J Clin Invest. 2020 Jul 1;130(7):3361-3369. doi: 10.1172/JCI136225.
Herpesviruses infect virtually all humans and establish lifelong latency and reactivate to infect other humans. Latency requires multiple functions: maintaining the herpesvirus genome in the nuclei of cells; partitioning the viral genome to daughter cells in dividing cells; avoiding recognition by the immune system by limiting protein expression; producing noncoding viral RNAs (including microRNAs) to suppress lytic gene expression or regulate cellular protein expression that could otherwise eliminate virus-infected cells; modulating the epigenetic state of the viral genome to regulate viral gene expression; and reactivating to infect other hosts. Licensed antivirals inhibit virus replication, but do not affect latency. Understanding of the mechanisms of latency is leading to novel approaches to destroy latently infected cells or inhibit reactivation from latency.
疱疹病毒几乎感染所有人类，并建立终身潜伏和重新激活以感染其他人类。潜伏需要多种功能：在细胞核中维持疱疹病毒基因组；在有丝分裂细胞中将病毒基因组分配到子细胞；通过限制蛋白质表达来避免被免疫系统识别；产生非编码病毒 RNA（包括 microRNA）来抑制裂解基因表达或调节细胞蛋白表达，否则这些表达可能会消除病毒感染的细胞；调节病毒基因组的表观遗传状态以调节病毒基因表达；重新激活以感染其他宿主。已授权的抗病毒药物可抑制病毒复制，但不影响潜伏。对潜伏机制的理解正在导致新的方法来破坏潜伏感染的细胞或抑制潜伏状态下的重新激活。
