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通过给ＢＡＬＢ／Ｃ小鼠腹腔接种ＣＶＢ３ｍ后３、６、９、１２、１５、３０天分批随机处死小鼠，取心脏进行检测发现：感染后９～１５天，病毒性心肌炎（ＶＭＣ）检出率可达９２．３０％。感染后３～９天，心肌中可分离出病毒，而病毒核酸（ＣＶＢＲＮＡ）可持续存在于感染后３个月。应用电镜、原位末端标记法（ＴＵＮＥＬ）及免疫组化法检测发现：ＶＭＣ鼠心肌中可见心肌细胞和血管内皮细胞凋亡及ＴＧＦ－β１和Ｃ－ｍｙｃ蛋白的表达。感染后９～１５天，三者阳性率分别为７５．８６％、７２．４１％和８２．７６％，且分布区域基本一致。Ｐ５３蛋白摄影性率为１．９２％，无统计学意义。实验结果表明：ＣＶＢ３ｍ可诱发ＢＡＬＢ／Ｃ小鼠ＶＭＣ，而细胞凋亡可能参与ＶＭＣ的发生与发展。ＣＶＢ３ｍ、ＣＶＢＲＮＡ、ＴＧＦ－β１和Ｃ－ｍｙｃ蛋白可能在ＶＭＣ细胞凋亡调控机制中起一定作用。进而揭示细胞凋亡可能与ＤＣＭ、克山病的病程有关
The BALB / C mice were sacrificed on days 3, 6, 9, 12, 15 and 30 after inoculation of CVB3m by intraperitoneal inoculation. The heart was taken for detection. The results showed that at 9-15 days after infection, viral myocarditis Rate up to 92.30%. 3 to 9 days after infection, the virus can be isolated from the myocardium, while the viral nucleic acid (CVBRNA) persists at 3 months after infection. Electron microscopy, TUNEL and immunohistochemistry showed that apoptosis of cardiomyocytes and vascular endothelial cells and expression of TGF-β1 and C-myc were observed in myocardium of VMC. 9 to 15 days after infection, the positive rates of the three were 75.86%, 72.41% and 82.76%, respectively, and the distribution areas were basically the same. P53 protein imaging rate was 1.92%, no statistical significance. The experimental results show that: CVB3m can induce VMC in BALB / C mice, and apoptosis may be involved in the occurrence and development of VMC. CVB3m, CVBRNA, TGF-β1 and C-myc proteins may play a role in the regulation of VMC apoptosis. Further revealing that apoptosis may be related to DCM, Keshan disease duration