Abstract

Herpes zoster is a localized disease of the sensory ganglion, nerve and skin, caused by reactivation and replication of endogenous varicella-zoster virus (VZV) that has persisted as a latent infection in sensory and autonomic neurons following an earlier episode of varicella. It is characterized by unilateral radicular pain and a vesicular rash that is generally limited to the dermatome innervated by a single spinal or cranial sensory ganglion. Replication and spread of reactivated VZV within the sensory ganglion and adjacent neural structures causes necrosis of neurons and supporting cells, resulting in neuropathic pain and sensory dysfunction in the affected dermatome during the acute phase of herpes zoster.Neuropathic pain may persist after rash healing, a debilitating complication known as postherpetic neuralgia (PHN). The incidence and severity of herpes zoster and PHN increase markedly with increasing age in parallel with an age-related decline in VZV-specific cell mediated immunity (VZV CMI).Antiviral treatment can reduce the duration and severity of acute herpes zoster and prevent complications that result from continued VZV replication and spread, but it does not prevent the development of PHN.

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