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 also been suggested that a transforming event causes arterial smooth muscle cells to begin dividing and form a focus of proliferating cells.
The possibility of viral infection playing a role in the pathogenesis of atherosclerosis is compatible with the hypotheses described above, since viruses may cause cell destruction, alter cellular metabolism, or induce transformation of infected cells. Recent work in this area has been stimulated by the finding that atherosclerotic lesions, strikingly similar to those in human disease, were reproducibly induced in chickens by