The role of T cells in mouse cytomegalovirus myocarditis

Abstract

BALB/c mice infected with murine cytomegalovirus (MCMV) developed myocarditis. Athymic nu/nu mice infected with the virus did not develop myocarditis, in contrast to heterozygous T-cell competent nu/+mice. MCMV-infected BALB/c mice given cyclosporin A(CsA) a drug which inhibits the activation of T cells, showed a delay in the development of myocarditis relative to CsA-untreated mice infected with MCMV. However, BALB/c mice infected with MCMV, regardless of CsA treatment, developed both anti-MCMV antibodies and autoantibodies. Nu/nu mice infected with MCMV did not produce the anti-MCMV antibody response or the multiple autoantibody response which was observed in nu/+ MCMV-infected mice. Both nu/nu and CsA-treated animals displayed greater organ distribution of viral antigen than control MCMV-infected animals. These results suggest that the presence of a thymus is required for both the development of myocarditis and the multiple autoantibody response, which includes autoantibodies to cardiac muscle, and that CsA immunosuppression does not abrogate either myocarditis or the antibody response in mice following MCMV infection.