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This has been demonstrated by molecular detection of enteroviral RNA in human heart tissue, serologic associations with disease, and virus isolation from cases of fulminant myocarditis. The murine model of CVB\u2012associated myocarditis has demonstrated that CVB can be attenuated through mutations at different genomic sites. Human CVB3 isolates demonstrate varying degrees of cardiovirulence in the murine model; one site of virulence determination has been mapped to domain II of the 5\u2032 non\u2012translated region. The interplay of CVB replication and the immune response to that replication in the heart is a complex interaction determining the extent to which the virus replication is limited and the degree to which a pathogenic inflammation of cardiac muscle occurs. Studies of CVB3\u2012induced myocarditis in murine strains lacking subsets of the immune system or genes regulating the immune response have demonstrated a pivotal role of the T cell response to the generation of myocarditis. While CVB are associated with 20\u201325% of cases of myocarditis or cardiomyopathy, the severity of the disease and the existence of attenuated strains shown to generate protective immunity in animal models indicates that vaccination against the CVBs would be valuable. 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