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INTRODUCTION When I, fresh from obtaining my PhD in biochemistry at Yale University in 1939, began my studies of poliovirus, not much was known about the virus. No one knew [...]

Atherosclerotic plaques are accumulations of cholesterol, lipids, and debris that form inside the walls of arteries. These plaques are produced by the smooth muscle cells that compose part of the arterial wall, but the factors that regulate plaque deposition remain largely unknown. One possible factor is injury to the artery's lining due to viral infection. Results from several animal studies describe a possible association between atherosclerosis and virus, which causes cell destruction. Atherosclerotic lesions have been induced in chickens by avian herpesvirus (HSV). Following a high-cholesterol diet, atherosclerotic plaques were also detected in Japanese quail that were bred for susceptibility to the condition. DNA (genetic material) in susceptible quail contained sequences related to avian herpesvirus. Several human studies are also cited. Antibodies to human herpesvirus are present in more than 50 percent of people by age 35. Arterial tissue, primarily from people undergoing surgery to reduce arterial plaque, was evaluated for the presence of HSV and CMV (cytomegalovirus). Cultures of smooth muscle-like cells from plaque tissue and from uninvolved sections of artery (explants) were grown; proteins specific to CMV were found in both kinds of explant. Based on these results, it appears that CMV may act as an initiating factor in plaque genesis. Viral genetic material was detected in segments of abdominal and femoral (upper leg) arteries from patients undergoing surgery for vascular disease, and in abdominal arteries removed during autopsies of patients who did not have atherosclerosis. CMV DNA was found in 90 percent of the arterial tissue of the surgical patients, but in only 53 percent of the tissue obtained during postmortem examinations. Another study compared viral presence in patients who had undergone surgery for atherosclerotic disease and patients who had high blood cholesterol levels, but no apparent vascular disease. Significant differences in CMV antibody were found between the two groups. Studies of heart transplant patients reported that recipients who developed CMV soon after transplantation had a higher rate of atherosclerosis, a leading cause of death in these patients. CMV may infect and damage cells, without killing them, and may be involved in the early stages of atherosclerotic disease. Overall, evidence from several sources indicates that viruses may play an important role in the pathogenesis of human atherosclerosis. (Consumer Summary produced by Reliance Medical Information, Inc.)