泡沫病毒（FV）具有独特的生物学特性，可能是以HIV为代表的正反转录病毒和以HBV为代表的嗜肝DNA病毒之间进化的桥梁。FV在毒粒结构、基因组组成、生活周期、宿主范围等方面与HIV类似，但其感染个体表现为终身潜伏感染，未发现其引发任何疾病。可以肯定，宿主中存在某些抗FV感染、抑制其完成生活周期的机制，成功地抑制了FV的复制。研究表明，干扰素抗病毒效应是其中重要因素。本实验室前期研究发现干扰素调控蛋白（IRF-1）及其调控基因IFP35和BST2可显著抑制FV复制，本项目拟以IRF-1抑制FV复制效应为研究出发点，分析其在干扰素抑制泡沫病毒复制中的作用，确定关键效应基因及其作用机制，并初探FV感染对此类抗病毒效应的影响，以解析泡沫病毒潜伏感染形成的机理，加深对干扰素抗病毒效应机制的认识，为探究相关反转录病毒感染与致病特性间的差异提供新视角。

Foamy viruses (FVs) have unique biological characteristics. In some respects, FVs appear to bridge the gap between retroviruses and the Hepadnaviridae. Although the viron structure and arrangement of the genome of FV are similar to that of HIV, they establish lifelong latent infections without accompanying pathology in their native hosts. Therefore, there must be some factors that play important roles in inhibiting FV. Interferons are believed to play a protective role against the lytic replication of FV. Our previous work demonstrated that interferon regulatory factor-1 (IRF-1) and its target genes IFP35 and BST2 significantly inhibited the replication of FV. In this project, we set out to define how the replication of FV is inhibited by IRF-1 and the role of IRF-1 in interferon-mediated anti-FV response. Besides, some of the IRF-1 target genes will be investigated to determine which one plays a key role in mediating the anti-FV activity. Collectively, these data will help us to further understand the anti-viral function of interferon. Furthermore, understanding the mechanisms responsible for latent infection induced by FV may yield insight into pathogenesis by other retroviruses.