新城疫病毒(NDV)是危害我国养禽业的重要病原。病毒感染诱导细胞凋亡既是宿主对病毒感染的防御反应，也可能病毒造成机体损伤的一种重要方式；同时，为了在宿主细胞中更好的增殖，病毒又需要在一定程度上延缓细胞凋亡。NDV可诱导细胞凋亡，但是其是否可劫持宿主细胞的某些信号转导系统延缓细胞凋亡目前仍不清楚。我们的前期研究发现，新城疫病毒感染CEF细胞的早期可激活PI3K/AKT信号通路延缓宿主细胞凋亡。因此，本项目在前期研究基础上，以NDV体内外感染及病毒蛋白为研究对象，利用抑制剂、基因功能干扰、激光共聚焦、Co-IP和流式细胞术等手段，从不同的层次和角度研究NDV/编码蛋白、PI3K/AKT信号途径及细胞凋亡之间的关系，鉴定和验证其中的关键病毒蛋白及宿主分子，以期揭示NDV感染早期激活PI3K/AKT信号通路延缓宿主细胞凋亡的分子机制，从而为阐明NDV感染与致病提供新的理论基础。

Newcastle disease virus (NDV) is an important pathogen that endangers China's poultry industry. Apoptosis during an infection is both a form of the host’s defense mechanism and one of the main ways for virus to inflict damage onto the host. At the same time, however, in order to proliferate and diffuse within the host’s cellular system, the virus needs to delay the apoptotic process to a certain extent as well. It is evident that NDV could induce apoptosis, but the answer to whether it is capable of hijacking the signal transduction system of host cells thus delaying the apoptotic process remains unclear. Previous studies have shown that the PI3K/AKT intracellular signaling pathway becomes active during early stages of NDV infection in CEF cells, prompting host cells to slow down the apoptosis. Hence, building on previous discoveries, this project aims at deciphering the complex relationship between NDV, protein-encoding, PI3K/AKT intracellular signaling pathway, and apoptosis during the early stages of a NDV infection by tackling NDV as well as its viral protein using various methods such as inhibitor utilization, gene interference, laser confocal, Co-IP, and flow cytometry; thus identify the key factor of virus and host in the process; and, in doing so, provides novel theoretical knowledge about NDV infection for future application.