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Review

VZV: molecular basis of persistence (latency and reactivation)

In: Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge: Cambridge University Press; 2007. Chapter 38.
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Review

VZV: molecular basis of persistence (latency and reactivation)

Jeffrey I. Cohen.
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Excerpt

Primary infection with varicella-zoster virus (VZV) causes varicella manifested by fever and a vesicular rash. During primary infection the virus disseminates in lymphocytes to the skin and other organs, and replicates in and establishes a latent infection in the nervous system (Croen et al., 1988). Early studies demonstrated viral DNA in human trigeminal and dorsal root ganglia by in situ hybridization and Southern blotting (Gilden et al., , ; Hyman et al., 1983). More recent studies, using PCR, have demonstrated latent VZV in multiple cranial nerve, dorsal root, and autonomic ganglia (Furuta et al., , ; Gilden et al., ; Mahalingham et al., 1990). The virus can reactivate from these sites to cause herpes zoster.

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