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Studies on the pathogenesis of atrial myocarditis in mice infected with Coxsackie virus B3
Abstract:
Coxsackie virus B3 (CB3) was inoculated intraperitoneally into BALB/c mice to determine whether atrial myocarditis is due primarily to virus multiplication in the atrial myocardium or is secondary to the effects of virus multiplication in the ventricular myocarditis. Ventricular changes were observed in 15 (71%) out of 21 mice. The lesions consisted of hyaline or granular degeneration and necrosis with or without calcium deposits of the muscle fibres and inflammatory mononuclear cell infiltration. Histopathological changes in the atrial myocardium were found in 14 (67%) out of 21 mice. The lesions in the atrial myocardium were oedema or thickening of the endocardium, degeneration and necrosis of the muscle fibres and inflammatory mononuclear cell infiltration. The incidence and degrees of intensity of the histopathological changes in the atrial myocardium were less than those of the ventricular myocardium in mice inoculated with CB3, but no difference in the nature of the histopathological changes between the atrial and ventricular myocardium were observed. A high virus titer was found in the atrial myocardium as well as in the ventricular myocardium, and virus antigen was detected in the degenerating or necrotizing muscle fibres in the atrial myocardium by immunofluorescent technique. It is clear that CB3 could produce not only ventricular myocarditis, but also atrial myocarditis. We conclude, therefore, that damage of the atrial myocardium is due to direct action of the virus.
Insights
Coxsackie virus B3 (CB3) causes both atrial and ventricular myocarditis in mice. Direct viral action on the atrial myocardium leads to inflammation and damage, similar to ventricular effects.
Area of Science:
- Virology
- Cardiovascular Pathology
- Immunology
Background:
- Coxsackie virus B3 (CB3) is a known cause of myocarditis.
- The specific mechanisms of atrial myocarditis by CB3 are not fully understood.
- Distinguishing primary viral effects from secondary inflammation is crucial.
Purpose of the Study:
- To investigate whether atrial myocarditis is a direct result of CB3 replication in the atria.
- To compare the histopathological changes in atrial and ventricular myocarditis induced by CB3.
- To determine the role of direct viral action in atrial myocardial damage.
Main Methods:
- Intraperitoneal inoculation of BALB/c mice with Coxsackie virus B3 (CB3).
- Histopathological examination of atrial and ventricular myocardium for lesions and inflammation.
- Virus titration and immunofluorescent detection of viral antigen in myocardial tissues.
Main Results:
- CB3 induced histopathological changes in both atrial (67%) and ventricular (71%) myocarditis.
- Lesions included degeneration, necrosis, and mononuclear cell infiltration in both atria and ventricles.
- High virus titers and detectable viral antigen in atrial myocardium confirmed direct viral infection.
Conclusions:
- Coxsackie virus B3 directly causes atrial myocarditis.
- Atrial myocardial damage is due to the direct action of the virus, not secondary to ventricular inflammation.
- CB3 is capable of infecting and damaging both atrial and ventricular heart tissues.
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