Heemskerk M H, Schoemaker H M, Spaan W J, Boog C J
Institute of Infectious Diseases, Faculty of Veterinary Medicine, University of Utrecht, The Netherlands.
Immunology. 1995 Apr;84(4):521-7.
Coronavirus-induced acute hepatitis is a complex event and the role of different components of the immune system with regard to defined viral proteins and the course of the infection is not yet clear. We have analysed the cytotoxic T-lymphocyte (CTL) response in mouse hepatitis virus (MHV-A59) infection. Surprisingly, we detected only a very clear virus-specific major histocompatibility complex (MHC) class II-restricted cytotoxicity in mice infected with MHV-A59. We found no evidence of activation of the classical CD8+ MHC class I-restricted CTL. The virus-specific CD4+ CTL derived from two different mouse strains having different MHC haplotypes recognized the same immunodominant epitope. This epitope, comprising the amino acid residues 329-343 of the viral S-glycoprotein, was recognized both at the polyclonal level and by virus-specific CTL clones. Transfer studies using a MHV-A59-specific CD4+ CTL clone showed significant protection against a lethal challenge with MHV-A59, implicating that these CD4+ CTL play a pivotal role in the protection against MHV-A59 infections.
冠状病毒诱导的急性肝炎是一个复杂的事件，免疫系统不同组成部分针对特定病毒蛋白及感染过程所起的作用尚不清楚。我们分析了小鼠肝炎病毒（MHV-A59）感染中的细胞毒性T淋巴细胞（CTL）反应。令人惊讶的是，我们在感染MHV-A59的小鼠中仅检测到非常明显的病毒特异性主要组织相容性复合体（MHC）II类限制性细胞毒性。我们没有发现经典的CD8+ MHC I类限制性CTL被激活的证据。来自具有不同MHC单倍型的两种不同小鼠品系的病毒特异性CD4+ CTL识别相同的免疫显性表位。该表位由病毒S糖蛋白的329-343位氨基酸残基组成，在多克隆水平以及病毒特异性CTL克隆中均被识别。使用MHV-A59特异性CD4+ CTL克隆进行的转移研究显示，对MHV-A59的致死性攻击具有显著的保护作用，这表明这些CD4+ CTL在抵抗MHV-A59感染中起关键作用。
