EB病毒免疫逃逸的分子机制  

Molecular mechanism for EB virus escape from host cell defense

作　　者：刘愿[1] 刘卓然[1] 

机构地区：[1]南华大学附属第二医院检验科,湖南衡阳421001

出　　处：《微生物学免疫学进展》2016年第3期76-81,共6页Progress In Microbiology and Immunology

基　　金：湖南省科技厅资助项目(2012FJ3103)

摘　　要：EB病毒(Epstein-Barr vius,EBV)是一种最广泛的对人类感染的γ疱疹病毒,与人类多种疾病尤其是恶性肿瘤有关。其致病的一个重要条件是能够在人体B细胞中长期潜伏,并且在人体免疫力低下时被激活并增殖,这表明EB病毒存在逃逸宿主细胞免疫的机制。从潜伏期EB病毒基因表达的下调、干扰抗原加工和提呈、调节细胞毒性T细胞(Cytotoxic lymphocyte,CTL)免疫应答、干扰细胞因子的作用、干扰CTL的活动及抑制宿主细胞凋亡、抑制辅助性T细胞1(Helper T cell 1,Th1)免疫应答等方面,对EB病毒免疫逃逸的分子机制作一简要综述。Epstein-Barr virus （EBV） is a kind of human gamma herpesvirus that infects extensively to human beings, it is associated with human diseases, especially malignant tumor. An important condition for the pathogenesis of EBV is it in a latent form to parasitize inside human B cells for a long time, in addition, EBV will be activated and proliferate when the human immunity is deficient, which shows that EBV has a mechanism to evade from host cell immunity. Thus a brief summary will focus on the molecular mechanism for EBV immune escape, including down regulation gene expression of viral antigen in a latent state, interference with antigen processing and presenting, interference with regulation of cytotoxic lymphocyte （CTL） response, interference with cytokine effect, and inhibition of target ceil apoptosis, inhibition of Thl response and so on.

关 键 词：EB病毒 免疫逃逸 分子机制 细胞毒性T细胞 

分 类 号：R392.11[医药卫生—免疫学]