Molecular mechanisms in enterovirus and parvovirus B19 associated myocarditis and inflammatory cardiomyopathy

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Abstract
Enteroviruses are considered as important agents of acute and chronic myocarditis. Molecular studies in murine coxsackievirus B3 (CVB3) myocarditis have confirmed the decisive role of virus replication in initiating and maintaining cytopathic effects in myocytes, thus sustaining chronic inflammation. At the molecular level, interference with myocyte function is mediated by specific cleavage of host cell proteins by viral proteinases. There is also evidence that virus-induced activation of distinct cellular signal transduction pathways promotes enteroviral replication and myocardial dysfunction. More recently, additional viruses such as adenoviruses and, in particular, parvovirus B19 (PVB19) have been associated with inflammatory cardiomyopathy. Molecular pathology of PVB19-associated myocarditis is characterized by infection of intracardiac endothelial cells, followed by intravascular accumulation, adhesion and penetration of inflammatory cells, resulting in endothelial dysfunction with secondary myocyte necrosis, which may clinically present with symptoms similar to that of myocardial infarction during acute infection.

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