传染性法法氏囊炎病毒（IBDV）是一种高度接触性传染病，引起雏鸡的免疫机能下降，导致继发感染，迅速提高死亡率，对养禽业构建巨大威胁。IBDV分子量最大的结构蛋白VP1是病毒的聚合酶，负责病毒基因组的复制与转录。我们的前期研究意外发现VP1除发生泛素化修饰、SUMO1修饰以外，还可以发生磷酸化修饰。本项目拟在前期研究基础上，进一步解析周期蛋白依赖性激酶CDK1磷酸化VP1的分子机制，确定其磷酸化位点，探索VP1 SUMO1修饰与CDK1磷酸化VP1的关联机制；借助课题组建立的Minigenome报告系统以及IBDV反向遗传操作系统，构建VP1突变载体，拯救VP1突变重组病毒，比较分析VP1磷酸化位点突变对VP1聚合酶活性、病毒复制及致病性的影响，为阐明IBDV VP1生物学功能调节奠定理论基础。

Infectious bursal disease virus (IBDV) is a highly contagious infectious disease that causes the immunity inhibition of young chickens, leading to secondary infections, rapidly increasing mortality, which is posing a huge threat to the poultry industry. The polymerase of VP1, the structural protein with the largest molecular weight of IBDV, is responsible for the replication and transcription of the viral genome. Our previous research unexpectedly discovered that in addition to ubiquitination modification as well as SUMO1 modification of VP1, VP1 also undergoes phosphorylation. Based on the previous research, this project intends to further analyze the molecular mechanism of VP1 phosphorylated by cyclin dependent kinase CDK1, and determine its phosphorylation site, and explore the relationship mechanism between VP1 SUMO1 modification and CDK1 phosphorylated VP1; With the assistance of the Minigenome reporting system and IBDV reverse genetic operating system, we plane to construct VP1 mutation vector, rescue VP1 mutant recombinant virus, compare and analyze the effect of VP1 phosphorylation site mutation on VP1 polymerase activity, virus replication and pathogenicity. The molecular mechanism of VP1 phosphorylation and its biological significance provides a theoretical foundation for elucidating the regulation of the biological function of IBDV VP1.