<unk>  shows a cardiac tropism partly due to the high expression of<unk>  and adenovirus receptors (CAR) in cardiomyocytes.<unk>  B genome is approximately 7.4 Kb and translated as a polycistronic polyprotein. Upon translation, the polyprotein is cleaved by two essential viral proteases, 2A and 3C. The viral protease 2A cleaves the proteins in a sequence specific manner. These viral proteases can also act on host proteins exerting negative effects on the residing cell. Enteroviral protease 2A can cleave the cytoskeletal dystrophin protein in cardiomyocytes disrupting the dystrophin glycoprotein (DCG) complex. The cleavage site of dystrophin by protease 2A occurs in the hinge 3 region of the protein resulting a disruption of DCG complex and loss of sarcolemma integrity and increasing myocyte permeability. This eventually results in similar cardiac deformities observed in dilated cardiomyopathy caused by hereditary defects in dystrophin in DMD patients. Additionally, dystrophin deficiency has been shown to increase the severity in dilated cardiomyopathy in a mouse model for DMD. The increased susceptibility of dystrophin deficient heart to<unk><unk>  dilated cardiomyopathy is attributed to more efficient release of the virus from infected cells resulting an increase in viral-mediated cytopathic effects. Viral-induced dilated cardiomyopathy can be characterized using different methods. A 2011 study showed in<unk>  infected heart proteome, increased levels of fibrotic extracellular matrix proteins and reduced amounts of energy-producing enzymes can be observed suggesting they could be characteristic in enteroviral cardiomyopathy. There are notable differences between the hereditary dilated cardiomyopathy in DMD and acute coxsackieviral-mediated cardiomyopathy. # The amount of virally infected cardiomyocytes varies in different stages of the disease. In a mouse model, at the acute stage (7 days after infection with<unk>  B3) approximately 10% of the myocytes are infected and could affect overall cardiac function. In chronic murine infection, the percentage of infected cardiomyocytes are much lower. # Unlike in the DMD, in<unk> , acute cleavage of dystrophin in cardiomyocytes is unlikely to<unk> any prompt compensatory mechanism since host cell translation mechanism is defective in the infected cells.
Coxsackievirus-induced cardiomyopathy
Viral cardiomyopathy
Amyloid cardiomyopathy
Alcoholic cardiomyopathy
Idiopathic giant-cell myocarditis
Eosinophilic myocarditis
HIV associated cardiomyopathy
Diabetic cardiomyopathy