Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Jul;13(3):509-13.
doi: 10.1007/s13311-016-0430-x.

Issues in the Treatment of Neurological Conditions Caused by Reactivation of Varicella Zoster Virus (VZV)

Affiliations
Review

Issues in the Treatment of Neurological Conditions Caused by Reactivation of Varicella Zoster Virus (VZV)

Peter G E Kennedy. Neurotherapeutics. 2016 Jul.

Abstract

Varicella zoster virus (VZV) is a ubiquitous neurotropic human herpesvirus. Primary infection usually causes varicella (chicken pox), after which virus becomes latent in ganglia along the entire neuraxis. Decades later, virus reactivates to produce herpes zoster (shingles), a painful dermatomally distributed vesicular eruption. Zoster may be further complicated by postherpetic neuralgia, VZV vasculopathy, myelitis, and segmental motor weakness. VZV reactivation has also been associated with giant cell arteritis. This overview discusses treatment of various conditions that often require both corticosteroids and antiviral drugs. Treatment for VZV-associated disease is often based on case reports and small studies rather than large-scale clinical trials. Issues that require resolution include the optimal duration of such combined therapy, more effective treatment for postherpetic neuralgia, whether some treatments should be given orally or intravenously, the widening spectrum of zoster sine herpete, and the role of antiviral therapy in giant cell arteritis.

Keywords: Antiviral agents; Corticosteroids; Postherpetic neuralgia; Varicella zoster virus; Vasculitis.

PubMed Disclaimer

References

    1. Gilden DH, Kleinschmidt-DeMasters BK, LaGuardia JJ, Mahalingam R, Cohrs RJ. Neurologic complications of the reactivation of varicella-zoster virus. N Engl J Med. 2000;342:635–645. doi: 10.1056/NEJM200003023420906. - DOI - PubMed
    1. Mitchell BM, Bloom DC, Cohrs RJ, Gilden DH, Kennedy PGE. Herpes simplex virus-1 and varicella-zoster virus latency in human ganglia. J Neurovirol. 2003;9:194–204. doi: 10.1080/13550280390194000. - DOI - PubMed
    1. Kennedy PGE, Cohrs RJ. Varicella-zoster virus human ganglionic latency—a current summary. J Neurovirol. 2010;16:411–418. doi: 10.1007/BF03210846. - DOI - PubMed
    1. Kennedy PGE, Grinfeld E, Gow JW. Latent varicella-zoster virus is located predominantly in neurons in human trigeminal ganglia. Proc Natl Acad Sci U S A. 1998;95:4658–4662. doi: 10.1073/pnas.95.8.4658. - DOI - PMC - PubMed
    1. Ouwendijk WJ, Choe A, Nagel MA, et al. Restricted varicella-zoster virus transcription in human trigeminal ganglia obtained soon after death. J Virol. 2012;86:10203–10206. doi: 10.1128/JVI.01331-12. - DOI - PMC - PubMed

MeSH terms