抄録
This review delineates the impact of molecular biology on the diagnosis and pathogenesis of coxsackie B viral myocarditis. The etiological role of the coxsackie B viruses in acute myocarditis is well established. A hallmark of most coxsackie B virus infections is extension cytopathology of the host cell. Recent evidence from studies of a nonlytic infection show that a coxsackie B virus can alter an infected cell which results from persistent infection. There are two other mechanisms for cardiac injury during coxsackie B virus infection. The first phase usually occurs during the first week after infection, and is probably a direct result of lytic infection to the myocytes and of the accompanying inflammatory response. The second phase of coxsackie B virus-induced myocarditis is accompanied by an autoimmune response to heart tissue, which occurs 3 weeks after infection. Genetic factors probably play a role, but their contribution has not yet been evaluated.
