Coxsackievirus B-3 myocarditis. Identification of different pathogenic mechanisms in DBA/2 and Balb/c mice.
DBA/2 and Balb/c mice, both H-2d, develop myocardial inflammation and necrosis when infected with a heart-adapted strain of coxsackievirus Group B, Type 3. Similar inoculation of C57Bl/6 (H-2b) animals results in minimal myocarditis despite equivalent heart virus titers in the three stains. Thus, the host's genetic constitution influences the pathogenesis of the infection. Anti-mouse thymocyte serum and monoclonal Iad antibody effectively prevent myocarditis induction in DBA/2 and Balb/c mice, which demonstrates the importance of the immune system in this disease. Cytolytic T lymphocytes lysing virus-infected and uninfected myocytes and heart-reactive autoantibodies occur in both myocarditis-susceptible strains. Cellular immunity causes the myocardial injury in Balb/c mice. Complement depletion of Balb/c mice using cobra venom factor fails to alter the disease. Similar treatment of DBA/2 animals abrogates inflammation and necrosis, which suggests that heart-reactive antibodies in this strain are primarily responsible for initiating myocardial damage.
D000818:Animals; D000914:Antibodies, Viral / Q000032:analysis; D003165:Complement System Proteins / Q000276:immunology; D003384:Coxsackievirus Infections / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D003602:Cytotoxicity, Immunologic; D029822:Enterovirus B, Human / Q000302:isolation & purification; D006321:Heart / Q000382:microbiology; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D007165:Immunosuppression Therapy; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008811:Mice, Inbred DBA; D009205:Myocarditis / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D000914:Antibodies, Viral; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D003165:Complement System Proteins