Ongoing viral replication is required for gammaherpesvirus 68-Induced vascular damage

A. J. Dal Canto, H. W. Virgin IV, S. H. Speck

Research output: Contribution to journalArticle

49 Scopus citations

Abstract

The role of autoimmunity in large-vessel vasculitis in humans remains unclear. We have previously shown that infection of gamma interferon receptor knockout (IFN-γR-/-) mice with gammaherpesvirus 68 (γHV68) results in severe inflammation of the large elastic arteries that is pathologically similar to the lesions observed in Takayasu's arteritis, the nongranulomatous variant of temporal arteritis, and Kawasaki's disease (K. E. Weck et al., Nat. Med. 3:1346-1353, 1997). Here we define the mechanism of damage to the elastic arteries. We show that there is a persistent productive infection of the media of the large elastic vessels. In addition, we demonstrate that persistent virus replication is necessary for chronic arteritis, since antiviral therapy of mice with established disease resulted in increased survival, clearance of viral antigen from the media of the affected vessel, and dramatic amelioration of arteritic lesions. These data argue that ongoing virus replication, rather than autoimmunity, is the cause of γHV68-induced elastic arteritis.

Original languageEnglish
Pages (from-to)11304-11310
Number of pages7
JournalJournal of virology
Volume74
Issue number23
DOIs
StatePublished - Dec 1 2000

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