病毒性疾病时刻威胁人类健康。固有免疫在机体抵抗病毒感染中起到至关重要的作用；为有效清除病毒的同时避免机体过度活化，宿主体内存在多种调节分子对固有免疫活化信号进行精确调控。去泛素化酶USP36能够介导组蛋白H2B去泛素化修饰；但其在抗病毒固有免疫调节中的作用并不清楚。我们发现USP36缺陷显著上调RNA及DNA病毒感染介导的I型干扰素及干扰素诱导基因表达，免疫共沉淀显示USP36能够特异性与组成型及单泛素化修饰的H2B结合并介导H2B的去泛素化修饰，提示USP36可能通过靶向H2B对抗病毒相关基因转录活性进行调控。我们将进一步明确USP36在病毒感染中的功能，确定USP36通过H2B单泛素化调控抗病毒固有免疫反应的作用靶点及作用机制，并在小鼠体内进行验证。我们的研究对补充及完善固有免疫调控网络、探寻新的抗病毒药物靶点具有重要理论意义。

Viral diseases are the main threats to human health. Since innate immunity plays a vital role in defending viruses, host existing various regulatory factors to finetune innate immune responses, thus to effectively eliminate viruses and avoid overactivation. The deubiquitinase USP36 is considered to mediate the deubiquitination of monoubiquitinated histone H2B. However, the regulatory roles in the antiviral innate immune responses are remained unclear. We found that USP36 deficiency dramatically increased the expression of RNA and DNA viruses induced type I interferon and interferon- stimulated genes (ISGs). USP36 coprecipitated with constitutive and monoubiquitinated H2B and then mediated the deubiquitination of H2B, which indicated USP36 regulating the transcriptional level of antiviral associated genes by targeting H2B. In our future work, we will further explicit the regulatory roles of USP36 in virus infection models, and identify the targets and mechanisms of H2B monoubiquitination in regulating antiviral innate immunity through USP36. We will also confirm the roles of USP36 in vivo. Our research will supplement the regulatory network of innate immunity, and provide new potential drug targets for preventing and controlling viral diseases.