Kennedy Peter G E, Cohrs Randall J
Department of Neurology, Glasgow University, Southern General Hospital, Glasgow, Scotland, UK.
J Neurovirol. 2010 Nov;16(6):411-8. doi: 10.1007/BF03210846. Epub 2010 Sep 27.
Varicella-zoster virus (VZV) is a ubiquitous human herpes virus typically acquired in childhood when it causes varicella (chickenpox), following which the virus establishes a latent infection in trigeminal and dorsal root ganglia that lasts for the life of the individual. VZV subsequently reactivates, spontaneously or after specific triggering factors, to cause herpes zoster (shingles), which may be complicated by postherpetic neuralgia and several other neurological complications including vasculopathy. Our understanding of VZV latency lags behind our knowledge of herpes simplex virus type 1 (HSV-1) latency primarily due to the difficulty in propagating the virus to high titers in a cell-free state, and the lack of a suitable small-animal model for studying virus latency and reactivation. It is now established beyond doubt that latent VZV is predominantly located in human ganglionic neurons. Virus gene transcription during latency is epigenetically regulated, and appears to be restricted to expression of at least six genes, with expression of gene 63 being the hallmark of latency. However, viral gene transcription may be more extensive than previously thought. There is also evidence for several VZV genes being expressed at the protein level, including VZV gene 63-encoded protein, but recent evidence suggests that this may not be a common event. The nature and extent of the chronic inflammatory response in latently infected ganglia is also of current interest. There remain several questions concerning the VZV latency process that still need to be resolved unambiguously and it is likely that this will require the use of newly developed molecular technologies, such as GeXPS multiplex polymerase chain reaction (PCR) for virus transcriptional analysis and ChIP-seq to study the epigenetic of latent virus genome ( Liu et al, 2010 , BMC Biol 8: 56).
水痘带状疱疹病毒（VZV）是一种普遍存在的人类疱疹病毒，通常在儿童期感染，引发水痘，之后该病毒在三叉神经节和背根神经节建立潜伏感染，并伴随个体终身。VZV随后会自发地或在特定触发因素作用下重新激活，引发带状疱疹，可能并发带状疱疹后神经痛以及包括血管病变在内的其他几种神经并发症。我们对VZV潜伏的了解落后于对单纯疱疹病毒1型（HSV-1）潜伏的认识，主要原因在于难以在无细胞状态下将该病毒增殖至高滴度，以及缺乏用于研究病毒潜伏和重新激活的合适小动物模型。现在已经毫无疑问地确定，潜伏的VZV主要位于人类神经节神经元中。潜伏期间病毒基因转录受到表观遗传调控，似乎仅限于至少六个基因的表达，基因63的表达是潜伏的标志。然而，病毒基因转录可能比以前认为的更为广泛。也有证据表明几种VZV基因在蛋白质水平表达，包括VZV基因63编码的蛋白质，但最近的证据表明这可能并非常见现象。潜伏感染神经节中慢性炎症反应的性质和程度也是当前研究的热点。关于VZV潜伏过程仍有几个问题需要明确解决，很可能这需要使用新开发的分子技术，如用于病毒转录分析的GeXPS多重聚合酶链反应（PCR）和用于研究潜伏病毒基因组表观遗传学的ChIP-seq（Liu等人，2010年，《BMC生物学》8：56）。
