传染性法氏囊病（IBD）是由传染性法氏囊病病毒（IBDV）感染引起的一种危害3-6周龄雏鸡的烈性，高度接触性传染性疾病。IBDV感染的靶器官主要为雏鸡的中枢免疫器官法氏囊，引起雏鸡法氏囊严重损伤，导致免疫抑制。我们在前期的研究中，证实了IBDV VP4蛋白与宿主细胞靶蛋白GILZ相互作用，抑制宿主细胞I型干扰素的表达，促进病毒在细胞中的复制，初步阐明了IBDV感染宿主细胞后引起免疫抑制的分子机理。本课题在此基础上进一步研究VP4与GILZ相互作用的分子机理，确定VP4与GILZ相互作用的关键氨基酸位点、探索VP4与GILZ互作的生化过程（包括泛素化、磷酸化等），进一步解析VP4蛋白在IBDV感染宿主引起免疫抑制的机理，为揭示IBDV引起免疫抑制的机理提供依据。

Infectious Bursal Disease(IBD), which is caused by Infectious Bursal Disease virus(IBDV), is a highly contagious infectious disease. The target organ of IBDV is the Bursa of Fabricius. IBDV infection can cause severe damages in Bursa of Fabricius, Infectied chickens show severe immunosuppression, which increases the risks of infecting other diseases. However, the underlying mechanism that causes immunosuppression remains unclear. Our previous research showed that VP4 inhibits expression of type I interferons through interaction with host protein GILZ. Based on these findings, we further investigate the underlying mechanism of VP4-GILZ interaction to determine the crucial amino acids for such interaction and to examine whether GILZ’s ubiquitination or phosphorylation involved during VP4-GILZ interaction. This project will further our understandings roles of VP4 in IBDV induced immunosuppresion and help to elucidate the pathogenesis of IBDV.