Bowie Andrew G, Zhan Jun, Marshall William L
Viral Immune Evasion Group, Department of Biochemistry, Trinity College, Dublin 2, Ireland.
J Cell Biochem. 2004 Apr 15;91(6):1099-108. doi: 10.1002/jcb.20026.
Viruses utilize a variety of strategies to evade the host immune response and replicate in the cells they infect. The comparatively large genomes of the Orthopoxviruses and gammaherpesviruses encode several immunomodulatory proteins that are homologous to component of the innate immune system of host cells, which are reviewed here. However, the viral mechanisms used to survive host responses are quite distinct between these two virus families. Poxviruses undergo continuous lytic replication in the host cytoplasm while expressing many genes that inhibit innate immune responses. In contrast, herpesviruses persist in a latent state during much of their lifecycle while expressing only a limited number of relatively non-immunogenic viral proteins, thereby avoiding the adaptive immune response. Poxviruses suppress, whereas latent gammaherpesviruses activate, signaling by NF-kappaB, yet both viruses target similar host signaling pathways to suppress the apoptotic response. Here, modulation of apoptotic and NF-kappaB signal transduction pathways are examined as examples of common pathways appropriated in contrasting ways by herpesviruses and poxviruses.
病毒利用多种策略来逃避宿主的免疫反应并在它们感染的细胞中进行复制。正痘病毒和γ疱疹病毒相对较大的基因组编码了几种与宿主细胞先天免疫系统成分同源的免疫调节蛋白，本文对此进行综述。然而，这两个病毒家族用于在宿主反应中存活的病毒机制截然不同。痘病毒在宿主细胞质中进行持续的裂解复制，同时表达许多抑制先天免疫反应的基因。相比之下，疱疹病毒在其生命周期的大部分时间里处于潜伏状态，只表达数量有限的相对无免疫原性的病毒蛋白，从而避免适应性免疫反应。痘病毒抑制，而潜伏的γ疱疹病毒激活核因子κB信号传导，然而这两种病毒都靶向相似的宿主信号通路来抑制凋亡反应。在这里，以凋亡和核因子κB信号转导通路的调节为例，探讨疱疹病毒和痘病毒以不同方式利用的共同通路。
