Coxsackievirus B-3 myocarditis. Identification of different pathogenic mechanisms in DBA/2 and Balb/c mice

Am J Pathol. 1986 Feb;122(2):284-91.


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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies, Viral / analysis
  • Complement System Proteins / immunology
  • Coxsackievirus Infections* / genetics
  • Coxsackievirus Infections* / immunology
  • Coxsackievirus Infections* / microbiology
  • Cytotoxicity, Immunologic
  • Enterovirus B, Human / isolation & purification
  • Heart / microbiology
  • Immunoglobulin G / analysis
  • Immunoglobulin M / analysis
  • Immunosuppression
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred DBA
  • Myocarditis / etiology*
  • Myocarditis / genetics
  • Myocarditis / immunology
  • T-Lymphocytes / immunology


  • Antibodies, Viral
  • Immunoglobulin G
  • Immunoglobulin M
  • Complement System Proteins