Coxsackievirus-induced myocarditis in mice: a model of autoimmune disease for studying immunotoxicity
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Updated: Jul 18, 2026
Noninvasive Assessment of Cardiac Abnormalities in Experimental Autoimmune Myocarditis by Magnetic Resonance Microscopy Imaging in the Mouse
Published on: June 20, 2014
DeLisa Fairweather1, Noel R Rose
1Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, MD 21205, USA.
Insights
A new mouse model using coxsackievirus B3 (CVB3) effectively mimics human autoimmune heart disease, including myocarditis and dilated cardiomyopathy (DCM). This model aids research into heart inflammation and its causes.
Area of Science:
- Immunology
- Cardiology
- Virology
Background:
- Cardiovascular disease is a leading global cause of death, with inflammation playing a significant role in Western populations.
- Myocarditis, or heart muscle inflammation, is a primary cause of sudden death in young adults.
- Genetically susceptible individuals can develop chronic myocarditis, dilated cardiomyopathy (DCM), and congestive heart failure after acute myocarditis.
Purpose of the Study:
- To describe a novel animal model for studying autoimmune myocarditis and DCM.
- To investigate the mechanisms of viral infection and environmental factors in cardiac inflammation and immune dysregulation.
Main Methods:
- Induction of autoimmune myocarditis and DCM in susceptible mice via intraperitoneal inoculation with heart-passaged coxsackievirus B3 (CVB3).
- Monitoring of cardiac inflammation, myocarditis, and DCM progression at specific time points post-infection (days 7-14 and 28-56 pi).
Main Results:
- CVB3 inoculation successfully induced acute cardiac inflammation within 7-14 days post-infection.
- The induced inflammation progressed to chronic myocarditis and DCM by 28-56 days post-infection in susceptible mice.
- The model demonstrated the development of autoimmune heart disease, mirroring human conditions.
Conclusions:
- The CVB3-induced mouse model provides a valuable tool for dissecting the roles of viral infection and xenobiotics in cardiac immune dysregulation.
- This model facilitates a deeper understanding of the interplay between environmental exposures and the development of heart disease.
- Further research using this model can address challenges in immunotoxicology related to heart disease.
Abstract:
Excellent animal models are available for virus-induced and autoimmune heart disease that are remarkably similar to human disease. Developing good animal models for heart disease is crucial because cardiovascular disease is now the leading cause of death in the United States and is estimated to be the leading cause of death in the world by the year 2020. A significant proportion of heart disease in Western populations is associated with inflammation. Myocarditis, or inflammation of the heart muscle, is the major cause of sudden death in young adults. Although most individuals recover from acute myocarditis, genetically susceptible individuals may go on to develop chronic myocarditis and dilated cardiomyopathy (DCM) resulting in congestive heart failure. In this article, we describe a model of autoimmune myocarditis and DCM induced by inoculation with heart-passaged coxsackievirus B3 (CVB3). Intraperitoneal inoculation of susceptible mice with CVB3 induces acute cardiac inflammation from days 7 to 14 postinfection (pi) that progresses to chronic myocarditis and DCM from day 28 to at least 56 pi. The model of CVB3-induced myocarditis presented here allows dissection of the contribution of viral infection and xenobiotics on immune dysregulation and inflammation in the heart. An improved understanding of the interaction between environmental exposures and the development of heart disease represents a clear challenge for immunotoxicologists.
