代谢在机体抗病毒机制以及病毒的免疫逃逸机制中很可能会发挥关键作用。本课题组在对抗病毒天然免疫明星分子MAVS相互作用蛋白分析中意外发现，代谢酶免疫应答基因1(IRG1)蛋白与MAVS相互结合，且在病毒刺激后表达显著升高。进一步研究发现IRG1能抑制病毒复制，显著正向调节病毒诱导的I型干扰素产生。由此推测IRG1很可能通过影响MAVS的功能状态或通过重塑细胞代谢状态，影响抗病毒天然应答及免疫细胞抗病毒。本课题拟通过已构建的敲除小鼠等探究其正向调控抗病毒天然免疫的生物学机制；通过转录组和代谢组高通量组学分析寻找IRG1缺失之后细胞代谢状态改变的证据，并聚焦其中最为重要的代谢通路；通过质谱、免疫共沉淀等筛选IRG1的相互作用蛋白及其相互作用方式；通过对相关临床样本的采集和分析，挖掘其在临床应用中的价值。本课题的完成可为病毒性感染防治方法的研发提供新的靶点和新的思路，具有理论意义和潜在的应用价值。

Metabolism is likely to play a key role in the mechanism of antivirus and the immune escape mechanism of the virus. In this project, we found that the immune enzyme gene 1 (IRG1) can interact with MAVS and the expression of IRG1 increased significantly after viral stimulation. Further studies have found that IRG1 can inhibit viral replication and significantly positively regulate the production of virus-induced type I interferon. Therefore, it is presumed that IRG1 may affect the natural response to antiviral and immune cells by affecting the functional status of MAVS or by remodeling the metabolic state of cells. This project will explore the biological mechanisms of its positive regulation of antiviral innate immunity and will obtain the evidence of the transcriptome and metabolome metabolism changes for IRG1 deletion. We will focus on the most important metabolic pathways to explore its mechanisms. We will also excavate its value in clinical applications through the collection and analysis of the related clinical samples. The completion of this project will provide new targets and new ideas for the prevention and control methods of viral infection, which has theoretical significance and potential application value.