OBJECTIVE: To assess the expression of coxsackievirus B3 (CB3) myocarditis in mice with pre-existing CB4 myocardial disease. DESIGN: Double blind comparative study of CB3 myocarditis in CD1 mice with or without prior CB4 induced cardiac damage. INTERVENTIONS: Antecedent myocardial injury was produced by CB4 infection intraperitoneally at age two days. Two to three weeks later, when CB4 myocarditis was established, infected and control animals were inoculated intraperitoneally with CB3. They were then sacrificed over a 45-day period. Virus and neutralizing antibody titres were measured on days 3 and 13 after CB3 infection, respectively. The incidence of myocarditis and the intensity of histopathological changes (assessed according to a semiquantitative grading scale from 0 to 4) over a 45-day period were compared. MAIN RESULTS: Among animals with prior CB4 disease, CB3 titres were lower (2.3 +/- 1.7 versus 3.6 +/- 0.8, tissue culture infective dose 50, P = 0.05) and neutralizing antibody response was slightly higher. The incidence of myocarditis was diminished (59.1 versus 89.3%, P = 0.01) and the indices of pathological changes were lower but the differences were not significant (0.68 +/- .54 versus 1.10 +/- 0.20, 1.38 +/- 0.43 versus 1.50 +/- 0.25, 0.56 +/- 0.56 versus 1.26 +/- 0.75, 0.38 +/- 0.58 versus 1.30 +/- 0.78, 0.12 +/- 0.28 versus 0.47 +/- 0.2 on days 3, 9, 13, 30 and 45 post infection, respectively, P > 0.1). CONCLUSION: These results demonstrate that prior exposure to CB4 offers some protection from subsequent CB3 infection. Moreover, they show that antecedent CB4 myocardial damage does not predispose to a worsened expression of CB3 myocarditis.
OBJECTIVE: To assess the expression of coxsackievirus B3 (CB3) myocarditis in mice with pre-existing CB4myocardial disease. DESIGN: Double blind comparative study of CB3 myocarditis in CD1 mice with or without prior CB4 induced cardiac damage. INTERVENTIONS: Antecedent myocardial injury was produced by CB4infection intraperitoneally at age two days. Two to three weeks later, when CB4myocarditis was established, infected and control animals were inoculated intraperitoneally with CB3. They were then sacrificed over a 45-day period. Virus and neutralizing antibody titres were measured on days 3 and 13 after CB3 infection, respectively. The incidence of myocarditis and the intensity of histopathological changes (assessed according to a semiquantitative grading scale from 0 to 4) over a 45-day period were compared. MAIN RESULTS: Among animals with prior CB4 disease, CB3 titres were lower (2.3 +/- 1.7 versus 3.6 +/- 0.8, tissue culture infective dose 50, P = 0.05) and neutralizing antibody response was slightly higher. The incidence of myocarditis was diminished (59.1 versus 89.3%, P = 0.01) and the indices of pathological changes were lower but the differences were not significant (0.68 +/- .54 versus 1.10 +/- 0.20, 1.38 +/- 0.43 versus 1.50 +/- 0.25, 0.56 +/- 0.56 versus 1.26 +/- 0.75, 0.38 +/- 0.58 versus 1.30 +/- 0.78, 0.12 +/- 0.28 versus 0.47 +/- 0.2 on days 3, 9, 13, 30 and 45 post infection, respectively, P > 0.1). CONCLUSION: These results demonstrate that prior exposure to CB4 offers some protection from subsequent CB3 infection. Moreover, they show that antecedent CB4myocardial damage does not predispose to a worsened expression of CB3 myocarditis.