新城疫病毒的P基因可以编码P、V 和W 3种蛋白，其中V蛋白与病毒拮抗宿主干扰素的抗病毒作用有关。前期研究发现，一株朱鹮源新城疫病毒P/V/W蛋白在N端存在连续15个氨基酸缺失，且其在DF-1细胞上诱导的干扰素水平是未缺失株的1/7,V基因转染试验也获得相似的结果。据此，我们认为该区段的缺失可能使该株新城疫病毒获得更强的逃逸宿主天然免疫系统的能力。本项目拟通过比较研究2株朱鹮源NDV（一个N端15aa缺失，另一个未缺失）对PAMP产生及PRRs诱导干扰素抗病毒信号通路的调控，确定P/V/W基因缺失区域在新城疫病毒拮抗干扰素系统中的作用，从而揭示新城疫病毒朱鹮分离株拮抗宿主干扰素系统的机制，首次确定N端110～124位15个氨基酸区域也是NDV V蛋白拮抗宿主干扰素的主要功能域，为新城疫病毒及其他副黏病毒逃逸宿主天然免疫的机理研究提供新的资料。

P gene of NDV can encode three proteins, P , V and W. Among which, the V protein is the inhibitor of IFN. In our previous work, we has reported that the P gene of NDV isolated from Crested Ibis had 45nt naturally deletion at N-terminal, which directly results in 15aa deletion at N terminus of P , V and W protein. Interestingly, we also discovered that the IFN expression level induced by Crested Ibis NDV is only 1/7 of the other NDV isolate without 45nt deletion in corresponding domain. Similar result was further confirmed by transfection with plasmids expressing full length V gene and 45nt deleted V gene. Based on above results, we presume that the deletion may contribute Crested Ibis NDV to escape from host innate immune system. Though comparison the regulatory effect of two NDV isolates from Crested Ibis (with or without 15aa ) on PAMP production and IFN-mediated antiviral signal pathway, we can conclude whether 15aa deletion at the N terminus of P/V/W proteins play essential role for IFN inhibition or not. The data will provide more information for study the host antiviral mechanism of paramyxoviruses.