| First Author | Grun JB | Year | 1988 |
| Journal | Microb Pathog | Volume | 4 |
| Issue | 6 | Pages | 417-30 |
| PubMed ID | 2848174 | Mgi Jnum | J:24867 |
| Mgi Id | MGI:72607 | Doi | 10.1016/0882-4010(88)90027-7 |
| Citation | Grun JB, et al. (1988) Pathogenesis of acute myocardial necrosis in inbred mice infected with coxsackievirus B3. Microb Pathog 4(6):417-30 |
| abstractText | The pathogenesis of myocardial necrosis due to CB3W infection was studied in BALB/c and C3H/HeJ mice. BALB/c mice infected with 5 x 10(4) pfu were found to die of massive hepatic coagulative necrosis before myocardial changes occurred. Reducing the inoculum size to 5 x 10(2) pfu resulted in sublethal hepatic involvement and multifocal myocardial coagulative necrosis by day 7 p.i. In contrast, C3H/HeJ mice survived infection and developed multifocal myocardial coagulative necrosis, but not liver disease following inoculation with as much as 5 x 10(6) pfu of CB3W. As with BALB/c mice infected with 5 x 10(2) pfu, myocardial lesions became apparent in C3H/HeJ mice a few days after peak cardiac virus titer was attained. Minimal inflammatory infiltrate was seen following development of cellular necrosis and was restricted to the areas of virus-induced pathologic change. However, no evidence was found for virus-specific cytotoxic T cell activity or for delayed type hypersensitivity responses. Furthermore, myocardial necrosis in CB3W-infected, T cell-depleted C3H/HeJ mice was as severe as in CB3W-infected, immunocompetent mice. These data have led us to conclude that cardiac lesions were due to virus-induced cytopathology rather than immunopathogenic mechanisms. |
