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Neurol Clin. 2008 Aug;26(3):675-97, viii. doi: 10.1016/j.ncl.2008.03.011.

Varicella zoster virus infection: clinical features, molecular pathogenesis of disease, and latency.

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  • 1Department of Neurology, University of Colorado School of Medicine, 4200 East 9th Avenue, Mail Stop B182, Denver, CO 80262, USA.


Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis. Years later, in association with a decline in cell-mediated immunity in elderly and immunocompromised individuals, VZV reactivates and causes a wide range of neurologic disease. This article discusses the clinical manifestations, treatment, and prevention of VZV infection and reactivation; pathogenesis of VZV infection; and current research focusing on VZV latency, reactivation, and animal models.

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