Virus Infection of Endothelial Cells

Abstract

Endothelial injury is important in the pathogenesis of thrombosis, atherosclerosis, disseminated intravascular coagulation, and vasculitis. The ability of several common human viruses to infect cultures of endothelial cells obtained from human umbilical veins or bovine thoracic aorta was demonstrated. Indicators of infection included cytopathology, viral growth curves, and antigen detection by immunofluorescence. Herpes simplex virus type 1, adenovirus type 7, measles virus, and parainfluenza virus type 3 infected both human venous and bovine aorta endothelium. Mumps virus, poliovirus type 1, and echovirus type 9 grew only in human venous cells; coxsackievirus B4 infected only bovine arterial cultures; and cytomegalovirus, influenza A/Victoria/75 (H3N2) virus, and respiratory syncytial virus failed to grow in either cell culture. During replication some viruses caused acute lytic changes; some produced chronic, less destructive alterations; and other induced no apparent cytopathology. The results suggest that viral replication within endothelium may be important in the pathogenesis of viral disease of initiation of vessel-wall injury.

Respiratory Syncytial Virus Infection of Human Lung Endothelial Cells Enhances Selectively Intercellular Adhesion Molecule-1 Expression

“…The infection of HUVEC is still contradictorily discussed. Friedmann et al (19) reported that RSV was not able to infect HUVEC or bovine thoracic aorta endothelium. In contrast, Visseren et al (20) observed that RSV infection of HUVEC can occur and that infection increases their procoagulant activity.…”

The effect of herpesvirus infection on the expression of cell adhesion molecules on cultured human dermal microvascular endothelial cells

“…As a preliminary study, we treated HD-MEC with 10 5 and 10 6 plaque-forming units (PFU) HSV-1, because the MOI (multiplicity of infection) of HSV to endothelial cells was 5 in a previous study [5]. Typical cytopathic effect was seen after 24 and 48 h of the treatment of 10 5 PFU HSV-1, but not of 10 6 PFU HSV-1.…”

“…Experimental models of endothelial damage indicate the importance of endothelial cells in the pathogenesis of immune vasculitis, atherosclerosis, thrombosis, and disseminated intravascular coagulation [5]. Mechanisms of experimental injury to endothelium include mechanical trauma, hypercholesterolemia, hemodynamic stress, and immune attack.…”

“…Infectious agents such as Rickettsia rickettsii, meningococci, and Aspergillus can damage vessel walls. Viruses such as herpes simplex have also been implicated in injuries to endothelial cells or vessel walls [5]. The effector cell populations against herpesviruses in human peripheral blood have been shown to include NK cells, killer cells, cytotoxic lymphocytes and B lymphocytes [6].…”

Effect of acetylsalicylic acid on pulmonary arteriosclerosis induced by a one-year Dirofilaria immitis infection.

“…Examples include dietary regimens to increase plasma lipid levels, 1 removal of endothelial cells by balloon catheters, 2 ' 3 air-drying of exposed vascular surfaces, 4 homocystine infusion, 5 viral infections, 6 vascular grafting, 7 " 9 and parasite infection. 10 " 12 Each vascular injury model has advantages, along with sufficient disadvantages to cause caution in relating the experimental results to human atherosclerosis.…”