Immunological and virological study of viral myocarditis and dilated cardiomyopathy by using PCR, in situ hybridization and immunohistochemical technique

点击翻译按钮获取中文摘要

1)Murine coxsackie B3 virus myocarditis: On days 5, 7 and 9 after virus inoculation, necrotic cardiocytes were surrounded by many CD4^+ cells and macrophages (Mac), and a few CD8^+ cells. Using in situ hybridization method, coxsackie B virus cDNA signal was detected in and around the necrotic foci. Immunoelectron microscopy revealed that virus antigen and MHC1 were present in the plasma membrane, sarcoplasmic reticulum (SR) and Golgi complex of apparently intact cardiocytes on days 5, 7, 9 and 14.CD8^+ cells were conjugated with apparently viable or degenerated cardiocytes, and MHC1 was also located on the plasma membrane of their cardiocytes. Variable expression of MHC2 was found in the cell membrane of small round cells including Mac. CD4^+ cells and Mac often infiltrated in the necrotic foci. Mac were sometimes in close contact with CD4^+ cells. It has been generally assumed that cytotoxic T cells recognize both virus antigen and MHC1, and then lyse target cells in viral infection. In our experiments MHC1 appeared to be involved in development of cardiocyte lysis by CD8^+ cells. MHC2 was detected in the membrane of Mac which were often in contact with CD4^+ cells. The contact suggested an activation of helper T cells. MHC1 and MHC2 may play an important role in antigen recognition and subsequent cell-to-cell interactions in cell-mediated immunity of myocarditis.2)Myocardial biopsies from patients with viral myocarditis and dilated cardiomyopathy(CDM): T cells and natural killer cells often infiltrated in the myocardial biopsies from patients with viral myocarditis. Many CD8^+ cells sometimes were seen in the necrotic foci. In the patients with CDM a few T cells infiltrated in the myocardium, and T4/T8 ratios in the myocardium were less than 1.0. By using PCR 32% of DCM patients demonstrated coxsackie B virus RNA signals. These findings suggest that viral infection involved in pathogenesis of DCM.