Chow L H
Department of Medicine, University of Western Ontario, London, Canada.
Lab Anim Sci. 1993 Apr;43(2):133-5.
The mechanism of cardiac muscle damage in virus-induced myocarditis remains to be fully understood. In particular, a direct role for viral replication has been obscured by evidence of immune-mediated injury. The combined use of severe combined immunodeficient (scid) and doubly mutant scid/beige mice of different genetic backgrounds has provided a unique opportunity to study the consequences of viral proliferation apart from the influence of immunologic responses. In these immunodeficient animals, inoculation with coxsackievirus B3 caused severe myocardial injury, indicating a profound and direct pathogenic potential of viral infection. These studies, in turn, serve to illustrate the value of the scid mutation in experimental biology, as defined among different genetic backgrounds and combined with other mutations.
病毒诱导的心肌炎中心肌损伤的机制仍有待充分了解。特别是,免疫介导损伤的证据掩盖了病毒复制的直接作用。不同遗传背景的严重联合免疫缺陷(scid)小鼠和双突变scid/米色小鼠的联合使用为研究病毒增殖的后果提供了独特的机会,而不受免疫反应的影响。在这些免疫缺陷动物中,接种柯萨奇病毒B3会导致严重的心肌损伤,表明病毒感染具有深远的直接致病潜力。反过来,这些研究也说明了scid突变在实验生物学中的价值,该突变在不同遗传背景中定义,并与其他突变相结合。