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Rev Med Virol. 2002 Sep-Oct;12(5):327-34.

Varicella-zoster virus latency in human ganglia.

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Glasgow University Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, Scotland, UK.


Varicella-zoster virus (VZV) is a human herpesvirus which causes varicella (chickenpox) as a primary infection, and, following a variable period during which it remains in latent form in trigeminal and dorsal root ganglia, reactivates in later life to cause herpes zoster (shingles). VZV is a significant cause of neurological disease including post-herpetic neuralgia which may be persistent and highly resistant to treatment, and small and large vessel encephalitis. VZV infections are more frequent with advancing age and in immunocompromised individuals. An understanding of the mechanisms of latency is crucial in developing effective therapies for VZV infections of the nervous system. Such studies have been hampered by the difficulties in working with the virus and also the lack of a good animal model of VZV latency. It is known that the ganglionic VZV burden during latency is low. Two of the key questions that have been addressed are the cellular site of latent VZV and the identity of the viral genes which are transcribed during latency. There is now a consensus that latent VZV resides predominantly in ganglionic neurons with less frequent infection of non-neuronal satellite cells. There is considerable evidence to show that at least five viral genes are transcribed during latency. Unlike herpes simplex virus-1 latency, viral protein expression has been demonstrated during VZV latency. A precise knowledge of which viral genes are expressed is crucial in devising novel antiviral therapy using expressed genes as therapeutic targets. Whether gene expression at both the transcriptional and translational levels is more extensive than currently reported will require much more work and probably new molecular technology.

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