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European Heart Journal 1991 12(Supplement D):124-129; doi:10.1093/eurheartj/12.suppl_D.124
Copyright © 1991 by the European Society of Cardiology.
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© 1991 The European Society of Cardiology

Anti-coxsackievirus B3 neutralizing antibodies with pathological potential

C. J. Gauntt, H. M. Arizpe, A. L. Higdon, R. Rozek, R. Crawley and M. W. Cunningham

Departments of Microbiology, Pathology and Laboratory Animal Resources, The University of Texas Health Science Center at San Antonio San Antonio, Texas and Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center Oklahoma City, Oklahoma, U.S.A.

Address for correspondence: Charles J. Gauntt, Ph.D., The University of Texas Health Science Center at San Antonio, Department of Microbiology, 7703 Floyd Curt Drive, San Antonio, Texas 78284-7758, U.S.A.

Adolescent CD-1 mice inoculated with coxsackievirus B3 (CVB33) will develop acute myocarditis with focal lesions by 7 days post-inoculation (p.i.). Administration of murine sera containing anti-CVB33-neutralizing antibodies into CVB33-inoculated mice at 3 days p.i. will exacerbate myocarditis, suggesting the presence of pathological antibodies. To study potential pro-inflammatory properties of virus-induced antibodies, a panel of anti-CVB33-neutralizing monoclonal antibodies (mAbs) was generated. Several studies demonstrated shared epitopes between CVB33 particles and cultured murine cardiac or neonatal skin fibroblasts: (1) one or more mAbs bound to cultured cardiac fibroblasts; (2) several mAbs can participate in complement-mediated lysis of neonatal skin fibroblasts; and (3) at least one mAbs stimulated synthesis of a macrophage chemoattractant from cultured neonatal skin fibroblasts. Injection of one mAb in three doses, each of about 5 µg, into adolescent male CD-1 mice induced focal myocarditic lesions which were similar to CVB33-induced lesions. One mAb induced a diffuse interstitial hypercellularity in most mice and two mAbs did not induce detectable cardiopathology. These data suggest that some anti-CVB3m neutralizing idiotypes (antibodies) which initially can provide protection via virus clearance mechanisms can also bind to cross-reacting epitopes on normal tissues. Binding of antibodies to normal heart tissues could stimulate proinflammatory reactions by several mechanisms and sustain myocarditis.

Key Words: Myocarditis • coxsackievirus • animal model • autoimmune disease • monoclonal antibodies • shared epitopes • myosin epitopes • mechanisms of pathogenicity


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