Inoculation of DBA/2 mice with the M variant of the EMC virus induces severe, rapid-onset myocarditis, providing an excellent animal model for studying the pathogenesis of viral myocarditis.
Rapid EMC myocarditis model enables earlier lesion timing studies; leaves open human translation.
Severe myocarditis was induced in inbred DBA/2 mice inoculated with M variant of EMC virus. Yellowish-white patches were seen on the surface of the ventricles and atria, and histologically, myocardial necrosis and calcification was evident on the fourth day after virus inoculation. Myocardial lesions appeared earlier and were more extensive than we observed in previous myocarditis induced by Coxsackie B viruses. Spontaneous perimyocardial lesions were observed in control DBA/2 mice, which were exclusively limited to the right ventricle; however, these lesions were different in localization from lesions observed in infected mice in which extensive myocardial lesions were noted. This animal model is considered to be excellent for studies on the pathogenesis and natural history of viral myocarditis.
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Matsumori et al. (1981) studied this question.
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