LATENT VIRAL INFECTION AND ATHEROSCLEROSIS

Abstract

Atherosclerotic plaques consist of complex accumulations produced by arterial smooth muscle cells, which proliferate excessively at the site of plaque formation. To explain the onset of this abnormal cellular proliferation, it has been suggested that injury to the endothelial lining of the artery results in exposure of underlying smooth muscle cells to hormones, low-density lipoproteins, and various growth-promoting factors associated with serum and platelets. It has been suggested that a transforming event causes arterial smooth muscles to begin dividing and form a focus of proliferating cells.

The possibility of viral infection playing a role in atherogenesis is compatible with the hypothesis described above, since viruses may cause cell destruction, alter cellular metabolism, or induce transformation of infected cells.

The evidence for involvement of one or more members of the herpesvirus family in human atherosclerosis is much more circumstantial, but it is increasing (Melnick eta!, 1990).

Our study aims to find an aetiological association between herpes simplex virus type II & cytomegalovirus infections and atherosclerosis.