人巨细胞病毒（HCMV）感染宿主细胞的过程中，需要“挟持”宿主细胞因子帮助其完成复制，而宿主细胞的抗病毒反应也会被激活，这种病毒和宿主的相互作用决定了病毒的最终命运，研究参与这些相互作用的宿主蛋白有助于发现新的抗病毒蛋白并发展抗病毒药物，具有重要意义。本项目前期工作运用基于质谱的蛋白质组学技术首次对HCMV感染的宿主细胞的核、质蛋白分别进行了定量分析，发现了261个在HCMV感染前后发生了变化的宿主蛋白，随后初步功能研究表明UB2V2等变化蛋白能够影响HCMV的复制。本项目将在此基础上继续对UB2V2展开深入研究，探索其是否通过TRIM32蛋白影响Ⅰ型干扰素的激活，从而影响HCMV复制，阐明其影响病毒复制的分子机制。本项目还将对其它变化的宿主蛋白进行初步功能研究，探索其影响HCMV复制的分子机制，为抗HCMV研究提供潜在的分子靶标。

During infection, HCMV will hijack various host cell factors to promote their replication, while host cells in turn will activate antiviral responses. The balance of virus-host interactions determines the outcome of viral infection and disease progression. A better understanding of these host-virus interactions may lead to the identification of potential drug targets and the development of novel antiviral agents. To identify host proteins involved in HCMV-host interactions, in our previous research, we performed subcellular quantitative proteomic analysis of HCMV-infected HEL cells, and found 261 host proteins were differentially regulated in cytoplasmic or nuclear fractions. Subsequent functional study indicated that UB2V2 and several other host proteins can influence the replication of HCMV. In this project, we will perform further functional study on UB2V2, and explore how UB2V2 influence the activation of type Ⅰ interferons through TRIM32, thus influence the replication of HCMV. We will also explore whether other regulated host proteins can influence the replication of HCMV, and perform functional study on some of them. Our project will provide targets for anti-HCMV research.