Ongoing viral replication is required for gammaherpesvirus 68-induced vascular damage.

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 Virol

journal_title

Journal of virology

authors

Dal Canto AJ,Virgin HW 4th,Speck SH

doi

10.1128/jvi.74.23.11304-11310.2000

subject

Has Abstract

pub_date

2000-12-01 00:00:00

pages

11304-10

issue

23

eissn

0022-538X

issn

1098-5514

journal_volume

74

pub_type

杂志文章