Varicella zoster virus infections

Abstract

Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which the virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause zoster (shingles), dermatomal-distribution pain and rash on an erythematous base in 1-3 dermatomes. Zoster may develop anywhere on the body. Skin lesions resolve within 1-2 weeks, while complete cessation of pain usually takes 4-6 weeks. Unfortunately, zoster can be followed by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, vasculopathy, meningoencephalitis, cerebellitis, myelopathy, and multiple ocular disorders. VZV reactivation also produces chronic radicular pain without rash (zoster sine herpete). In fact, all of the neurological and ocular disorders listed above may also develop without rash. This review covers clinical, laboratory and pathological features of neurological complications of VZV reactivation, including diagnostic testing to verify active VZV infection in the nervous system and the potential value of examining saliva for VZV DNA in patients with neurological disease without rash. Additional perspectives are provided by discussions of the VZV genome, VZV latency, viral pathology, pathogenesis and immunity, and of the value of vaccination of elderly individuals to boost cell-mediated immunity to VZV and prevent VZV reactivation.