Miller F W, Love L A, Biswas T, McClintock P R, Notkins A L, Plotz P H
Arthritis Rheum. 1987 May;30(5):549-56. doi: 10.1002/art.1780300509.
Recent research findings implicate picornaviruses in the etiology of human polymyositis/dermatomyositis and suggest that genetic factors play a role in susceptibility to these diseases. We compared 2 variants of encephalomyocarditis (EMC) virus for their ability to induce polymyositis in adult mice, and evaluated what role the genetic background of the host plays in the degree of myositis induced. While BALB/c mice developed minimal myositis when infected with a diabetogenic variant (EMC-D), the same strain inoculated with a newly isolated myopathic variant (EMC-221A) developed viral dose-dependent elevations in muscle-associated enzymes, bilateral limb muscle weakness, and the histopathologic changes of severe polymyositis. Mice with different genetic backgrounds showed significantly different susceptibilities to EMC-221A. These data suggest that the severity of polymyositis induced by EMC virus is influenced by both the viral and host genomes.
近期研究结果表明,微小核糖核酸病毒与人类多发性肌炎/皮肌炎的病因有关,并提示遗传因素在这些疾病的易感性中起作用。我们比较了脑心肌炎(EMC)病毒的两种变体在成年小鼠中诱导多发性肌炎的能力,并评估宿主的遗传背景在诱导的肌炎程度中所起的作用。当用致糖尿病变体(EMC-D)感染时,BALB/c小鼠仅出现轻微的肌炎,而接种新分离的肌病变体(EMC-221A)的同一品系小鼠则出现与病毒剂量相关的肌肉相关酶升高、双侧肢体肌肉无力以及严重多发性肌炎的组织病理学变化。具有不同遗传背景的小鼠对EMC-221A的易感性存在显著差异。这些数据表明,EMC病毒诱导的多发性肌炎的严重程度受病毒基因组和宿主基因组的共同影响。