NDV Clone30和IBDV VP2L不同形式的二联苗通过JAK-STAT信号通路影响NDV复制的分子机制研究

疫苗接种仍是预防ND和IBD最普遍的方法，多联疫苗逐渐取代单一疫苗，商品化的多联疫苗都是将多种病毒或蛋白混合制备成多联灭活疫苗。本课题组研究发现Clone30+VP2L蛋白的免疫效果低于rClone30-VP2L和Clone30疫苗的免疫效果；rClone30-VP2L疫苗的免疫效果高于Clone30疫苗，与预期的结果相反。表明NDV Clone30和IBDV VP2L不同形式的二联苗会影响NDV的复制，但其机制仍不清楚。本项目通过体外沉默JAK1或STAT1的DF1细胞、抑制剂Fludarabine处理的DF1细胞、动物实验以及蛋白组学分析研究NDV Clone30和IBDV VP2L不同形式的二联苗影响NDV复制的分子机制是通过IFN-α/β-JAK1/TYK2-STAT1/STAT2信号轴完成的，为rClone30-VP2L疫苗能够商品化及二联和多联疫苗的研发提供了重要的理论基础。

Vaccination is the most common method to prevent of Newcastle disease (ND) and Infectious bursal disease (IBD). Multivalent vaccine is gradually replacing single-vaccine. Commercialized multivalent vaccines are available a combination of multiple viruses or proteins to produce a polyvalent inactivated vaccine. Our study has found that the immune effect of Clone30+VP2L protein was lower than that of rClone30-VP2L and Clone30 vaccine. The immune effect of rClone30-VP2L vaccine were higher than those of Clone30 vaccine, it is contrary to what was expected. These results indicated that the different forms of NDV Clone30 and IBDV VP2L could affect the replication of NDV, but its exact mechanism is still unclear. This project will study the molecular mechanism of NDV Clone30 and IBDV VP2L vaccine affecting NDV replication by IFN-α/β-JAK1/TYK2-STAT1/STAT2 signal axis through in vitro silencing of JAK1 or STAT1 DF1 cells, DF1 cells treated with the inhibitor Fludarabine, animal experiment and proteomic analysis. It provides an important theoretical basis for the commercialization of rClone30-VP2L vaccine and the development of divalent and multivalence vaccines.