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1
Mechanisms determining innate resistance to ectromelia virus infection in C57BL mice.决定C57BL小鼠对埃可病毒感染天然抗性的机制。
Infect Immun. 1983 Sep;41(3):1391-4. doi: 10.1128/iai.41.3.1391-1394.1983.
2
The cell-mediated immune response to ectromelia virus infection. I. Kinetics and characteristics of the primary effector T cell response in vivo.对埃可病毒感染的细胞介导免疫反应。I. 体内主要效应T细胞反应的动力学和特征。
Cell Immunol. 1976 Mar 15;22(2):271-82. doi: 10.1016/0008-8749(76)90029-0.
3
H-2-linked control of resistance to ectromelia virus infection in B10 congenic mice.B10同源小鼠中H-2连锁的抗痘苗病毒感染抗性控制。
Immunogenetics. 1983;18(3):255-65. doi: 10.1007/BF00952964.
4
Genetic factors in the stimulation of T cell responses against ectromelia virus-infected cells: role of H-2K, H-2D, and H-2I genes.刺激针对感染痘苗病毒细胞的T细胞反应中的遗传因素：H-2K、H-2D和H-2I基因的作用。
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Effects of solid tumors on the resistance of mice to viral and bacterial infections.实体瘤对小鼠抵抗病毒和细菌感染能力的影响。
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Depression of protective mechanism during the early phase of a viral infection in tumor-bearing mice and prevention by PSK.荷瘤小鼠病毒感染早期保护机制的抑制及PSK的预防作用
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Mousepox in inbred mice innately resistant or susceptible to lethal infection with ectromelia virus. IV. Studies with the Moscow strain.对埃可病毒致死性感染具有先天抗性或易感性的近交系小鼠中的鼠痘。IV. 莫斯科毒株的研究。
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Abrogation of resistance to severe mousepox in C57BL/6 mice infected with LP-BM5 murine leukemia viruses.C57BL/6小鼠感染LP-BM5鼠白血病病毒后对重症鼠痘抵抗力的消除。
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Genetic study on susceptibility of different mouse lines to ectromelia virus.不同品系小鼠对痘苗病毒易感性的遗传学研究。
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Chromosomal locations and gonadal dependence of genes that mediate resistance to ectromelia (mousepox) virus-induced mortality.介导对埃可病毒（鼠痘）病毒诱导死亡抵抗力的基因的染色体定位和性腺依赖性
J Virol. 1991 Apr;65(4):1946-51. doi: 10.1128/JVI.65.4.1946-1951.1991.

引用本文的文献

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Enhanced resistance in STAT6-deficient mice to infection with ectromelia virus.STAT6基因缺陷小鼠对埃可病毒感染的抵抗力增强。
Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6812-7. doi: 10.1073/pnas.111151098. Epub 2001 May 22.
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Expression of mouse interleukin-4 by a recombinant ectromelia virus suppresses cytolytic lymphocyte responses and overcomes genetic resistance to mousepox.重组埃可病毒表达小鼠白细胞介素-4可抑制细胞溶解性淋巴细胞反应并克服对鼠痘的遗传抗性。
J Virol. 2001 Feb;75(3):1205-10. doi: 10.1128/JVI.75.3.1205-1210.2001.
3
Identification of nitric oxide synthase 2 as an innate resistance locus against ectromelia virus infection.一氧化氮合酶2作为抗痘苗病毒感染的先天抗性基因座的鉴定。
J Virol. 1998 Sep;72(9):7703-6. doi: 10.1128/JVI.72.9.7703-7706.1998.
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Differential pathogenesis of lethal mousepox in congenic DBA/2 mice implicates natural killer cell receptor NKR-P1 in necrotizing hepatitis and the fifth component of complement in recruitment of circulating leukocytes to spleen.同源DBA/2小鼠中致死性鼠痘的差异发病机制表明，自然杀伤细胞受体NKR-P1与坏死性肝炎有关，而补体第五成分与循环白细胞向脾脏募集有关。
Am J Pathol. 1997 Apr;150(4):1407-20.
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Different roles for CD4+ and CD8+ T lymphocytes and macrophage subsets in the control of a generalized virus infection.CD4+和CD8+ T淋巴细胞以及巨噬细胞亚群在控制全身性病毒感染中的不同作用。
J Virol. 1996 Dec;70(12):8301-9. doi: 10.1128/JVI.70.12.8301-8309.1996.
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Granzyme A is critical for recovery of mice from infection with the natural cytopathic viral pathogen, ectromelia.颗粒酶A对于小鼠从自然细胞病变性病毒病原体——埃可病毒感染中恢复至关重要。
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7
Importance of interferons in recovery from mousepox.干扰素在小鼠痘恢复过程中的重要性。
J Virol. 1993 Jul;67(7):4214-26. doi: 10.1128/JVI.67.7.4214-4226.1993.
8
Ectromelia virus replication in major target organs of innately resistant and susceptible mice after intravenous infection.静脉感染后，痘苗病毒在先天抗性和易感小鼠主要靶器官中的复制
Arch Virol. 1993;129(1-4):65-75. doi: 10.1007/BF01316885.
9
H-2-linked control of resistance to ectromelia virus infection in B10 congenic mice.B10同源小鼠中H-2连锁的抗痘苗病毒感染抗性控制。
Immunogenetics. 1983;18(3):255-65. doi: 10.1007/BF00952964.
10
Abrogation of resistance to severe mousepox in C57BL/6 mice infected with LP-BM5 murine leukemia viruses.C57BL/6小鼠感染LP-BM5鼠白血病病毒后对重症鼠痘抵抗力的消除。
J Virol. 1987 Feb;61(2):383-7. doi: 10.1128/JVI.61.2.383-387.1987.

本文引用的文献

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Mouse-pox; infectious ectromelia of mice; a review.鼠痘；小鼠传染性缺肢症；综述
J Immunol. 1949 Dec;63(4):341-73.
2
GROWTH OF VIRULENT AND ATTENUATED ECTROMELIA VIRUS IN CULTURED MACROPHAGES FROM NORMAL AND ECTROMELIAIMMUNE MICE.强毒和减毒鼠痘病毒在正常及对鼠痘免疫小鼠的培养巨噬细胞中的生长情况
J Immunol. 1964 Jun;92:837-42.
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THE RESISTANCE OF A2G MICE TO MYXOVIRUSES.A2G小鼠对黏液病毒的抵抗力。
J Immunol. 1963 Jun;90:942-51.
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Histopathogenesis of mousepox. II. Cutaneous infection.鼠痘的组织病理学发病机制。II. 皮肤感染。
Br J Exp Pathol. 1962 Oct;43(5):462-8.
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Identification of peritoneal macrophages in mouse radiation chimeras.小鼠辐射嵌合体中腹膜巨噬细胞的鉴定。
Transplantation. 1963 Apr;1:217-23. doi: 10.1097/00007890-196301020-00009.
6
Macrophages as a cellular expression of inherited natural resistance.巨噬细胞作为遗传性天然抵抗力的一种细胞表现形式。
Proc Natl Acad Sci U S A. 1962 Feb;48(2):160-5. doi: 10.1073/pnas.48.2.160.
7
Studies on the innate resistance of mice to infection with mousepox. I. Resistance and antibody production.小鼠对鼠痘感染的先天抵抗力研究。I. 抵抗力与抗体产生。
Aust J Exp Biol Med Sci. 1960 Aug;38:271-88. doi: 10.1038/icb.1960.29.
8
Hematopoietic origin of macrophages as studied by chromosome markers in mice.通过小鼠染色体标记研究巨噬细胞的造血起源
J Exp Med. 1968 May 1;127(5):943-52. doi: 10.1084/jem.127.5.943.
9
The origin of alveolar macrophages in mouse radiation chimeras.小鼠辐射嵌合体中肺泡巨噬细胞的起源。
J Exp Med. 1972 Sep 1;136(3):630-43. doi: 10.1084/jem.136.3.630.
10
Mechanisms of recovery from a generalized viral infection: mousepox. 3. Regression infectious foci.全身性病毒感染（鼠痘）的恢复机制。3. 感染灶的消退
J Exp Med. 1971 May 1;133(5):1090-104. doi: 10.1084/jem.133.5.1090.

决定C57BL小鼠对埃可病毒感染天然抗性的机制。

Mechanisms determining innate resistance to ectromelia virus infection in C57BL mice.

作者信息

O'Neill H C, Blanden R V

出版信息

Infect Immun. 1983 Sep;41(3):1391-4. doi: 10.1128/iai.41.3.1391-1394.1983.

DOI:10.1128/iai.41.3.1391-1394.1983
PMID:6309671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC264656/
Abstract

The mechanism for innate resistance to ectromelia virus, which is controlled by a single gene in C57BL mice, was investigated. The cells or factors involved appear to be radioresistant and to impose an early barrier to viral penetration and spread via lymphatics or blood to the target organs, i.e., liver and spleen.

摘要

研究了C57BL小鼠中由单个基因控制的对痘苗病毒先天抗性的机制。所涉及的细胞或因子似乎具有抗辐射性，并对病毒通过淋巴管或血液渗透和传播到靶器官（即肝脏和脾脏）形成早期屏障。