Varicella zoster virus infection.

Abstract

Varicella zoster virus (VZV) is an exclusively human alphaherpesvirus that infects >90% of the global population. Primary infection typically causes varicella (chickenpox), after which VZV establishes lifelong latency in ganglionic neurons along the entire neuroaxis. Virus reactivation, typically triggered by age-associated immune dysfunction or immune suppressive conditions, produces herpes zoster (shingles) that can be complicated by post-herpetic neuralgia. In limited instances, VZV reactivation (and rarely primary infection) also produces multisystem disease including vasculopathy, cranial neuropathies, myelopathy and cardiovascular or gastrointestinal complications; these complications can occur without, or temporally dissociated from, rash. Diagnosis of varicella or herpes zoster relies on clinical presentation of a disseminated or dermatomal-distribution rash, respectively; diagnosis of VZV infection (owing to replicating virus) is more challenging when cases are atypical and/or occur without rash. Prevention strategies include administration of live attenuated varicella vaccine and recombinant zoster vaccine. VZV infection is treated with antiviral drugs including oral valacyclovir (drug of choice), famciclovir, acyclovir or amenamevir; for severe or disseminated disease, intravenous acyclovir or foscarnet (when other drugs fail) are used. Critical challenges remain in recognizing and diagnosing atypical presentations, developing novel therapeutics, establishing the causal role of VZV in vascular and neurodegenerative disease, and achieving broader vaccine implementation worldwide.