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J Virol. 1996 Jul;70(7):4811-5. doi: 10.1128/JVI.70.7.4811-4815.1996.
2
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3
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J Virol. 1994 Jun;68(6):4049-52. doi: 10.1128/JVI.68.6.4049-4052.1994.
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Transcriptome analysis following neurotropic virus infection reveals faulty innate immunity and delayed antigen presentation in mice susceptible to virus-induced demyelination.神经亲和性病毒感染后的转录组分析揭示了易感染病毒诱导脱髓鞘的小鼠固有免疫缺陷和抗原呈递延迟。
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MHC class II-alpha chain knockout mice support increased viral replication that is independent of their lack of MHC class II cell surface expression and associated immune function deficiencies.MHC II 类-α链敲除小鼠支持病毒复制增加,这与其 MHC II 类细胞表面表达缺失和相关免疫功能缺陷无关。
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Protection against lethal encephalomyocarditis virus infection in the absence of serum-neutralizing antibodies.在缺乏血清中和抗体的情况下对致死性脑心肌炎病毒感染的保护作用。
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本文引用的文献

1
Theiler's virus persistence and demyelination in major histocompatibility complex class II-deficient mice.泰勒氏病毒在主要组织相容性复合体II类缺陷小鼠中的持续感染与脱髓鞘病变
J Virol. 1996 Mar;70(3):1729-37. doi: 10.1128/JVI.70.3.1729-1737.1996.
2
Theiler's virus infection of beta 2-microglobulin-deficient mice.β2-微球蛋白缺陷小鼠的泰勒氏病毒感染
J Virol. 1993 Jan;67(1):589-92. doi: 10.1128/JVI.67.1.589-592.1993.
3
Class I-deficient resistant mice intracerebrally inoculated with Theiler's virus show an increased T cell response to viral antigens and susceptibility to demyelination.用泰勒氏病毒脑内接种I类缺陷抗性小鼠,可显示出对病毒抗原的T细胞反应增强以及对脱髓鞘的易感性增加。
Eur J Immunol. 1993 Sep;23(9):2287-93. doi: 10.1002/eji.1830230935.
4
Abrogation of resistance to Theiler's virus-induced demyelination in H-2b mice deficient in beta 2-microglobulin.在缺乏β2-微球蛋白的H-2b小鼠中,对泰勒氏病毒诱导的脱髓鞘的抗性消除。
J Immunol. 1993 Jul 1;151(1):266-76.
5
FVB mice transgenic for the H-2Db gene become resistant to persistent infection by Theiler's virus.携带H-2Db基因的转基因FVB小鼠对泰勒氏病毒的持续感染产生抗性。
J Virol. 1994 Jun;68(6):4049-52. doi: 10.1128/JVI.68.6.4049-4052.1994.
6
Class II-restricted T cell responses in Theiler's murine encephalomyelitis virus-induced demyelinating disease. V. Mapping of a dominant immunopathologic VP2 T cell epitope in susceptible SJL/J mice.II类分子限制性T细胞应答在泰勒鼠脑脊髓炎病毒诱导的脱髓鞘疾病中的作用。V. 易感SJL/J小鼠中主要免疫病理VP2 T细胞表位的定位
J Immunol. 1994 Jan 15;152(2):908-18.
7
Analysis of proteolipid protein and P0 transcripts in mice infected with Theiler's virus.
Microb Pathog. 1993 Feb;14(2):123-31. doi: 10.1006/mpat.1993.1013.
8
Inhibition of Theiler's virus-mediated demyelination by peripheral immune tolerance induction.通过诱导外周免疫耐受抑制泰勒病毒介导的脱髓鞘
J Immunol. 1995 Jul 15;155(2):947-57.
9
Class II-restricted T cell responses in Theiler's murine encephalomyelitis virus-induced demyelinating disease. VI. Potentiation of demyelination with and characterization of an immunopathologic CD4+ T cell line specific for an immunodominant VP2 epitope.Ⅱ类分子限制性T细胞应答在泰勒鼠脑脊髓炎病毒诱导的脱髓鞘疾病中的作用。VI. 针对免疫显性VP2表位的免疫病理CD4⁺ T细胞系对脱髓鞘的增强作用及其特性
J Immunol. 1994 Jan 15;152(2):919-29.
10
DA strain of Theiler's murine encephalomyelitis virus induces demyelination in nude mice.泰勒氏小鼠脑脊髓炎病毒的DA毒株可在裸鼠中诱发脱髓鞘病变。
Ann Neurol. 1984 May;15(5):494-9. doi: 10.1002/ana.410150516.

用泰勒氏病毒DA株感染II类缺陷小鼠。

Infection of class II-deficient mice by the DA strain of Theiler's virus.

作者信息

Fiette L, Brahic M, Pena-Rossi C

机构信息

Unité des Virus Lents, URA 1157 Centre National de la Recherche Scientifique, Institut Pasteur, France.

出版信息

J Virol. 1996 Jul;70(7):4811-5. doi: 10.1128/JVI.70.7.4811-4815.1996.

DOI:10.1128/JVI.70.7.4811-4815.1996
PMID:8676513
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC190423/
Abstract

The DA strain of Theiler's virus causes, in susceptible strains of mice, a persistent infection of the white matter of the spinal cord accompanied by chronic inflammation and primary demyelination. In resistant strains, including all H-2b strains, mice clear the infection after 1 to 2 weeks. We inoculated RHAbetao/o mice, an H-2b strain which does not express class II molecules. We found that they are susceptible to persistent infection and that they develop foci of chronic inflammation with demyelination. However, these foci are smaller and contain fewer demyelinated axons than those observed in susceptible SJL/J or beta2m-/- mice.

摘要

泰勒氏病毒的DA毒株在易感小鼠品系中会导致脊髓白质的持续性感染,并伴有慢性炎症和原发性脱髓鞘。在包括所有H-2b品系在内的抗性品系中,小鼠在1至2周后清除感染。我们接种了RHAbetao/o小鼠,这是一种不表达II类分子的H-2b品系。我们发现它们易受持续性感染,并且会出现伴有脱髓鞘的慢性炎症病灶。然而,这些病灶比在易感的SJL/J或β2m-/-小鼠中观察到的病灶更小,且脱髓鞘轴突更少。