The presencc of autoantibodies in the scra of patients with myocarditis has suggeted that autoimmunity is a sequela of myocarditis. In this study, we examined anti-vimentin antibodies in a murinc model of myocarditis. Four-week-old male DBA/2 mice were inoculated intraperitoneally with 10 plaque-forming units of encephalomyocarditis (EMC) virus. The surviving mice were killed on Days 0 (n = 7), 2 (n = 6), 5 (n = 6), 7 (n = 6), 9 (n = 6), 14 (n = 5), 60 (n -6) and 540 (n = 3) after virus inoculation. The presence of anti-vimentin autoantibodies in the sera of mice was determined by ELISA. The optical density (OD) of anti-vimentin IgG and IgM autoantibodies of day 0 mice was 0.03 i 0.03 and 0.12 i 0.08, respectively. when positive antibody was defined as over the mean value plus 2-standard deviations of the scra of day 0 mice, anti-vimentin IgG antibodies werc negative before day 5 but positive in all mice on day 9. Both IgG and IgM OD of the sera from day 9 mice (IgC; 0.26i0.12, IgM; 0.30k0.08) were significantly higher than thosc of the sera from day 0 mice (p<0.005) and decreased thereafter on day 14. In the chronic stage, five of six mice werc positive on day 60 and two of threc mice were positive on day 540. Although further studies arc needed to elucidate the pdthogcnetic role of anti-vimentin antibodies, these antibodies may be a parameter of the interstitial injury.