Key Points
- To examine the molecular mechanisms underlying enterovirus persistence, immune evasion, and chronic inflammation leading to myocarditis and dilated cardiomyopathy.
- Analyzed in situ hybridization data from human myocardial tissue across acute myocarditis, chronic myocarditis, and end-stage dilated cardiomyopathy.
- Reviewed experimental murine models of chronic myocarditis inoculated with coxsackievirus B3 to evaluate host-virus interactions and immune surveillance evasion.
- Enterovirus genomic material is detectable within myocardial tissue across all clinical stages of myocarditis and in subset populations with end-stage dilated cardiomyopathy.
- Coxsackievirus B3 evades host immunological surveillance in a host-dependent manner, maintaining viral persistence and chronic myocardial inflammation.
- Identification of viral persistence provides diagnostic utility and supports the evaluation of targeted antiviral strategies, including interferons.
Structured PICO
PPopulationPatients with acute and chronic enterovirus-induced myocarditis and end-stage dilated cardiomyopathy, as well as murine models of chronic myocarditis (coxsackievirus B3)
Enterovirus persistence plays a role in the pathogenesis of chronic myocarditis and dilated cardiomyopathy, highlighting potential targets for specific antiviral therapies like interferons.