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Coxsackievirus B3 (CVB3) infections induce myocardial inflammation which is presumably mediated by autoimmune mechanisms in the experimental murine model. Naturally occurring antibodies that also bind to myocytes have been identified that can either abrogate or enhance cardiac injury by modulating the immune response. Monoclonal antibodies derived from CVB3-infected mice were immobilized to plastic and overlaid with spleen cells obtained from mice infected with 5 x 10(4) plaque forming units of CVB3 0 to 8 days earlier. Controls consisted of either myocytes or virus adsorption monolayers. After incubation, non-adherent lymphocytes were removed, the adherent cells were recovered and cultured on either virus or myocytes for 48 h at 37 degrees C. The lymphocytes were removed and any antibody binding to the virus or myocytes was detected using goat anti-mouse IgG and IgM in a urease enzyme-linked immunoadsorption assay (ELISA). The original unfractionated spleen cell population added directly to the ELISA wells showed reactivity to both virus and myocytes. Cells adsorbed to myocytes made primarily myocyte-reactive antibody and cells adsorbed to virus made primarily virus-reactive antibody. Cells adsorbed to the heart-reactive mAB (10A1) made primarily virus-specific antibody suggesting this autoantibody might be an anti-idiotype of the virus-reactive response.
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