Abstract
Coxsackievirus B4 (CB4) infection in infant ICR Swiss mice induces synchronous peaks in both virus titres and pathologic changes in the heart. Among surviving mice, transmural necrosis is followed by fibrosis and ventricular aneurysm. Rabbit antimouse thymocyte serum (ATS) was given before CB4 infection to determine the effects of thymus-dependent functions upon the course of disease. The mortality in ATS-treated mice was 75.9% (65 of 83 mice died) compared to 21.3% (16 of 75 mice died) in normal rabbit serum-treated controls. Pathologic studies showed that ATS-treated mice had more extensive myofibre necrosis and subsequent mineralization, but during the first 10 days of infection, leukocytic infiltration was decreased. Splenic follicles were not present until the 17th day after infection in this treated group. Serum CB4-neutralizing antibodies were similar in mice from the group treated with ATS and normal rabbit serum. These findings indicate that ATS-suppressible functions contribute importantly to virus elimination, perhaps by an increase in macrophage phagocytosis of CB4.
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