Hufnagel G, Chapman N, Tracy S
Philipps University of Marburg, Department of Cardiology, Germany.
Eur Heart J. 1995 Dec;16 Suppl O:18-9. doi: 10.1093/eurheartj/16.suppl_o.18.
The most extensively studied animal model of coxsackievirus B3 (CVB3)-induced inflammatory heart muscle disease is the murine model. In the acute and chronic phase of the disease, it has been suggested that autoimmune mechanisms play a major role in the pathogenesis of the disease. In this study, C3H mice without functional T- and B-lymphocytes (C3H SCID) were inoculated either with a cardiovirulent (CVB3/20) or a non-cardiovirulent (CVB3/0) strain of coxsackievirus B3. Both viruses caused myocarditis in SCID mice. Furthermore, it could be demonstrated, that CVB3/0 had mutated to a cardiovirulent phenotype, able to cause myocarditis in immunocompetent mice.
柯萨奇病毒B3(CVB3)诱导的炎症性心肌病研究最为广泛的动物模型是小鼠模型。在该疾病的急性期和慢性期,有人提出自身免疫机制在疾病发病机制中起主要作用。在本研究中,将无功能性T淋巴细胞和B淋巴细胞的C3H小鼠(C3H SCID)接种了具有心脏毒性的(CVB3/20)或无心脏毒性的(CVB3/0)柯萨奇病毒B3毒株。两种病毒均在SCID小鼠中引起了心肌炎。此外,还可以证明,CVB3/0已突变为具有心脏毒性的表型,能够在免疫活性小鼠中引起心肌炎。