Farrell H E, Davis-Poynter N J
Department of Microbiology, the University of Western Australia, Western Australia, Australia.
Semin Cell Dev Biol. 1998 Jun;9(3):369-78. doi: 10.1006/scdb.1998.0246.
The outcome of a virus infection is strongly influenced by interactions between host immune defences and virus 'antidefence' mechanisms. For many viruses, their continued survival depends on the speed of their attack:their capacity to replicate and transmit to uninfected hosts prior to their elimination by an effective immune response. In contrast, the success of persistent viruses lies in their capacity for immunological subterfuge: the evasion of host defence mechanism by either mutation (covered elsewhere in this issue, by Gould and Bangham, pp. 331-338) or interference with the action of host cellular proteins that are important components of the immune response. This review will focus on the strategies employed by persistent viruses against two formidable host defences against virus infection: the CD8+ cytotoxic T lymphocyte (CTL) and natural killer (NK) cell responses.
病毒感染的结果受到宿主免疫防御与病毒“反防御”机制之间相互作用的强烈影响。对于许多病毒而言，它们能否持续存活取决于其攻击速度：即在被有效的免疫反应清除之前，它们进行复制并传播到未感染宿主的能力。相比之下，持续性病毒的成功在于其免疫逃避能力：通过突变（本期其他地方由古尔德和班汉姆论述，第331 - 338页）或干扰作为免疫反应重要组成部分的宿主细胞蛋白的作用来逃避宿主防御机制。本综述将聚焦于持续性病毒针对病毒感染的两种强大宿主防御机制所采用的策略：CD8 + 细胞毒性T淋巴细胞（CTL）反应和自然杀伤（NK）细胞反应。
