副粘病毒通过P基因的mRNA编辑编码V、W等蛋白来拮抗宿主的IFN系统，且NiV V/W蛋白的mRNA水平随感染状态而实时变化。我们发现NDV V蛋白拮抗IFN的能力与毒力密切相关。因此推断，NDV在感染细胞和机体中P基因编辑频率也应动态变化，病毒可能在感染不同免疫状态的机体、细胞时，通过P基因编辑频率改变以调控V/W的水平来拮抗IFN等免疫因子与病毒在组织、细胞中的感染、增殖程度。本研究拟以5株不同毒力与基因型的NDV感染细胞、SPF鸡和免疫状态不同的鸡，测定不同时间点P基因编辑频率、IFN等免疫因子的量、细胞与组织病变程度、病毒滴度及排毒量，从体外和体内水平阐明NDV感染过程中P基因编辑频率的动态变化与病毒毒力、增殖能力和免疫状态间的关系，揭示NDV P/V/W基因编辑频率的变化在影响病毒增殖与突破机体免疫防御中发挥的作用，为进一步阐明NDV致病机理与免疫机制提供新的资料。

Paramyxovirus antagonize the host IFN system by mediating viral IFN-antagonistic proteins, V, W and so on, which are encoded by a process of viral phosphoprotein (P)-gene mRNA editing. And the expression levels of mRNA of V and W proteins of Nipah virus are dynamic variation during different time of virus infection. We found that the ability of IFN antagonism of NDV V protein is closely related to its virulence. Thus infer that the editing frequency of the P gene must be dynamic during Newcastle disease virus (NDV) infection in cells and hosts. In different situation of infection or different immune state of cells and hosts, virus may adjust the level of V/W by changing the P gene editing frequency to antagonize IFN and other immune factors and the viral infection and proliferation in cells and tissues. Total five NDV isolates with different virulence and genotypes will be used for infection in chicken cells, SPF chickens and different immune state chickens in this study. And the editing frequencies of its P gene, IFN and other immune cytokines expression levels, pathological changes of cells and tissues, viral titers and detoxifications will be analysized during different infection time. This study will clarify the relationships between the frequency variation of P gene mRNA editing and viral virulence, proliferation, immune state in the process of NDV infection in vitro and in vivo. Will eventually reveal the role of the variation of NDV P/V/W gene editing frequencies in affecting virus proliferation and the mechanisms of breaking the host immune defense, which would provide a new information to further clarify the NDV pathogenesis and immune mechanism.