酶体融合，从而逃避细胞自噬抗病毒机制。鉴于细胞自噬在流感病毒感染中扮演关键角色，本项目拟基于前期全基因组CRISPR/Cas9敲除筛选鉴定的宿主因子COG8为研究对象，解析COG8影响流感病毒诱导细胞自噬的作用机制；从宿主和病毒双角度挖掘出COG8调控细胞自噬溶酶体影响流感病毒感染的分子机制，为COG8作为抗流感病毒药物靶点提供理论依据。

Influenza virus infection causes serious infectious respiratory diseases, which pose a major threat to human health and public health. Therefore, studying the pathogenic mechanism of influenza virus and virus-host interaction is of great significance for the development of effective antiviral strategies. Autophagy acts as an intracellular degradation mechanism to effectively inhibit viral infection. However, influenza virus infection impedes the fusion of autophagosome with lysosome, thereby evading the autophagic antiviral mechanism. In view of the critical role of cellular autophagy in influenza virus infection, based on the previous genome-wide CRISPR/Cas9 knockout screen and identification, the aim of this project is analyzing the mechanism of host factor COG8 on influenza virus-induced autophagy. Meanwhile, From the aspect angle of both host and virus, the molecular mechanism of COG8-reuglated autolysosome affecting influenza virus infection was explored. In conclusion, the results obtained from this project will provide a theoretical basis for COG8 as a target for anti-influenza virus drugs.