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Intricacies of cardiac damage in coxsackievirus B3 infection: implications for therapy
Chandirasegaran Massilamany1, Arunakumar Gangaplara2, Jay Reddy1
1School of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583.
Insights
Coxsackievirus B (CVB)3 infection can cause heart disease like myocarditis and dilated cardiomyopathy (DCM). In mice, CVB3 infection generates cardiac myosin-specific CD4 T cells that transfer disease, suggesting an autoimmune link.
Area of Science:
- Cardiology
- Immunology
- Virology
Background:
- Heart disease is a leading cause of death globally.
- Myocarditis is a significant cause of heart failure in young adults, often leading to dilated cardiomyopathy (DCM).
- Existing treatments for DCM are limited, with heart transplantation being the only definitive option.
Purpose of the Study:
- To investigate the role of Coxsackievirus B (CVB)3 in the pathogenesis of myocarditis and dilated cardiomyopathy (DCM).
- To explore the potential autoimmune mechanisms underlying CVB3-induced heart disease.
- To present findings from a mouse model relevant to human disease.
Main Methods:
- Induction of myocarditis in susceptible mice using human isolates of Coxsackievirus B (CVB)3.
- Analysis of viral damage and host immune response in the CVB3 infection model.
- Investigation of CD4 T cell responses specific to cardiac myosin.
Main Results:
- CVB3 infection in mice mimics human post-infectious myocarditis.
- CVB3 infection is associated with the generation of cardiac myosin-specific CD4 T cells.
- These cardiac myosin-specific CD4 T cells can transfer myocarditis to naive recipient mice.
Conclusions:
- CVB3-induced myocarditis involves both direct viral damage and host-mediated autoimmune responses.
- The generation of cardiac myosin-specific CD4 T cells plays a crucial role in disease pathogenesis.
- These findings suggest potential therapeutic targets for myocarditis and DCM.
Abstract:
Heart disease is the leading cause of death in humans, and myocarditis is one predominant cause of heart failure in young adults. Patients affected with myocarditis can develop dilated cardiomyopathy (DCM), a common reason for heart transplantation, which to date is the only viable option for combatting DCM. Myocarditis/DCM patients show antibodies to coxsackievirus B (CVB)3 and cardiac antigens, suggesting a role for CVB-mediated autoimmunity in the disease pathogenesis; however, a direct causal link remains to be determined clinically. Experimentally, myocarditis can be induced in susceptible strains of mice using the human isolates of CVB3, and the disease pathogenesis of postinfectious myocarditis resembles that of human disease, making the observations made in animals relevant to humans. In this review, we discuss the complex nature of CVB3-induced myocarditis as it relates to the damage caused by both the virus and the host's response to infection. Based on recent data we obtained in the mouse model of CVB3 infection, we provide evidence to suggest that CVB3 infection accompanies the generation of cardiac myosin-specific CD4 T cells that can transfer the disease to naïve recipients. The therapeutic implications of these observations are also discussed.
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