Related Experiment Videos
[Pathogenesis, diagnosis and therapy of heart disease caused by enteroviruses (molecular biological study)]
Insights
Human enteroviruses, like coxsackieviruses, can persist in heart muscle, causing myocarditis and dilated cardiomyopathy. Research is exploring viral persistence mechanisms and host factors for new therapeutic strategies against enteroviral heart disease.
Area of Science:
- Virology
- Cardiology
- Immunology
Context:
- Enteroviruses, including group B coxsackieviruses (CVB), are detected in myocardial tissue of patients with myocarditis and dilated cardiomyopathy.
- Evidence suggests enterovirus persistence in the human heart, supported by murine models showing coxsackievirus B3 (CVB3) evading immune surveillance.
Purpose:
- To analyze the molecular mechanisms of enterovirus persistence in the heart.
- To characterize viral and host factors influencing the course of myocardial enterovirus infections.
- To explore therapeutic strategies for human enteroviral heart disease.
Summary:
- Molecular hybridization confirms enteroviruses in heart tissue of patients with myocarditis and dilated cardiomyopathy, indicating potential persistent infection.
- Studies in murine models demonstrate enterovirus persistence and immune evasion, highlighting host-dependent mechanisms.
- Research focuses on understanding viral and host factors driving enterovirus persistence in the myocardium.
Impact:
- Establishes a causal link between enterovirus infection and heart muscle diseases, with therapeutic implications.
- Contraindicates immunosuppressive steroid treatment for patients with myocardial enterovirus infection.
- Highlights the potential of antiviral agents like interferons for new therapeutic strategies in enteroviral heart disease.
Abstract:
Molecular hybridization studies have demonstrated that human enteroviruses, including group B coxsackieviruses (CVB), are detectable in myocardial tissue of patients with acute and chronic myocarditis. As well, such infections are observed in some patients with end-stage dilated cardiomyopathy indicating the possibility of persistent heart muscle infection. Enterovirus persistence in the human heart is supported by the discovery in various murine models of chronic myocarditis, demonstrating that coxsackievirus B3 (CVB3), typically a cytolytic virus, is capable of evading immunological surveillance in a host-dependent manner. Currently attention is focused on the analysis of molecular mechanisms of virus persistence, the characterization of viral and host factors and their impact in determining the natural course of myocardial enterovirus infections. The evidence for a causal linkage of enterovirus infection with heart muscle diseases has emerged therapeutic implications. From the view of a virologist, immunosuppressive treatment of patients revealing enterovirus infection in the myocardium with steroids is clearly contraindicated. The evaluation of potent antiviral agents, such as interferons, in established in vitro and in vivo model systems of enterovirus infection is expected to contribute significantly to new therapeutic strategies in human enteroviral heart disease.