ABSTRACT
Varicella-zoster virus is a herpesvirus. It infects the throat, replicates in local lymph nodes, and then is carried to the skin by circulating T cells. Replication in the skin gives rise to the characteristic primary infection, varicella, or chickenpox. Virus also enters nerve terminals and is transported to nerve cell bodies throughout the spinal cord and cranial nerves, the site of latency of VZV. Upon reactivation from latency, virus travels down the nerves to reach that area of skin supplied by the nerve, giving rise to the characteristic secondary infection, herpes zoster, or shingles. Activation of pattern-recognition receptors leads to a potent innate immune response with production of interferons and other inflammatory cytokines. The adaptive immune response, particularly cytotoxic T cells, is important for maintaining VZV in latency, as T-cell immunodeficient patients are prone to frequent and aggressive reactivations. Complications of chickenpox include pneumonia (adults only) and encephalitis; herpes zoster in the ophthalmic branch of the trigeminal nerve may result in zoster keratitis. The commonest complication of zoster is post-herpetic neuralgia. Diagnosis of infection is by detection of viral genome from a vesicle swabs. Treatment is with aciclovir or derivatives thereof. A live attenuated vaccine is licensed for use as primary prophylaxis. Vaccines for the prevention of shingles include a high dose form of the chickenpox vaccine, and an adjuvanted recombinant glycoprotein E subunit vaccine.
