Viruses in the Etiology of Atherosclerosis

To examine the possible role of viruses in the etiology of atherosclerosis, we searched for the presence of viral genomes in arterial tissues by in situ hybridization. Because chickens infected with Marek disease virus, a herpesvirus, develop atherosclerotic lesions after infection, we looked for th...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1983-10, Vol.80 (20), p.6386-6389
Main Authors: Benditt, Earl P., Barrett, Thomas, McDougall, James K.
Format: Article
Language:English
Subjects:
Animals
Arteriosclerosis - etiology
Arteriosclerosis - microbiology
Atherosclerosis
Cell lines
Cells, Cultured
Chickens
DNA, Viral - isolation & purification
Epstein Barr virus infections
Human herpesvirus 1
Humans
In situ hybridization
Infections
Lesions
Muscle, Smooth, Vascular - microbiology
Nucleic Acid Hybridization
RNA, Messenger - metabolism
RNA, Viral - metabolism
Simplexvirus - physiology
Smooth muscle myocytes
Specimens
Virus Replication
Viruses
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Summary:To examine the possible role of viruses in the etiology of atherosclerosis, we searched for the presence of viral genomes in arterial tissues by in situ hybridization. Because chickens infected with Marek disease virus, a herpesvirus, develop atherosclerotic lesions after infection, we looked for the presence of herpesvirus or parts thereof in human artery wall tissue, particularly in individuals with evidence of atherosclerosis. Herpesvirus probes were used on specimens of aortic wall removed from patients undergoing coronary bypass surgery. Evidence for the presence of herpes simplex viral mRNA was obtained in 13 specimens. Some of the specimens positive for herpes simplex virus appear to represent early stages in atherogenesis. Evidence for the presence of cytomegalovirus or Epstein-Barr viral genome was not observed in any of the specimens examined. We have also shown that herpes simplex virus can infect human fetal smooth muscle cells in culture. There are several ways in which viruses could operate in the pathogenesis of atherosclerosis: They could induce proliferation of artery wall intimal smooth muscle cells via injury or by genomic alterations leading to clonal expansion of intimal smooth muscle cell populations. We suggest that expression of at least a part of the herpesvirus genome in arterial smooth muscle cells may in some cases be instrumental in initiating or maintaining this enhanced cell proliferation. Furthermore, viral agents could explain other puzzling features in the occurrence of atherosclerosis and the attendant heart disease and strokes.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.80.20.6386