Enteroviral Replication and Cardiocyte Injury in the Myocardium from patients with Dilated Cardiomyopathy and Perforin Knockout Mice with Viral Myocarditis

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(1)Experimental Coxsackievirus B3 Myocarditis in Perforin Knockout (pfk) Mice.We examined light and (LM) electron-microscopic (EM) changes of the myocardium obtained from pfk and wild(C57BL/6) mice with Coxsackievirus B3(CVB3) myocarditis. The mice were sacrificed on days 5-28 after virus inoculation. On days 8 and 14 many cardiocytes underwent necrosis with infiltration of lymphocytes and macrophages. By immuno-EM perforin were often observed in the granules of lymphocytes. The lymphocytes were sometimes in close contact with plasma membrane of cardiocytes. In pfk mice, cardiocyte necrosis was less than in wild mice, although significant number of lymphocytes infiltrated in the myocardium. These findings suggest that perforin plays an important role in the development of lymphcyte-mediated cardiocyte injury.(2)Enteroviral RNA Replicatin in 26 Cases of Dilated Cardiomyopathy (DCM) with Refractory Heart FailureWe performed light microscopic in situ hybridization (ISH) and virological analyses of myocardial specimens obtained by partial left ventriculectomy. Myocardial specimens were tested for the presence and localization of enteroviral RNA in the myocardium by PCR and ISH. In PCR studies, both sense and antisense viral RNA were detected in the myocardium of seven patients(38%). The presence of these RNAs indicates active viral replication in the myocardium. On ISH, 3 patients had evidence of active replication of enteroviral genomes. Viral signals were found in degenerating cardiocytes, interstitial inflammatory cells and endothelial cells of small vessels. We detected both sense and antisense enteroviral RNA in various myhocardial lesions. Our results suggest that active viral replication plays a role in the development of myocardial lesions in DCM patients.