Okada I, Matsumori A, Tomioka N, Kawai C
Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.
J Pathol. 1992 Jul;167(3):341-7. doi: 10.1002/path.1711670313.
Successive infection of coxsackievirus B3 and encephalomyocarditis virus was investigated as a disease model of chronic myocarditis. Four-week-old C3H/He mice were inoculated with coxsackievirus B3 and then inoculated with encephalomyocarditis virus at 8 weeks old. The hearts were evaluated on histopathological changes compared with those of non-infected mice and mice infected with either virus alone. At 10 weeks old, the hearts of the mice infected successively with both viruses showed co-existence of fibrosis surrounding calcified lesions and marked cellular infiltration with myocardial necrosis. These findings resembled chronic active myocarditis in humans, unlike the lesions due to either virus alone. At 12 weeks old, the hearts of all the infected mice showed fibrosis with scarce cellular infiltration. The successively infected hearts also showed a significantly higher heart weight to body weight ratio than that of the non-infected control mice, and localized wall thinning in the damaged regions. Thus, we conclude that successive infection additively causes myocardial damage that resembles chronic myocarditis and may produce a heart condition similar to dilated cardiomyopathy.
研究了柯萨奇病毒B3和脑心肌炎病毒的连续感染作为慢性心肌炎的疾病模型。给4周龄的C3H/He小鼠接种柯萨奇病毒B3,然后在8周龄时接种脑心肌炎病毒。与未感染小鼠和仅感染一种病毒的小鼠相比,对心脏进行组织病理学变化评估。在10周龄时,先后感染两种病毒的小鼠心脏显示钙化病变周围存在纤维化,伴有明显的细胞浸润和心肌坏死。这些发现类似于人类的慢性活动性心肌炎,与仅由一种病毒引起的病变不同。在12周龄时,所有感染小鼠的心脏均显示纤维化,细胞浸润稀少。先后感染的心脏与未感染的对照小鼠相比,心脏重量与体重之比也显著更高,并且在受损区域出现局部室壁变薄。因此,我们得出结论,连续感染会累加性地导致类似于慢性心肌炎的心肌损伤,并可能产生类似于扩张型心肌病的心脏状况。