The role of U1 snRNA RNVU1-18 in the regulation of host innate immunity against RNA viruses
作者单位：CAMS Key Laboratory of Synthetic Biology Regulatory Elements Chinese Academy of Medical Sciences &Peking Union Medical College Suzhou Institute of Systems Medicine
会议名称：《第十四届全国免疫学学术大会》
会议日期：2021年
学科分类：1001[医学-基础医学(可授医学、理学学位)] 100102[医学-免疫学] 10[医学]
关 键 词：Infectious disease small nuclear RNA U1 snRNA non-coding RNA antiviral immunity type I interferon
摘 要：Rapid and robust induction of type I interferon(IFN-I) is a key event for the host against invaded viruses. Non-coding RNAs(ncRNAs) including microRNAs, long non-coding RNAs, and circular RNAs play important roles in the fine regulation of IFN-I production and IFNAR downstream signaling pathways. However, it is not clear whether small nuclear RNAs(snRNAs) involve in the regulation of IFN-I-dependent antiviral immunity. snRNA, a type of ncRNA between 100～300bp, is stably, widely, and highly expressed in cells, and very conserved among numerous species. SnRNAs mainly control the splicing of mRNA precursors, which is critical for the basic activities of life. However, the function of snRNAs in viral infectious diseases has not been reported. The E3 ubiquitin ligase TRIM25 mediates the K63 ubiquitination of the viral RNA sensor RIG-I, thereby facilitating the activation of the RIG-I downstream signaling pathway and the production of IFN-I. Our Results have shown that U1 snRNA RNVU1-18 is upregulated in the influenza virus-infected cells. RNVU1-18 interacts with TRIM25 to promotes the activation of RIG-I and its downstream antiviral signaling pathways. Our study has explored the role of RNVU1-18 in host antiviral immunity and clarified the molecular mechanisms, which will provide novel targets and strategies for the prevention and treatment of the infectious diseases caused by viruses including influenza viruses and SARS-CoV-2.