VZV vasculopathy and postherpetic neuralgia: progress and perspective on antiviral therapy.

Abstract

Two serious complications of varicella-zoster virus (VZV) reactivation are vasculopathy and postherpetic neuralgia (PHN). Clinical-virologic analyses have proven that VZV vasculopathy is caused by chronic active virus infection in cerebral arteries. Conclusive evidence that PHN is caused by persistent or productive VZV infection is less compelling because human ganglia are not accessible during life for pathologic and virologic examination. However, the notion that PHN may reflect a smoldering VZV ganglionitis is supported by 1) the detection of VZV DNA and proteins in peripheral blood mononuclear cells of many patients with PHN; 2) studies of multiple patients with zoster sine herpete, which indicate a productive VZV ganglionitis; and 3) a favorable response of some patients with zoster sine herpete and PHN to antiviral treatment. Few studies have used antiviral therapy to manage PHN with conflicting results. Larger, double-blind studies, which give IV antiviral drug, are needed.

• Authors: Donald H Gilden, Randall J Cohrs, Ravi Mahalingam
• Journal: Neurology (Neurology) Vol. 64 Issue 1 Pg. 21-5 (Jan 11 2005) ISSN: 1526-632X [Electronic] United States
• PMID: 15642898 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, P.H.S., Review)

Topics

• Animals
• Herpes Zoster Oticus (pathology)
• Herpesvirus 3, Human (pathogenicity)
• Humans
• Virus Activation (physiology)