Ressing Maaike E, van Gent Michiel, Gram Anna M, Hooykaas Marjolein J G, Piersma Sytse J, Wiertz Emmanuel J H J
Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Department of Molecular Cell Biology, Leiden University Medical Center, Leiden, The Netherlands.
Curr Top Microbiol Immunol. 2015;391:355-81. doi: 10.1007/978-3-319-22834-1_12.
Epstein-Bar virus (EBV) is widespread within the human population with over 90% of adults being infected. In response to primary EBV infection, the host mounts an antiviral immune response comprising both innate and adaptive effector functions. Although the immune system can control EBV infection to a large extent, the virus is not cleared. Instead, EBV establishes a latent infection in B lymphocytes characterized by limited viral gene expression. For the production of new viral progeny, EBV reactivates from these latently infected cells. During the productive phase of infection, a repertoire of over 80 EBV gene products is expressed, presenting a vast number of viral antigens to the primed immune system. In particular the EBV-specific CD4+ and CD8+ memory T lymphocytes can respond within hours, potentially destroying the virus-producing cells before viral replication is completed and viral particles have been released. Preceding the adaptive immune response, potent innate immune mechanisms provide a first line of defense during primary and recurrent infections. In spite of this broad range of antiviral immune effector mechanisms, EBV persists for life and continues to replicate. Studies performed over the past decades have revealed a wide array of viral gene products interfering with both innate and adaptive immunity. These include EBV-encoded proteins as well as small noncoding RNAs with immune-evasive properties. The current review presents an overview of the evasion strategies that are employed by EBV to facilitate immune escape during latency and productive infection. These evasion mechanisms may also compromise the elimination of EBV-transformed cells, and thus contribute to malignancies associated with EBV infection.
爱泼斯坦-巴尔病毒（EBV）在人群中广泛传播，超过90%的成年人受到感染。针对原发性EBV感染，宿主会启动一种抗病毒免疫反应，包括先天性和适应性效应功能。尽管免疫系统在很大程度上可以控制EBV感染，但病毒并未被清除。相反，EBV在B淋巴细胞中建立潜伏感染，其特征是病毒基因表达有限。为了产生新的病毒后代，EBV从这些潜伏感染的细胞中重新激活。在感染的增殖阶段，超过80种EBV基因产物会表达，向已致敏的免疫系统呈现大量病毒抗原。特别是EBV特异性的CD4+和CD8+记忆性T淋巴细胞能在数小时内做出反应，有可能在病毒复制完成和病毒颗粒释放之前摧毁产生病毒的细胞。在适应性免疫反应之前，强大的先天性免疫机制在原发性和复发性感染期间提供第一道防线。尽管有如此广泛的抗病毒免疫效应机制，EBV仍会终身持续存在并继续复制。过去几十年进行的研究揭示了大量干扰先天性和适应性免疫的病毒基因产物。这些包括EBV编码的蛋白质以及具有免疫逃避特性的小非编码RNA。本综述概述了EBV在潜伏期和增殖性感染期间用于促进免疫逃逸的逃避策略。这些逃避机制也可能损害对EBV转化细胞的清除，从而导致与EBV感染相关的恶性肿瘤。
