NDLI: Enhanced thrombin generation and platelet binding on herpes simplex virus-infected endothelium.

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Enhanced thrombin generation and platelet binding on herpes simplex virus-infected endothelium.

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Enhanced thrombin generation and platelet binding on herpes simplex virus-infected endothelium.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jacob, H. S. White, J. G. Goodman, J. L. Tracy, P. B. Visser, M. R. Vercellotti, G. M.
Description	Author Affiliation: Visser MR ( Department of Medicine, University of Minnesota, Minneapolis 55455.);
Abstract	Atherosclerotic lesions have been reported to contain herpes simplex virus 1 (HSV-1) genomic material. This, and other previous evidence, suggests that latent viral infection may be an atherogenic trigger. Moreover, active HSV-1 lesions manifest marked fibrin deposition in microvessels. In this report we show that very early infection of human endothelial cells with HSV-1 appears to alter surface conformation as detected by merocyanine 540 staining. Concomitantly, the efficiency of prothrombinase complex assembly increases, resulting in a 2- to 3-fold accelerated rate of thrombin generation on the cell surface. Increased thrombin generation is probably doubly procoagulant, since we also demonstrate that thrombin-induced platelet accumulation on HSV-infected endothelium (50.7 +/- 9.3%) is increased compared to uninfected endothelium (9.5 +/- 2.1%; P less than 0.002). Associated with HSV infection, prostacyclin secretion in response to thrombin is diminished by a factor of 20, probably explaining the enhanced platelet attachment. We conclude that HSV infection shifts endothelial cell properties from anticoagulant to procoagulant, both by promoting prothrombinase complex formation and function and by increasing platelet binding, well before cell disruption takes place. Virus-induced changes in the endothelial plasma membrane and diminished prostacyclin secretion are suggested as the pathways for this pathophysiologic mechanism, which may be germane to atherosclerotic thrombosis as well as HSV-mediated tissue necrosis.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	21
Volume Number	85
Language	English
Publisher	National Academy of Sciences
Publisher Date	1988-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Arteriosclerosis Microbiology Blood Platelets Metabolism Endothelium Herpes Simplex Pathology Thrombin Biosynthesis Blood Cell Adhesion Cell Aggregation Indomethacin Pharmacology Pyrimidinones Simplexvirus Thromboplastin Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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