COXSACKIEVIRUS B-3 MYOCARDITIS - IDENTIFICATION OF DIFFERENT PATHOGENIC MECHANISMS IN DBA/2 AND BALB/C MICE

  • 1 February 1986
    • journal article
    • research article
    • Vol. 122  (2) , 284-291
Abstract
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 C57B1/6 (H-2b) animals results in minimal myocarditis despite equivalent heart virus titers in the three strains. 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.