Abstract
Varicella zoster virus (VZV) is a neurotropic alphaherpesvirus. Primary infection usually results in varicella (chickenpox), after which the virus becomes latent in ganglionic neurons along the entire neuraxis. As the VZV-specific cell-mediated immunity to VZV declines with age and immunosuppression, VZV can reactivate, resulting in zoster (shingles). Furthermore, zoster is often complicated by multiple neurological and ocular disorders. Among the most serious is VZV vasculopathy where the productive virus infection of cerebral arteries leads to stroke. The diverse manifestations, laboratory features, pathogenesis and treatment of VZV vasculopathy have been updated recently [ [1] Gilden D. Cohrs R.J. Mahalingam R. Nagel M.A. VZV vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis and treatment. Lancet Neurol. 2009; 8: 731-740 Abstract Full Text Full Text PDF PubMed Scopus (382) Google Scholar ].
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