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Varicella zoster virus infection.

  • Author(s): Gershon, Anne A
  • Breuer, Judith
  • Cohen, Jeffrey I
  • Cohrs, Randall J
  • Gershon, Michael D
  • Gilden, Don
  • Grose, Charles
  • Hambleton, Sophie
  • Kennedy, Peter GE
  • Oxman, Michael N
  • Seward, Jane F
  • Yamanishi, Koichi
  • et al.

Published Web Location

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381807/
No data is associated with this publication.
Abstract

Infection with varicella zoster virus (VZV) causes varicella (chickenpox), which can be severe in immunocompromised individuals, infants and adults. Primary infection is followed by latency in ganglionic neurons. During this period, no virus particles are produced and no obvious neuronal damage occurs. Reactivation of the virus leads to virus replication, which causes zoster (shingles) in tissues innervated by the involved neurons, inflammation and cell death - a process that can lead to persistent radicular pain (postherpetic neuralgia). The pathogenesis of postherpetic neuralgia is unknown and it is difficult to treat. Furthermore, other zoster complications can develop, including myelitis, cranial nerve palsies, meningitis, stroke (vasculopathy), retinitis, and gastroenterological infections such as ulcers, pancreatitis and hepatitis. VZV is the only human herpesvirus for which highly effective vaccines are available. After varicella or vaccination, both wild-type and vaccine-type VZV establish latency, and long-term immunity to varicella develops. However, immunity does not protect against reactivation. Thus, two vaccines are used: one to prevent varicella and one to prevent zoster. In this Primer we discuss the pathogenesis, diagnosis, treatment, and prevention of VZV infections, with an emphasis on the molecular events that regulate these diseases. For an illustrated summary of this Primer, visit: http://go.nature.com/14xVI1.

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