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Pathogenesis of acute myocardial necrosis in inbred mice infected with coxsackievirus B3
Journal article   Peer reviewed

Pathogenesis of acute myocardial necrosis in inbred mice infected with coxsackievirus B3

Janet B. Grun, Maggie Schultz, Sydney D. Finkelstein, Richard L. Crowell and Burton J. Landau
Microbial pathogenesis, v 4(6), pp 417-430
1988
PMID: 2848174

Abstract

acute myocardial necrosis BALB/c mice C3H/HeJ mice Coxsackievirus B3 heart muscle disease hepatitis myocardiotropic virus variants
The pathogenesis of myocardial necrosis due to CB3W infection was studied in BALB/c and C3H/HeJ mice. BALB/c mice infected with 5 × 10 4 pfu were found to die of massive hepatic coagulative necrosis before myocardial changes occurred. Reducing the inoculum size to 5 × 10 2 pfu resulted in sublethal hepatic involvement and multifocal myocardial coagulative necrosis by day 7 p.i. In contrast, C3H/HeJ mice survived infection and developed multifocal myocardial coagulative necrosis, but not liver disease following inoculation with as much as 5 × 10 6 pfu of CB3W. As with BALB/c mice infected with 5 × 10 2 pfu, myocardial lesions became apparent in C3H/HeJ mice a few days after peak cardiac virus titer was attained. Minimal inflammatory infiltrate was seen following development of cellular necrosis and was restricted to the areas of virus-induced pathologic change. However, no evidence was found for virus-specific cytotoxic T cell activity or for delayed type hypersensitivity responses. Furthermore, myocardial necrosis in CB3W-infected, T cell-depleted C3H/HeJ mice was as severe as in CB3W-infected, immunocompetent mice. These data have led us to conclude that cardiac lesions were due to virus-induced cytopathology rather than immunopathogenic mechanisms.

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Web of Science research areas
Immunology
Microbiology
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