Rabausch-Starz I, Neu N, Müller-Hermelink H K
Pathologisches Institut, Universität Würzburg.
Verh Dtsch Ges Pathol. 1990;74:398-403.
A/J mice between 15 days and 10 weeks of age were infected intraperitoneally with Coxsackievirus B3 (CVB3). To search for virus in the myocardium various methods were applied: virus isolation from the myocardium, RNA extraction for dot blot hybridization and in situ hybridization. Two different RNA probes, one specific for CVB3 the other cross-reacting with other enteroviruses, were radioactively labeled with 35S or 32P by in vitro transcription. In paraffin sections histological alterations were assessed semiquantitatively. The animals developed acute myocarditis with myolysis and virus in the myocardium until 14 days after infection. The second stage of the disease was characterized by a persistent inflammatory infiltrate. At this stage no virus could be shown in the myocardium. Antibodies against cardiac myosin appeared 16 days after infection. Autoimmune mechanisms thus seem to be a most relevant factor for persistent inflammation after the acute viral phase of the disease.
15日龄至10周龄的A/J小鼠经腹腔感染柯萨奇病毒B3（CVB3）。为了在心肌中寻找病毒，应用了多种方法：从心肌中分离病毒、提取RNA用于斑点杂交和原位杂交。两种不同的RNA探针，一种对CVB3特异，另一种与其他肠道病毒交叉反应，通过体外转录用35S或32P进行放射性标记。在石蜡切片中，对组织学改变进行半定量评估。感染后14天内，动物出现急性心肌炎，伴有肌溶解和心肌中的病毒。疾病的第二阶段以持续的炎症浸润为特征。在此阶段，心肌中未发现病毒。感染后16天出现抗心肌肌凝蛋白抗体。因此，自身免疫机制似乎是疾病急性期后持续炎症的一个最相关因素。
