禽多瘤病毒（Avian Polyomavirus, APV）是一种DNA病毒，与没有致病性的哺乳动物多瘤病毒相比，APV对幼雏具有较强的致病性与危害。但是到目前为止，APV致病机制以及逃避宿主天然免疫的分子机制尚不清楚。干扰素系统（IFN）是机体抵抗病毒感染的重要防御系统，APV感染过程中IFN是否会被激活？APV是通过何种途径激活宿主IFN应答？以及APV又是如何逃避宿主IFN应答？以上科学问题目前都尚未被解析。本项目基于本课题组建立的APV感染细胞模型，初步发现APV感染可以激活I型IFN应答，而且其编码的两种只在APV中存在的VP4与VP4-delta蛋白具有抑制I型IFN应答的功能，但具体分子机制尚不清楚。本研究旨在基于APV感染细胞模型，系统研究并阐述APV激活与逃避宿主I型IFN天然免疫的分子机理，为APV致病机理研究与防控提供理论基础。

Avian Polyomavirus (APV) is a DNA virus, which is virulent to young birds comparedwith non-pathogenic mammalian polyomavirus. However, up to now, the pathogenesisof APV and the molecular mechanism of evading host innate immunity remain unclear.Interferon system (IFN) is an important host defense system against virusinfection. Will IFN be activated during APV infection? How does APV activate hostIFN response? And how does APV evade the host's IFN response? These scientificissues have not yet been resolved. Based on the established cell model of APVinfection, we preliminarily found that APV infection can activate type I IFNresponse, and the two VP4 and VP4-delta proteins only encoded in APV have thefunction of inhibiting type I IFN-response, but the specific molecular mechanismis still unclear. The purpose of this study is to systematically study andelucidate the molecular mechanism of APV activation and evasion of host type I IFNbased on APV infection cell model, therefore to provide theoretical basis for APVpathogenesis research and prevention and control.