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Updated: Aug 13, 2026
Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice
Published on: April 15, 2014
Encephalomyocarditis virus myocarditis in inbred strains of mice--chronic stage
Abstract:
Inbred strains of A/J, BALB/c, C3H/He, C57BL/6 and DBA/2 mice were inoculated with the M variant of encephalomyocarditis virus having a titer of 100 TCID50/0.1 ml. Myocardial lesions were seen in 73 of 150 BALB/c mice (48.7%), 160 of 259 C3H/He mice (61.8%) and 115 of 174 DBA/2 mice (66.1%). No pathologic findings were noted in A/J and C57BL/6 mice. In C3H/He and DBA/2 mice, dilatation and hypertrophy of the heart accompanying myocardial lesions persisted up to the 8th month after virus inoculation. The present study revealed that myocardial lesions similar to those in congestive (dilated) cardiomyopathy persisted for a long period after viral infection.
Insights
Viral infections can cause long-term heart damage. This study found that encephalomyocarditis virus (EMCV) infection in mice led to persistent myocardial lesions, mimicking dilated cardiomyopathy.
Area of Science:
- Virology
- Cardiology
- Immunology
Background:
- Viral infections are a known cause of myocarditis.
- The long-term cardiac sequelae of viral myocarditis are not fully understood.
- Encephalomyocarditis virus (EMCV) is a potential etiological agent for myocarditis.
Purpose of the Study:
- To investigate the long-term effects of encephalomyocarditis virus (M variant) infection on the myocardium in different mouse strains.
- To determine the susceptibility of various inbred mouse strains to EMCV-induced myocardial pathology.
- To characterize the persistence and nature of cardiac lesions following viral inoculation.
Main Methods:
- Inoculation of five inbred mouse strains (A/J, BALB/c, C3H/He, C57BL/6, DBA/2) with encephalomyocarditis virus (M variant).
- Assessment of myocardial lesions and pathological findings post-infection.
- Longitudinal observation of cardiac changes, including dilatation and hypertrophy, up to 8 months.
Main Results:
- Significant myocardial lesions were observed in BALB/c, C3H/He, and DBA/2 mice, with incidence rates of 48.7%, 61.8%, and 66.1%, respectively.
- No pathological findings were noted in A/J and C57BL/6 mice, indicating strain-specific susceptibility.
- In susceptible strains (C3H/He, DBA/2), cardiac dilatation and hypertrophy associated with myocardial lesions persisted for up to 8 months post-infection.
Conclusions:
- Encephalomyocarditis virus infection can induce persistent myocardial lesions in susceptible mouse strains.
- These long-term cardiac abnormalities resemble those seen in congestive (dilated) cardiomyopathy.
- Viral myocarditis may lead to chronic cardiac dysfunction and remodeling.
