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Abstract
Virologic findings reported in recent atherosclerosis literature may have profound
implications. To assess them, we have viewed atherosclerosis in a broad biologic context
and against a background of environmental, behavioral, and social change. Reasonable
grounds exist, we believe, for regarding atherosclerosis as a chronic, low-grade infectious
macroangiopathy which is aggravated by hypercholesterolemia and other recognized risk
factors. There are probably multiple infective pathogens and transmission routes.
The putative agents that initiate atherosclerosis might include ubiquitous viruses
that produce clinically unapparent infections in many animal species. Pathways for
their transmission to humans may include the food chain and contaminated water. Food-chain
transmission may have been largely responsible for the parallel increases of meat
consumption and mortality from coronary heart disease in the United States during
the middle third of the century. It provides a hypothetical basis for considering
thermal intervention as a heretofore unrecognized factor that may actually best account
for the surprising reversal of climbing heart disease mortality rates. Improved sanitation
and food hygiene as well as improvements in diet, lifestyle, and medical care may
have shaped the downward mortality curve. The virus hypothesis may reconcile apparent
epidemiologic conflicts and elucidate the natural history of atherosclerosis.
Keywords
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Article info
Publication history
Accepted:
February 1,
1990
Received in revised form:
January 17,
1990
Received:
August 13,
1989
Identification
Copyright
© 1990 Published by Elsevier Inc.