人细小病毒B19（B19病毒）是病毒性肾病的重要病原，与病情重、进展快、疗效及预后差的塌陷性肾小球病密切相关。我们前期研究证明B19病毒VP1独特区蛋白（VP1u蛋白）可诱发小鼠肾脏足细胞明显病变，并首先发现VP1u蛋白与细胞凋亡有关。但是，VP1u蛋白致足细胞病变的具体机制尚未阐明。本项目拟使用VP1u蛋白和已标记的VP1u蛋白作用于离体培养的足细胞，观察VP1u蛋白如何进入足细胞及在细胞内的分布，检测整合素、钙结合蛋白、TNF-α、NF-κB、Bax和Bcl-2等关键分子和蛋白的变化，并通过过表达或干涉实验分析证明关键分子通路机制（如TNFR信号通路），以期阐明B19病毒VP1u蛋白损伤肾脏足细胞的机理，对病毒性肾病的防治提供新的理论依据。

Human parvovirus B19 (B19) has been identified as one of the most important pathogenies of viral nephropathy. It has also been proved that B19 has close relationship with collapsing glomerulopathy (CG), which features severe clinical symptom, rapid progress, poor therapeutic outcome and prognosis. Our prior research indicates that the mice sustained renal lesions, marked in the podocytes, after being treated with the protein of virus protein 1 unique region (VP1u). We also firstly demonstrate that VP1u protein has close relationship with apoptosis. But the role of VP1u protein in the pathogenesis of B19-induced podocyte injury has not been well clarified. Based on the former research, we will add VP1u protein or marked VP1u protein in cultured podocytes, observe the distribution of VP1u protein in or on the podocytes, detect cell factors, apoptosis and cell surface markers changes, and analyse the changes of related signal passageways. At the end of this study, we hope to clarify the mechanism of the VP1u protein of B19 induces podocyte injury, and provid new theory in prevention and treatment of viral nephropathy.