Rowe Martin, Glaunsinger Britt, van Leeuwen Daphne, Zuo Jianmin, Sweetman David, Ganem Don, Middeldorp Jaap, Wiertz Emmanuel J H J, Ressing Maaike E
Division of Cancer Studies, University of Birmingham Medical School, Vincent Drive, Edgbaston, Birmingham B15 2TT, United Kingdom.
Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3366-71. doi: 10.1073/pnas.0611128104. Epub 2007 Feb 21.
Relatively little is known about immune evasion during the productive phase of infection by the gamma(1)-herpesvirus Epstein-Barr virus (EBV). The use of a unique system to isolate cells in lytic cycle allowed us to identify a host shutoff function operating in productively EBV-infected B cells. This impairment of protein synthesis results from mRNA degradation induced upon expression of the early lytic-cycle gene product BGLF5. Recently, a gamma(2)-herpesvirus, Kaposi sarcoma herpesvirus, has also been shown to encode a host shutoff function, indicating that host shutoff appears to be a general feature of gamma-herpesviruses. One of the consequences of host shutoff is a block in the synthesis of HLA class I and II molecules, reflected by reduced levels of these antigen-presenting complexes at the surface of cells in EBV lytic cycle. This effect could lead to escape from T cell recognition and elimination of EBV-producing cells, thereby allowing generation of viral progeny in the face of memory T cell responses.
对于γ1疱疹病毒爱泼斯坦-巴尔病毒（EBV）感染的增殖期免疫逃逸，人们了解得相对较少。利用一种独特的系统来分离处于裂解周期的细胞，使我们能够鉴定出在EBV感染活跃的B细胞中发挥作用的宿主关闭功能。蛋白质合成的这种损伤是由早期裂解周期基因产物BGLF5表达后诱导的mRNA降解所致。最近，γ2疱疹病毒卡波西肉瘤疱疹病毒也被证明编码一种宿主关闭功能，这表明宿主关闭似乎是γ疱疹病毒的一个普遍特征。宿主关闭的后果之一是HLA I类和II类分子合成受阻，这表现为EBV裂解周期中细胞表面这些抗原呈递复合物水平降低。这种效应可能导致EBV产生细胞逃避T细胞识别和清除，从而在面对记忆T细胞反应时产生病毒后代。
