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骨髓嵌合体揭示了非H-2造血细胞对泰勒氏病毒持续感染易感性的控制。

Bone marrow chimeras reveal non-H-2 hematopoietic control of susceptibility to Theiler's virus persistent infection.

作者信息

Aubagnac Stéphanie, Brahic Michel, Bureau Jean-François

机构信息

Unité des Virus Lents, CNRS URA 1930, Institut Pasteur, 75724 Paris Cedex 15, France.

出版信息

J Virol. 2002 Jun;76(11):5807-12. doi: 10.1128/jvi.76.11.5807-5812.2002.

DOI:10.1128/jvi.76.11.5807-5812.2002
PMID:11992010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC137043/
Abstract

The DA strain of Theiler's murine encephalomyelitis virus persists in the white matter of the spinal cords of susceptible mice. Previous results showed that the difference in susceptibility to viral persistence between the susceptible SJL/J strain and the resistant B10.S strain was due to multiple non-H-2 loci. The respective roles of hematopoietic and nonhematopoietic cells in this difference have been evaluated with bone marrow chimeras. The results show that non-H-2 loci with a major effect on susceptibility are expressed in hematopoietic cells. However, the study of the SJL.B10-D10Mit180-D10Mit74 congenic line suggests that other loci expressed in nonhematopoietic cells also play a role.

摘要

泰勒氏小鼠脑脊髓炎病毒的DA株在易感小鼠脊髓的白质中持续存在。先前的结果表明,易感的SJL/J株和抗性的B10.S株对病毒持续感染的易感性差异是由多个非H-2基因座引起的。已经用骨髓嵌合体评估了造血细胞和非造血细胞在这种差异中的各自作用。结果表明,对易感性有主要影响的非H-2基因座在造血细胞中表达。然而,对SJL.B10-D10Mit180-D10Mit74同源系的研究表明,在非造血细胞中表达的其他基因座也起作用。

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J Virol. 2002 Jun;76(11):5807-12. doi: 10.1128/jvi.76.11.5807-5812.2002.
2
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本文引用的文献

1
Viral load increases in SJL/J mice persistently infected by Theiler's virus after inactivation of the beta(2)m gene.在β2m基因失活后,持续感染泰勒氏病毒的SJL/J小鼠体内病毒载量增加。
J Virol. 2001 Aug;75(16):7723-6. doi: 10.1128/JVI.75.16.7723-7726.2001.
2
High numbers of viral RNA copies in the central nervous system of mice during persistent infection with Theiler's virus.在感染泰勒氏病毒的小鼠持续感染期间,其中枢神经系统中存在大量病毒RNA拷贝。
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Roles of the H-2D(b) and H-K(b) genes in resistance to persistent Theiler's murine encephalomyelitis virus infection of the central nervous system.H-2D(b)和H-K(b)基因在抵抗中枢神经系统持续性泰勒氏鼠脑脊髓炎病毒感染中的作用。
J Gen Virol. 2001 May;82(Pt 5):1043-1047. doi: 10.1099/0022-1317-82-5-1043.
4
H-2D(b-/-) mice are susceptible to persistent infection by Theiler's virus.H-2D(b-/-)小鼠易受泰勒氏病毒的持续感染。
J Virol. 2000 Jun;74(12):5470-6. doi: 10.1128/jvi.74.12.5470-5476.2000.
5
Viral load and a locus on chromosome 11 affect the late clinical disease caused by Theiler's virus.病毒载量和11号染色体上的一个基因座会影响由泰勒氏病毒引起的晚期临床疾病。
J Virol. 1999 Oct;73(10):7965-71. doi: 10.1128/JVI.73.10.7965-7971.1999.
6
The Th1/Th2 balance does not account for the difference of susceptibility of mouse strains to Theiler's virus persistent infection.Th1/Th2平衡并不能解释小鼠品系对泰勒氏病毒持续感染易感性的差异。
J Immunol. 1999 Jun 15;162(12):7330-4.
7
Two loci, Tmevp2 and Tmevp3, located on the telomeric region of chromosome 10, control the persistence of Theiler's virus in the central nervous system of mice.位于10号染色体端粒区域的两个基因座Tmevp2和Tmevp3控制着泰勒氏病毒在小鼠中枢神经系统中的持续性。
Genetics. 1999 May;152(1):385-92. doi: 10.1093/genetics/152.1.385.
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Genetics of susceptibility to Theiler's virus infection.泰勒氏病毒感染易感性的遗传学
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Protein 2A is not required for Theiler's virus replication.Theiler病毒复制不需要蛋白质2A。
J Virol. 1997 Dec;71(12):9549-56. doi: 10.1128/JVI.71.12.9549-9556.1997.
10
The immune system preferentially clears Theiler's virus from the gray matter of the central nervous system.免疫系统优先从中枢神经系统的灰质中清除泰勒氏病毒。
J Virol. 1997 Nov;71(11):8592-601. doi: 10.1128/JVI.71.11.8592-8601.1997.