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-gamma R(-/-)) 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. 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 gamma HV68-induced elastic arteritis.
journal_name
J Viroljournal_title
Journal of virologyauthors
Dal Canto AJ,Virgin HW 4th,Speck SHdoi
10.1128/jvi.74.23.11304-11310.2000subject
Has Abstractpub_date
2000-12-01 00:00:00pages
11304-10issue
23eissn
0022-538Xissn
1098-5514journal_volume
74pub_type
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pub_type: 杂志文章
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