The association of herpesvirus and atherosclerosis has been suggested by seroepidemiologic studies and detection of the virus in arterial tissues. To facilitate the studies of the pathologic role of herpesvirus in atherosclerosis, we have established an animal model of atherosclerosis by infection of rabbits with bovine herpesvirus type-4 (BHV-4). Since endothelial cells are highly susceptible to BHV-4, they might be the target cells and also act as latent reservoir cells for the virus. In this study, we investigated the effects of virus infection on the biological properties of endothelial cells. Infection of BHV-4 stimulated the biosynthesis and release of plasminogen activator inhibitor type-1 (PAI-1) from the endothelial cells. Infection of the virus per se did not increase the procoagulant activity of the cells. However, virus infection could stimulate the translocation of GMP-140 from the Weibel-Palade bodies of the endothelial cells to the cell surface. As a result, the binding of monocytes and polymorphonuclear neutrophils (PMNs) to the virus-infected endothelial cells increased. The virus-infected endothelial cells became procoagulant when raonocytes were added. Since virus infection might alter the properties of endothelial cells and increase adhesion of monocytes to the vessel wall, it could initiate inflammation reactions and increase the procoagulant activity of endothelial cells. We concluded that virus infection in the endothelial cells might play an important role in the pathogenesis of atherosclerosis and BHV-4 infection could be a good model for study this diesase.
|Number of pages||1|
|Journal||Fibrinolysis and Proteolysis|
|Issue number||SUPPL. 1|
|Publication status||Published - 2000 Dec 1|
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