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.
Key words
Endothelium - tissue factor viruses