Faculty Collaboration Database

Viral activation of the coagulation cascade: molecular interactions at the surface of infected endothelial cells. Cell 1990 May 18;61(4):657-62

Date

05/18/1990

Pubmed ID

2160855

DOI

10.1016/0092-8674(90)90477-v

Scopus ID

2-s2.0-0025277749 (requires institutional sign-in at Scopus site)   108 Citations

Abstract

Herpesviral infection of endothelial cells (ECs) induces arterial injury. We now demonstrate that such infection promoted enhanced monocyte-endothelial adhesion. Enhanced adhesion was blocked by monoclonal antibodies to the viral-encoded cell surface glycoprotein gC but not by antibodies to gD or gE. Adhesion was also blocked by treating ECs with specific thrombin inhibitors or by growing cells in prothrombin-depleted serum. We found that gC bound and promoted activation of factor X on infected ECs, thereby contributing to thrombin generation. Factor X also bound to transfected L cells that were induced to express gC. Cross-linking and immunoprecipitation studies demonstrated factor X-gC complex formation on the surface of these cells. We suggest that gC-dependent thrombin generation by herpes-infected endothelium may be an important mediator of vascular pathology during viral infection.

Author List

Etingin OR, Silverstein RL, Friedman HM, Hajjar DP

Author

Roy L. Silverstein MD Professor in the Medicine department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Blood Coagulation
Cell Adhesion
Cells, Cultured
Endothelium, Vascular
Factor V
Factor X
Factor Xa
Humans
Monocytes
Simplexvirus
Thrombin
Viral Envelope Proteins