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培养的新生BALB/c小鼠搏动心肌细胞感染柯萨奇B-2病毒4h加同种小鼠腹腔接种该病毒7d后的脾细胞共同孵育1d,后者能轻度加重被感染心肌细胞的超微结构改变,包括局部细胞膜边界模糊;细胞质内呈较为严重的胞浆浓缩、不均一和空隙形成及闰盘解离等。小鼠心肌细胞感染柯萨奇B-2病毒3d,其超微结构改变较感染4h者严重。实验结果提示T细胞介导免疫及病毒本身在急性病毒性心肌炎的发病中都起重要作用。
The cultured neonatal BALB/c mouse beating cardiomyocytes were infected with Coxsackie B-2 virus for 4 h and the same mice were inoculated intraperitoneally with the virus for 7 days. The spleen cells were incubated for 1 day, and the latter could slightly aggravate the supercardiocytes of the infected cardiomyocytes. Microstructure changes included blurring of local cell membrane boundaries; cytoplasm showed more severe cytoplasmic condensation, inhomogeneous and void formation, and disc dissociation. The mouse cardiomyocytes were infected with Coxsackie B-2 virus for 3 days, and their ultrastructural changes were more severe than those infected with 4 h. The experimental results suggest that T cell-mediated immunity and the virus itself play an important role in the pathogenesis of acute viral myocarditis.