Journal
JOURNAL OF VIROLOGY
Volume 74, Issue 23, Pages 11304-11310Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.74.23.11304-11310.2000
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Funding
- NCI NIH HHS [R01 CA052004, CA52004, R01 CA058524, R01 CA074730, R01 CA043143, CA58524, CA43143] Funding Source: Medline
- NHLBI NIH HHS [R01 HL060090] Funding Source: Medline
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The role of autoimmunity in large-vessel vasculitis in humans remains unclear. We have previously shown that infection of gamma interferon receptor knockout (IFN-gammaR(-/-)) mice with gammaherpesvirus 68 (gamma HV68) 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. Week 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 gamma HV68-induced elastic arteritis.
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