Fig. 1 The pathogenesis of myocarditis. Autoimmune myocarditis can be produced in genetically susceptible strains of mice by infection with coxsackievirus B3 (CB3). Myocarditis also can be induced by immunization with cardiac myosin with complete Freund’s adjuvant in the absence of an immune response to the virus7, 8. Myosin-specific T cells, present in genetically susceptible mice, are required. Both a type 1 T-helper-cell (TH1) response (cell-mediated immunity, or CMI), shown as lymphocytic infiltration of the heart, and a type 2 T-helper-cell (TH2) response, shown as myosin-specific autoantibodies, are present. The involvement of autoantibody in the disease is still uncertain. Horwitz et al. now report that virus-induced damage to the heart is necessary to initiate CB3-induced myocarditis, even in the presence of an immune response to the virus. These findings make it unlikely that a common immune response to the virus and the self antigen (‘molecular mimicry’) is responsible for this infection-induced autoimmune disease.