禽白血病是国家优先防控动物疫病，目前尚无有效疫苗，禽白血病病毒（ALV）持续感染是致禽白血病的主要原因，因此解析ALV感染机制是动物疫病领域重要问题。申请人及所在课题组前期利用高通量表达谱芯片，发现ALV致瘤组织中的p53信号通路发生改变，且进一步发现ALV致瘤组织中编码p53蛋白的Tumor Protein p53 (TP53) 基因发生突变，提示p53蛋白可能在ALV感染过程中发挥重要作用。本项目结合前期表达谱芯片筛选结果，加上申请人已建立的ALV体外持续感染细胞模型的进展，提出科学假说：ALV感染过程中，野生型p53蛋白限制ALV感染，ALV感染致TP53基因突变而对抗野生型p53蛋白对ALV感染的限制。本项目将进一步探索p53蛋白抑制ALV感染机制，且本项目对阐明ALV与宿主相互作用和揭示ALV与宿主共同进化规律均有重要意义，同时为禽白血病防治提供新思路和新靶点。

The diseases of the avian leukosis complex, a highly contagious viral disease affecting chickens, has been listed as disease control priorities. Avian leukosis virus (ALV) leads to the disease of avian leukosis complex, thus it is important to clarify how ALV infects Cells. The applicant has established in vivo and in vitro model for ALV infection. Microarray gene expression profiling and TP53 gene mutations in ALV-induced tumor reveal p53 involved in ALV infection. Our hypothesis is p53 inhibits ALV infection, but TP53 gene mutation upon ALV infection gives rise to p53 mutants inability to restrict viral infection. Dissecting the molecular mechanisms of p53-mediated inhibition in ALV infection will benefit the understanding for interaction and evolution between ALV and host, and provide valuable leads for strategies to blocking p53 mutation upon ALV infection as a therapeutic modality.