Response of Vascular Cells to Herpes Simplex Virus Infection

Abstract

Injury to blood vessel cells has been implicated in the development of a variety of vascular disorders including atherosclerosis (Ashford and Freiman, 1968; French, 1966), disseminated intravascular coagulation (Colman et al., 1972) and immune vasculitis (Rosenberg et al., 1971). Endothelial cell injury can arise from a variety of causes including hemodynamic stress (Stemerrnan et al., 1977), hypercholesterolemia (Ross and Harker, 1976), infectious agents (Friedman et al., 1981; Minick et al., 1979; Robbins, 1967), oxygen (Kistler et al., 1976) and other chemical agents such as homocysteine (Wall et al., 1980). Renewed interest in the relationship between vascular injury due to viral infection and atherosclerosis stems from recent observations which demonstrated that virus particles, virus antigens and virus DNA can be detected in vascular lesions of chickens (Fabricant et al., 1978; Minick et al., 1979) and humans (Benditt et al., 1983; Gyorkey et al., 1984; Melnick et al., 1983) with atherosclerosis. Viruses may produce vascular injury by mechanisms other than direct invasion of endothelium. Antigen-antibody complexes involving hepatitis B surface antigen have been isolated from the sera of some patients with periarteritis nodosa (Fye et al., 1977). Tumor formation as a result of viral infection is another possible mechanism by which viruses may induce vascular disease as is the case with cytomegalovirus and Kaposi’s sarcoma (Giraldo et al., 1980).