Duerst Rebecca J, Morrison Lynda A
Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, Missouri 63104, USA.
Viral Immunol. 2003;16(4):475-90. doi: 10.1089/088282403771926300.
Herpes simplex virus type 2 (HSV-2) is responsible for most cases of genital herpes and also can cause fatal disseminated disease in perinatally infected newborns. Sexually transmitted infections initiate in the skin or mucosa and quickly spread into peripheral nerves to establish latency. Innate immunity, the first line of defense during both primary and recurrent infection, is essential during this period of acute infection to limit initial viral replication and to facilitate an appropriate adaptive immune response. The innate immune response consists of a complex multilayered system of mechanical and secreted defenses, immediate chemokine and IFN responses, and rapidly recruited cellular defenses. HSV has devised equally elaborate strategies to evade or interfere with innate immunity. This review summarizes our current understanding of the innate immune responses to HSV-2 and the mechanisms by which HSV-2 can overcome these barriers. Newly emerging links between products of innate responses and the development of adaptive immune responses are also discussed.
2型单纯疱疹病毒（HSV-2）是大多数生殖器疱疹病例的病原体，也可在围产期感染的新生儿中引起致命的播散性疾病。性传播感染始于皮肤或黏膜，并迅速扩散到外周神经以建立潜伏状态。固有免疫是初次感染和复发感染期间的第一道防线，在急性感染期对于限制病毒的初始复制以及促进适当的适应性免疫反应至关重要。固有免疫反应由机械性和分泌性防御的复杂多层系统、即时趋化因子和干扰素反应以及迅速募集的细胞防御组成。HSV也设计了同样精巧的策略来逃避或干扰固有免疫。本综述总结了我们目前对HSV-2固有免疫反应以及HSV-2克服这些障碍机制的理解。还讨论了固有反应产物与适应性免疫反应发展之间新出现的联系。
