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Outbred mice infected by an encephalomyocarditis virus variant: a model for studying chronic viral heart disease
J P Kruppenbacher1, G Arnold, T Mertens
1Institut für Virologie, Universität zu Köln, Cologne, Germany.
Abstract:
Male 8 to 20-week-old NMRI mice (an outbred strain) infected with the encephalomyocarditis virus (EMCV) plaque variant (PV) 7 consistently develop a distinct myocarditis with a relatively low mortality (21%). Myocarditis occurs in essence independent of the virus dose applied, and other internal organs are not affected. Nevertheless, 3.5-week-old NMRI mice perished within 5 days of virus inoculation and exhibited disseminated myofibrillar degeneration (MFD); this obviously virus-induced myocardial damage was accompanied by scanty inflammatory infiltrates. EMCV PV7 infection of adult male C57Bl/6 and DBA/2 mice causes myocarditis comparable to that seen in NMRI mice. In DBA/2 mice, however, the virus-induced myocardial necrosis is complicated by subtotal calcification. This strain has a genetically determined "spontaneous" calcification of the myocardium, as shown by the study of uninfected controls. EMCV PV7-infected NMRI mice appear a promising model for study of long-term effects of viral myocarditis, possibly including cardiomyopathy. Furthermore, this outbred mouse strain offers the possibility of examining the pathogenesis of direct viral cytolysis and its relation to MFD as well as immunologically mediated cell damage.
Insights
Encephalomyocarditis virus (EMCV) infection in mice causes myocarditis, a heart inflammation. NMRI mice offer a promising model for studying viral myocarditis and its long-term effects, including cardiomyopathy.
Area of Science:
- Virology
- Cardiology
- Pathology
Background:
- Encephalomyocarditis virus (EMCV) plaque variant (PV) 7 consistently induces myocarditis in mice.
- Myocarditis development is largely independent of the EMCV dose and does not affect other organs.
- Younger mice exhibit disseminated myofibrillar degeneration (MFD) and myocardial damage with minimal inflammation.
Purpose of the Study:
- To characterize the myocarditis induced by EMCV PV7 in different mouse strains.
- To evaluate the potential of the NMRI mouse model for studying viral myocarditis and its sequelae.
- To investigate the relationship between direct viral cytolysis, MFD, and immune-mediated damage.
Main Methods:
- Infection of male NMRI, C57Bl/6, and DBA/2 mice with EMCV PV7.
- Assessment of myocarditis, mortality, and organ involvement.
- Histopathological examination for myofibrillar degeneration and calcification.
Main Results:
- NMRI mice consistently developed myocarditis with low mortality (21%).
- DBA/2 mice showed virus-induced myocardial necrosis complicated by spontaneous calcification.
- EMCV PV7 infection did not affect organs other than the heart.
Conclusions:
- EMCV PV7-infected NMRI mice represent a valuable model for studying viral myocarditis and potential cardiomyopathy.
- The model allows for investigation into direct viral cytolysis, MFD, and immune-mediated myocardial damage.
- DBA/2 mice present a unique model for studying the interplay between viral necrosis and genetic predisposition to myocardial calcification.