Matsumori A, Kawai C, Crumpacker C S, Abelmann W H
Department of Internal Medicine, Kyoto University, Japan.
Jpn Circ J. 1987 Jun;51(6):661-4. doi: 10.1253/jcj.51.661.
An animal model of dilated cardiomyopathy following encephalomyocarditis (EMC) virus has been developed. Virus was isolated from mouse hearts and viral antigens were detected in the myocardium until the second week of infection, but neither was found thereafter. Differences were found among different strains of mice in the frequency of occurrence and severity of myocarditis, and even in the character of the pathologic lesions. Thus, genetic factors may play an important role in the pathogenesis. Autoantibodies against heart developed and the distribution of cardiac myosin isoenzymes was altered during the course of myocarditis. Virus, vaccine, maternal vaccination, recombinant interferon alpha A/D and ribavirin were effective in protecting the mice from developing myocarditis. This animal model is suitable for studying the pathogenesis of viral myocarditis and evaluating preventive and therapeutic interventions of the condition.
已经建立了脑心肌炎(EMC)病毒感染后扩张型心肌病的动物模型。病毒从小鼠心脏中分离出来,在感染的第二周之前可在心肌中检测到病毒抗原,但此后均未发现。在不同品系的小鼠中,心肌炎的发生率、严重程度甚至病理病变特征都存在差异。因此,遗传因素可能在发病机制中起重要作用。在心肌炎过程中出现了针对心脏的自身抗体,并且心肌肌球蛋白同工酶的分布发生了改变。病毒、疫苗、母体接种、重组干扰素αA/D和利巴韦林可有效保护小鼠免于发生心肌炎。该动物模型适用于研究病毒性心肌炎的发病机制以及评估该疾病的预防和治疗干预措施。