Thromb Haemost 2000; 84(02): 319-324
DOI: 10.1055/s-0037-1614014
Review Article
Schattauer GmbH

Procoagulant Activity of Endothelial Cells after Infection with Respiratory Viruses

F. L. J. Visseren
1   From the University Medical Center Utrecht, Department of Internal and Vascular Medicine, The Netherlands
,
J. J. M. Bouwman
2   Diakonessen Hospital Utrecht, Department of Microbiology, The Netherlands
,
K. P. Bouter
3   Bosch Medical Centre, Den Bosch, Department of Internal Medicine, The Netherlands
,
R. J. A. Diepersloot
2   Diakonessen Hospital Utrecht, Department of Microbiology, The Netherlands
,
Ph. G. de Groot
4   University Hospital Utrecht, Department of Hematology, The Netherlands
,
D. W. Erkelens
1   From the University Medical Center Utrecht, Department of Internal and Vascular Medicine, The Netherlands
› Author Affiliations

The authors wish to thank Mrs. Mathea Verkerk for technical assistance, Dr. Peter Kreuz Wendedich von dem Borne for isolation of factor VII and X and Dr. Hence J. M. Verhage for technical advice on the tissue factor assay. This work was supported by a grant from the ‘Stichting Diabetes Research’, the Netherlands.
Further Information

Publication History

Received 26 June 1997

Accepted after resubmission 29 February 2000

Publication Date:
14 December 2017 (online)

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Summary

Influenza virus epidemics are associated with excess mortality due to cardiovascular diseases. There are several case reports of excessive coagulation during generalised influenza virus infection. In this study, we demonstrate the ability of respiratory viruses (influenza A, influenza B, parainfluenza-1, respiratory syncytial virus, adenovirus, cytomegalovirus) to infect lung fibroblasts and human umbilical vein endothelial cells in culture. All viral pathogens induced procoagulant activity in infected endothelial cells, as determined in a one-stage clotting assay, by causing an average 55% reduction in the clotting time. When factor VII deficient plasma was used clotting time was not reduced. The induction of procoagulant activity was associated with a 4- to 5-fold increase in the expression of tissue factor, as measured by the generation of factor Xa. Both experiments indicate that the procoagulant activity of endothelial cells in response to infection with respiratory viruses is caused by upregulation of the extrinsic pathway. Although both enveloped viruses and a non-enveloped virus (adenovirus) induced procoagulant activity in endothelial cells by stimulating tissue factor expression, the role of the viral envelope in the assembly of the prothrombinase complex remains uncertain.

We conclude that both enveloped and non-enveloped respiratory viruses are capable of infecting cultured human endothelial cells and causing a shift from anticoagulant to procoagulant activity associated with the induction of tissue factor expression.