Institute of Neuroscience and Psychology, University of Glasgow, Glasgow G61 1QH, UK.
Department of Infectious Diseases, Aarhus University Hospital, 8000 Aarhus, Denmark.
Viruses. 2021 Oct 7;13(10):2018. doi: 10.3390/v13102018.
Varicella-zoster virus (VZV) is a human herpes virus which causes varicella (chicken pox) as a primary infection, and, following a variable period of latency in neurons in the peripheral ganglia, may reactivate to cause herpes zoster (shingles) as well as a variety of neurological syndromes. In this overview we consider some recent issues in alphaherpesvirus latency with special focus on VZV ganglionic latency. A key question is the nature and extent of viral gene transcription during viral latency. While it is known that this is highly restricted, it is only recently that the very high degree of that restriction has been clarified, with both VZV gene 63-encoded transcripts and discovery of a novel VZV transcript (VLT) that maps antisense to the viral transactivator gene 61. It has also emerged in recent years that there is significant epigenetic regulation of VZV gene transcription, and the mechanisms underlying this are complex and being unraveled. The last few years has also seen an increased interest in the immunological aspects of VZV latency and reactivation, in particular from the perspective of inborn errors of host immunity that predispose to different VZV reactivation syndromes.
水痘带状疱疹病毒（VZV）是一种人类疱疹病毒，可引起原发性感染水痘（水痘），并在周围神经节中的神经元潜伏一段时间后，可能重新激活导致带状疱疹（带状疱疹）以及各种神经综合征。在这篇综述中，我们考虑了一些α疱疹病毒潜伏的最新问题，特别关注 VZV 神经节潜伏。一个关键问题是病毒潜伏期间病毒基因转录的性质和程度。虽然已知这是高度受限的，但直到最近才阐明了这种限制的程度非常高，包括 VZV 基因 63 编码的转录物和发现一种新的 VZV 转录物（VLT），该转录物与病毒转录激活基因 61 反义映射。近年来，人们还发现 VZV 基因转录存在显著的表观遗传调控，其机制复杂且正在逐步阐明。过去几年也增加了对 VZV 潜伏和重新激活的免疫学方面的兴趣，特别是从宿主免疫先天错误的角度出发，这些错误易导致不同的 VZV 重新激活综合征。
