Russell Tiffany A, Tscharke David C
John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.
PLoS Pathog. 2016 Jun 27;12(6):e1005729. doi: 10.1371/journal.ppat.1005729. eCollection 2016 Jun.
Herpes simplex virus (HSV) has provided the prototype for viral latency with previously well-defined acute or lytic and latent phases. More recently, the deep quiescence of HSV latency has been questioned with evidence that lytic genes can be transcribed in this state. However, to date the only evidence that these transcripts might be translated has come from immunological studies that show activated T cells persist in the nervous system during latency. Here we use a highly sensitive Cre-marking model to show that lytic and latent phases are less clearly defined in two significant ways. First, around half of the HSV spread leading to latently infected sites occurred beyond the initial acute infection and second, we show direct evidence that lytic promoters can drive protein expression during latency.
单纯疱疹病毒(HSV)为病毒潜伏提供了原型,其具有先前定义明确的急性或裂解期以及潜伏期。最近,HSV潜伏期的深度静止受到了质疑,有证据表明裂解基因可在这种状态下转录。然而,迄今为止,这些转录本可能被翻译的唯一证据来自免疫学研究,该研究表明活化的T细胞在潜伏期持续存在于神经系统中。在这里,我们使用一种高度敏感的Cre标记模型来表明,裂解期和潜伏期在两个重要方面的定义不那么清晰。首先,导致潜伏感染部位的HSV传播约有一半发生在初始急性感染之后;其次,我们提供了直接证据表明裂解启动子可在潜伏期驱动蛋白质表达。