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American Journal of Pathology, Vol 136, 159-167, Copyright © 1990 by American Society for Investigative Pathology

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Cardiovascular lipid accumulation with Coxsackie B virus infection in mice

NG Ilback, A Mohammed, J Fohlman and G Friman
Toxicology Lab, Swedish National Food Administration, Uppsala.

The authors used a myocarditic coxsackievirus B3 infection in Balb/c mice to investigate cardiovascular lipid accumulation and whether a cholesterol-enriched diet influences the development of the myocardial inflammatory reaction. It was found that, seven days after CB3 infection, the accumulation of 14C-cholesterol increased by 75% (P less than 0.001) in the heart and by 92% (P less than 0.001) in the aorta. This infection also caused extensive inflammatory lesions (4.5% of tissue section area) and lipid accumulation in the myocardium seven days after inoculation. Seven weeks on a 1% cholesterol-enriched diet did not affect the myocardial area damaged (3.9%), the lethality, or immune cell activity (T, B, and natural killer [NK] cells). The response pattern of myocardial lymphocyte subpopulations was studied with an immune histochemical staining technique. The number of Mac 2+ (macrophages), class II expressing cells, or the T cytotoxic, suppressor/T helper cell ratio was not changed by the cholesterol diet. The number of class II cells tended to increase (38%) with cholesterol and was positively correlated (P less than 0.001) with the Mac 2 expression regardless of the cholesterol diet. Although moderate diet- induced hypercholesterolemia did not alter host response to viral infection, these results support the idea that virus and immune cells may cooperate and play a role in arterial and myocardial lipid accumulation, possibly acting as initiating factors for atherosclerosis.

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