Wilson G L, Bellomo S C, Craighead J E
Diabetologia. 1983 Jan;24(1):38-41. doi: 10.1007/BF00275945.
The M variant of encephalomyocarditis virus (EMC) produces a disease similar to human insulin-dependent diabetes mellitus in some but not all strains of mice. This diabetogenic M variant was found to induce fivefold more interferon than non-diabetogenic strains of EMC in cultures of mouse L 929 fibroblasts. When interferon induced by the M variant was added to monolayers of B cells from both diabetes-'susceptible' CD-1 mice and 'resistant' C57 bl/6 mice before EMC infection, B cell damage and virus replication were delayed. In addition, viral production in B cell cultures from C57 bl/6 mice was reduced five- to tenfold. A similar effect was not found when cultures from CD-1 mice were treated with interferon. Thus, interferon might play an important role in modulating the severity of the initial infection of B cells.
脑心肌炎病毒（EMC）的M变种在部分而非所有品系的小鼠中会引发一种类似于人类胰岛素依赖型糖尿病的疾病。在小鼠L 929成纤维细胞培养物中，这种致糖尿病的M变种所诱导产生的干扰素比非致糖尿病的EMC品系多五倍。在EMC感染之前，将M变种诱导产生的干扰素添加到来自糖尿病“易感”的CD - 1小鼠和“抗性”的C57 bl/6小鼠的B细胞单层中时，B细胞损伤和病毒复制会延迟。此外，C57 bl/6小鼠B细胞培养物中的病毒产生量减少了五至十倍。用干扰素处理CD - 1小鼠的培养物时未发现类似效果。因此，干扰素可能在调节B细胞初始感染的严重程度方面发挥重要作用。
