EB病毒感染与多种肿瘤密切相关，建立无症状的潜伏感染是EBV逃避宿主免疫清除的主要手段，目前无法鉴别携带潜伏期EBV及未受感染的记忆性B细胞。课题组前期发现过表达EBV立早蛋白Zta细胞表面IFNGR1表达降低的现象，结合文献和既往工作基础，我们推测:Zta作为EBV由潜伏期进入裂解期的开关分子，在潜伏期与裂解期转换时通过下调IFNGR1进而影响IFN-γ信号通路参与的抗病毒免疫反应及机体抗病毒状态来逃避宿主免疫系统的清除，并进一步影响EBV相关肿瘤的免疫编辑过程。本研究拟以EBV相关肿瘤细胞系为模型，从转录调控的角度以双荧光素酶实验、EMSA和ChIP实验获得Zta调控IFNGR1的证据，并在EBV相关鼻咽癌组织中检测Zta与IFNGR1，分析两者表达的相关性,从而进一步揭示裂解期EBV逃避宿主免疫防御的机制，不但为EBV感染控制提供证据,并为EBV相关肿瘤早期干预及治疗提供线索。

EBV is an important onco-virus,which is estimated to be responsible for ~1% of all human cancers. To evade the host immune clearance, the virus usually establish a asymptomatic latent infection status, but it is unable to identify that whether memory B cells infec latent EBV or not to remove EBV infection. The early results of our group finded that the overexpression of EBV immediate early protein Zta reducing the cell surface expression of IFNGR1, combined with literature and previous work foundation, we hypothesized that: Zta as the switcher of EBV from latent period to lytic, through downregulating the IFNGR1expression can affect IFN-γ signal pathway which participates in the antiviral immune response and body's antiviral state evading the host immune clearance during the period of phase transition then affecting the “cancer immunoediting” pcrocess of EBV associated tumors. This research will take the EBV related cancer cell lines as the model, acquiring the evidence of Zta rregulating the transcription activity of IFNGR1 promoter by Dual-Luciferase Reporter assay system ,EMSA and ChIP. detecting the expression of Zta and IFNGR1 in EBV related nasopharyngeal carcinoma, analysis the correlation between them. If confirmed the mechanisms by which EBV inhibits the expression of IFNGR1 molecules, not only helps reveal the mechanism how EBV envade the immune clearance. Not only provide strategies for the antiviral therapy,but also provide infromtion for EBV associated tumors early intervation and treament.