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European Heart Journal 1995 16(Supplement O):56-58; doi:10.1093/eurheartj/16.suppl_O.56
Copyright © 1995 by the European Society of Cardiology.
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© 1995 The European Society of Cardiology

Coxsackievirus-induced chronic myocarditis in murine models

C. J. Gauntt*,, S. M. Tracy{dagger}, N. Chapman{dagger}, H. J. Wood*, P. C. Kolbeck{dagger}, A. G. Karaganis*, C. L. Winfrey* and M. W. Cunningham{dagger}{dagger}

* Department of Microbiology, The University of Texas Health Science Centre at San Antonio San Antonio, Texas
{dagger} Department of Pathology and Microbiology, University of Nebraska Medical Centre Omaha, Nebraska
{dagger}{dagger} Department of Microbiology and Immunology, The University of Oklahoma Health Sciences Center Oklahoma City, Oklahoma, U.S.A.

Charles J. Gauntt, PhD., Department of Microbiology. The University of Texas Health Science Centre at San Antonio, 7703 Floyd Curl Drive. San Antonio, Texas 78284-7758, US.A.

Challenge of several murine strains with two highly myocarditic variants of coxsackievirus B3 (CVB3) induced acute and chronic myocarditis, detectable at 21 and 45 days post-inoculation (p.L). In-situ hybridization of coronal heart sections showing chronic inflammation with a radiolabelled CVB3 probe detected viral genomic RNA at day 7 p.i. but rarely at 21 or 45 days p.L, suggesting few murine heart cells actively replicate virus during chronic myocardial inflammation. Data will be presented that favour an alternative hypothesis, i.e. autoimmune responses to shared epitopes among CVB3 proteins, cardiac myosin and myocardial cell surface proteins (molecular mimicry) can affect the severity of chronic inflammation. Mice inoculated with human cardiac myosin (HM) prior to a CVB3m challenge develop less myocarditis than mice inoculated with virus only, suggesting that antibodies stimulated by HM bind virus, reduce the virus burden and provide protection. Mice inoculated with HM only develop non-neutralizing antibodies against purified CVB3m particles. Several strains of mice inoculated with specific synthetic peptides of HM produce antibodies against CVB3m and/or develop cardiomyopathy. Thus antigen-challenged mice can produce antibodies which cross-react among CVB3m, HM or cardiac cells to protect or exacerbate heart disease.

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


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