Sedý John R, Spear Patricia G, Ware Carl F
Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.
Nat Rev Immunol. 2008 Nov;8(11):861-73. doi: 10.1038/nri2434.
Herpesviruses have evolved numerous strategies to subvert host immune responses so they can coexist with their host species. These viruses 'co-opt' host genes for entry into host cells and then express immunomodulatory genes, including mimics of members of the tumour-necrosis factor (TNF) superfamily, that initiate and alter host-cell signalling pathways. TNF superfamily members have crucial roles in controlling herpesvirus infection by mediating the direct killing of infected cells and by enhancing immune responses. Despite these strong immune responses, herpesviruses persist in a latent form, which suggests a dynamic relationship between the host immune system and the virus that results in a balance between host survival and viral control.
疱疹病毒已经进化出多种策略来颠覆宿主的免疫反应，以便它们能够与宿主物种共存。这些病毒“征用”宿主基因进入宿主细胞，然后表达免疫调节基因，包括肿瘤坏死因子（TNF）超家族成员的模拟物，这些基因启动并改变宿主细胞信号通路。TNF超家族成员在通过介导感染细胞的直接杀伤和增强免疫反应来控制疱疹病毒感染方面发挥着关键作用。尽管有这些强烈的免疫反应，疱疹病毒仍以潜伏形式持续存在，这表明宿主免疫系统与病毒之间存在动态关系，这种关系导致宿主生存与病毒控制之间的平衡。
