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Pathogenesis of chronic myocarditis in mice infected with coxsackie B3 viruses
Abstract:
Infection of 300 mice of the Swiss race with Coxsackie B3 viruses gave rise to chronic myocarditis and endocarditis. The virus was cultured from the heart muscle 9 days post infection. Between days 18 and 108 post infection, virtually all mice showed evidence of an active inflammatory process in the myocardium, and in one half there was proliferation of endothelial cells, and infitration and fibrosis in the endocardium. Immunomorphologic studies demonstrated the precence of antiheart antibodies in the blood serum, and Coxsackie B3 antigen and immunoglobulin deposits in the myocardium and endocardium. Highest levels of antivirus antibodies were observed 18 days post infection.
Insights
Coxsackie B3 virus infection causes chronic heart inflammation (myocarditis and endocarditis) in mice. This study details the inflammatory process and immune responses in infected mouse hearts.
Area of Science:
- Virology
- Immunology
- Cardiovascular Pathology
Background:
- Coxsackie B viruses are known human pathogens.
- Viral infections can trigger autoimmune responses and chronic heart disease.
Purpose of the Study:
- To investigate the development of chronic myocarditis and endocarditis following Coxsackie B3 virus infection in mice.
- To characterize the immunopathological changes in the heart tissue.
Main Methods:
- Infection of Swiss mice with Coxsackie B3 virus.
- Virus culturing from heart muscle.
- Histopathological examination of myocardium and endocardium.
- Immunomorphologic studies for antibodies, viral antigens, and immunoglobulin deposits.
Main Results:
- Chronic myocarditis and endocarditis were observed in infected mice.
- Coxsackie B3 virus was cultured from heart muscle up to 9 days post-infection.
- Active inflammation, endothelial cell proliferation, infiltration, and fibrosis were noted in the heart.
- Antiheart antibodies, Coxsackie B3 antigen, and immunoglobulin deposits were found in the myocardium and endocardium.
- Peak antivirus antibody levels occurred at 18 days post-infection.
Conclusions:
- Coxsackie B3 virus infection induces chronic inflammatory heart disease in mice.
- The findings suggest an autoimmune component in the pathogenesis of viral myocarditis.
- This model provides insights into the mechanisms of viral-induced cardiac pathology.