疱疹病毒与内质网应激

Herpesvirus and endoplasmic reticulum stress

摘要:

内质网是分泌型蛋白和膜蛋白折叠及翻译后修饰的主要场所。病毒感染所引起的宿主细胞内环境的改变可使细胞或病毒的未折叠和/或错误折叠蛋白在内质网中大量聚集，使内质网处于生理功能紊乱的应激状态。为了缓解这种应激压力，细胞会启动未折叠蛋白反应 (UPR)，并通过一系列分子的信号转导维持内质网稳态；同时病毒也会通过对UPR的精密调控营造有利于其复制与增殖的细胞内环境。疱疹病毒是一类有囊膜的DNA病毒，在病毒复制过程中，其表面大量的糖基化囊膜蛋白的合成及成熟依赖于内质网，并由此诱发内质网应激。现将对疱疹病毒感染与内质网应激的最新研究进展做一总结归纳。

Abstract:

Endoplasmic reticulum (ER) is an important organelle where folding and post-translational modification of secretory and transmembrane proteins take place. During virus infection, cellular or viral unfolded and misfolded proteins accumulate in the ER in an event called ER stress. To maintain the equilibrium homeostasis of the ER, signal-transduction pathways, known as unfolded protein response (UPR), are activated. The viruses in turn manipulate UPR to maintain an environment favorable for virus survival and replication. Herpesviruses are enveloped DNA viruses that produce over 70 viral proteins. Modification and maturation of large quantities of viral glycosylated envelope proteins during virus replication may induce ER stress, while ER stress play both positive and negative roles in virus infection. Here we summarize the research progress of crosstalk between herpesvirus infection and the virus-induced ER stress.