甲型流感病毒(IAV)的高效复制依赖于大量宿主因子。研究发现长链非编码RNA（lncRNAs）可以通过调节免疫应答来参与宿主的抗病毒防御过程，但目前对lncRNAs，尤其是干扰素非依赖型lncRNAs，在IAV复制中的生物学功能及其分子机制还知之甚少。我们前期工作首次发现干扰素非依赖型lncRNA IPAN能被IAV诱导表达，特异性促进IAV的复制。初步机制发现IPAN通过与病毒PB1结合，抑制RIG-I介导的PB1降解，从而保证了病毒RNA的合成，但对IPAN与RIG-I参与PB1降解的具体机制仍未可知。本项目将深入研究IPAN与病毒PB1相互作用机制及功能、IPAN沉默引起的PB1蛋白降解机制、宿主RIG-I介导PB1降解的分子机制，并鉴定IPAN结合蛋白，进行相关功能研究，以期全面阐明IPAN促进IAV病毒复制的分子机制，为lncRNAs调控病毒复制这一全新领域的深入研究奠定基础。

The productive infection of influenza A virus (IAV) requires the active involvement of many host factors. lncRNAs participate in host antiviral defense by modulating immune responses, but the roles and molecular mechanism of lncRNAs, especially IFN-independent lncRNAs in the IAV replication remains largely unknown. Our preliminary study for the first time found that IFN-independent IPAN is induced by IAV infection and specifically facilitates IAV replication. Preliminary mechanism study showed that IPAN inhibits RIG-I mediated PB1 degradation to warrant viral RNA synthesis by interaction with PB1 protein, but the detail mechanism of IPAN and RIG-I involved in PB1 degradation is not clear. In this proposed work, we will further study the mechanism and function of the interaction between IPAN and RIG-I, PB1degradation triggered by IPAN silencing and the mechanism of RIG-I mediated PB1 degradation. In addition, we will identify IPAN-binding proteins and investigate their function in the regulation of IAV replication by IPAN. The objective of this work are shed light in the molecular mechanisms of IAV replication facilitated by IPAN and to provide theoretical basis for further study on the new field of involvement of lncRNAs in viral replication.