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Neuropathol Appl Neurobiol. 2011 Aug;37(5):441-63. doi: 10.1111/j.1365-2990.2011.01167.x.

Review: The neurobiology of varicella zoster virus infection.

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  • 1Department of Neurology, University of Colorado School of Medicine, USA. don.gilden@ucdenver.edu

Abstract

Varicella zoster virus (VZV) is a neurotropic herpesvirus that infects nearly all humans. Primary infection usually causes chickenpox (varicella), after which virus becomes latent in cranial nerve ganglia, dorsal root ganglia and autonomic ganglia along the entire neuraxis. Although VZV cannot be isolated from human ganglia, nucleic acid hybridization and, later, polymerase chain reaction proved that VZV is latent in ganglia. Declining VZV-specific host immunity decades after primary infection allows virus to reactivate spontaneously, resulting in shingles (zoster) characterized by pain and rash restricted to one to three dermatomes. Multiple other serious neurological and ocular disorders also result from VZV reactivation. This review summarizes the current state of knowledge of the clinical and pathological complications of neurological and ocular disease produced by VZV reactivation, molecular aspects of VZV latency, VZV virology and VZV-specific immunity, the role of apoptosis in VZV-induced cell death and the development of an animal model provided by simian varicella virus infection of monkeys.

© 2011 The Authors. Neuropathology and Applied Neurobiology © 2011 British Neuropathological Society.

PMID:
21342215
[PubMed - indexed for MEDLINE]
PMCID:
PMC3176736
Free PMC Article

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