泡沫病毒（FV）是反转录病毒科泡沫病毒亚科唯一种。其毒粒结构、基因组组成及宿主范围等诸多特性与以HIV-1为代表的正反转录病毒高度相似，但感染个体后致病性迥异。这一特性表明，宿主存在抑制FV复制的机制，成功阻断了FV感染。多项研究表明，包括干扰素诱导基因在内的宿主固有免疫在其中发挥重要作用。本课题组前期工作证实，干扰素刺激基因TRIM14可抑制原型泡沫病毒PFV复制，这一抑制功能可能通过干扰病毒Tas的作用而实现。本项目拟进一步探究TRIM14抑制PFV复制的分子机制，分析泛素化修饰在其中作用及生化机理，初探泡沫病毒感染对TRIM14功能的影响，为深入理解病毒与宿主间制衡关系及制定新型病毒性疾病防控策略提供理论支撑。

Foamy virus (FV), same as human immunodeficiency virus (HIV), belongs to the retroviridae. There are many similarities between the two groups, such as the particle composition, the genome structure, the cytopathic effect of the tissue culture, and the host range. However, FV showed a lifelong latent infection and no disease was found till now, while HIV cause AIDS. It is certain that there are some mechanisms that inhibit FV replication in the host, which successfully block FV infection. There are some evidences that innate immunity, including interferon inducible genes, plays an important role in FV latency. Our recent results of screening assay and some confirmatory tests showed that TRIM14 can inhibit the prototype foamy virus (PFV) replication. Here, we apply to explore the mechanism of TRIM14 inhibition of PFV replication and analysis the function of ubiquitination related to TRIM14 inhibiting PFV and biochemical mechanism. Meanwhile，we will try to find the some details in the relationship between TRIM14 and PFV replication. The aim of the project is to provide experimental basis for the understanding of antiviral mechanism of TRIM family. The results will provide theoretical supports to understand the relationship between the virus and the host, and may help us to develop some new strategies to prevent the diseases caused by viruses.