CORONAVIRUS-INDUCED DEMYELINATION OCCURS IN THE PRESENCE OF VIRUS-SPECIFIC CYTOTOXIC T-CELLS
CORONAVIRUS-INDUCED DEMYELINATION OCCURS IN THE PRESENCE OF VIRUS-SPECIFIC CYTOTOXIC T-CELLS
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DOI：
10.1006/viro.1994.1237
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发表时间：
1994-05-01
期刊：
影响因子：
3.7
通讯作者：
PERLMAN, S
中科院分区：
文献类型：
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作者：
CASTRO, RF;EVANS, GD;PERLMAN, S
用小鼠肝炎病毒株JHM（MHV-JHM）感染的C57 B1/6小鼠而不是BALB/c小鼠发生迟发性、有症状的脱髓鞘性脑脊髓炎。在这份报告中，我们的特点是抗病毒细胞毒性T细胞在中枢神经系统和脾脏在急性和慢性阶段的MHV感染。数据显示，C57 B1/6小鼠显示出对表面（S）糖蛋白的细胞毒性T细胞（CTL）应答，并且这种应答可以在从急性和持续感染MHV-JHM的小鼠的脑和脊髓分离的淋巴细胞中证明。因此，慢性感染动物中枢神经系统中存在的抗S CTL活性不足以防止脱髓鞘过程。先前已经显示BALB/c小鼠产生针对核衣壳（N）蛋白的CTL应答（Stohlman等人，1992年）。由于C57 B1/6小鼠不对N蛋白产生应答，因此使用H-2基因座中重组的B10.A（18 R）小鼠评估N特异性应答在预防迟发性疾病中的作用。这些小鼠含有D和L基因座的d等位基因，并表现出针对N蛋白的CTL应答。然而，与BALB/e小鼠不同，这些动物发生迟发性症状性疾病。这些结果表明，N-特异性反应是部分保护对脱髓鞘疾病的发展，但其他因素也可能参与。(C)1994年出版社出版。
C57Bl/6, but not BALB/c, mice infected with mouse hepatitis virus strain JHM (MHV-JHM) develop a late onset, symptomatic demyelinating encephalomyelitis. In this report, we characterized anti-viral cytotoxic T cells in the central nervous system and spleen during the acute and chronic stages of the MHV infection. The data show that C57Bl/6 mice display a cytotoxic T cell (CTL) response to the surface (S) glycoprotein and this response can be demonstrated in lymphocytes isolated from the brains and spinal cords of mice both acutely and persistently infected with MHV-JHM. Thus, the anti-S CTL activity present in the central nervous system of chronically infected animals is not sufficient to prevent the demyelinating process. BALB/c mice have been shown previously to mount a CTL response against the nucleocapsid (N) protein (Stohlman et al., 1992). Since C57Bl/6 mice do not mount a response to the N protein, the role of the N-specific response in preventing the late onset disease was assessed using B10.A(18R) mice, recombinant in the H-2 locus. These mice contain the d alleles of the D and L loci and exhibit a CTL response against the N protein. However, unlike the BALB/e mice, these animals develop the late onset symptomatic disease. These results suggest that the N-specific response is partially protective against the development of the demyelinating disease, but that additional factors are also likely to be involved. (C) 1994 Academic Press, Inc.