Abstract
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 (Citation, BMC Biol 8: 56).
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Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.