病毒感染引起的慢性或突发传染病严重威胁人类生命健康，因此寻找有效的防控和治疗病毒感染的方法成为病毒学和免疫学的研究重点。固有免疫构筑起宿主抵抗病毒感染的第一道防线，在宿主清除病毒的免疫反应中发挥关键作用，然而目前关于抗病毒固有免疫的调控机制并不清楚。本课题前期研究发现特异性在免疫系统中表达的磷酸酶PAC1在巨噬细胞中能够被病毒感染诱导表达，提示PAC1参与抗病毒固有免疫过程。利用VSV病毒感染模型，研究发现PAC1能够抑制宿主抗病毒感染功能。本课题将在此基础上，通过一系列病毒免疫学相关实验明确PAC1对宿主抗病毒固有免疫的作用，利用磷酸化蛋白质组学和高通量RNA测序等分子生物学手段探究PAC1调控抗病毒固有免疫的分子机制。本课题有望发现一条全新的抗病毒免疫信号通路，为临床上防控和治疗病毒感染开辟新的途径。

Chronic or fulminant infectious diseases resulted from viral infection seriously threaten human health. Exploration of approaches to effectively prevent and treat viral infection is therefore a research focus in the field of virology and immunology. Innate immunity shapes the first line for host to defense against viral infection, which plays an essential role in eradication of invaded virus. Nevertheless, the mechanism governing regulation of antiviral innate immunity thus far remains elusive. Our preliminary studies showed that the immune cell-specific phosphatase PAC1 was induced in macrophages upon viral infection, suggesting that PAC1 is involved in the process of antiviral innate immunity. Employing VSV viral infection model, we found that PAC1 suppressed host antiviral capacity. Based on these findings, we will perform a series of viral immunological experiments to characterize the function of PAC1 in antiviral innate immunity. Furthermore, we will utilize high-throughput phosphoproteomics and RNA sequencing as well as other molecular biological techniques to investigate the molecular mechanism by which PAC1 modulates antiviral innate immunity. The implementation of this research project is conduced to uncover a novel signaling pathway regarding antiviral immunity and pave a new avenue for prevention and treatment of viral infection.