• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

强毒株和脱髓鞘性塞姆利基森林病毒在小鼠中枢神经系统中的增殖:对BALB/c和SJL小鼠的影响

Multiplication of virulent and demyelinating Semliki Forest virus in the mouse central nervous system: consequences in BALB/c and SJL mice.

作者信息

Smyth J M, Sheahan B J, Atkins G J

机构信息

Department of Microbiology, Moyne Institute, Trinity College, Dublin, Ireland.

出版信息

J Gen Virol. 1990 Nov;71 ( Pt 11):2575-83. doi: 10.1099/0022-1317-71-11-2575.

DOI:10.1099/0022-1317-71-11-2575
PMID:2174955
Abstract

The sites of multiplication in the mouse central nervous system (CNS) of the virulent L10 strain of Semliki Forest virus (SFV) and the L10-SFV-derived demyelinating M9 mutant were determined using both BALB/c and SJL mouse strains. In situ hybridization (ISH), using a cRNA probe to an SFV non-structural sequence, and immunogold-silver staining (IGSS), using polyclonal anti-SFV rabbit IgG, were the techniques utilized. For L10-SFV, viral RNA and antigen were detected in neurons and glial cells of both mouse strains. For BALB/c mice infected with M9-SFV, both neuronal and glial cell infection was less extensive than that obtained with L10. ISH or IGSS were generally not sensitive enough to detect viral RNA and antigen, respectively, in M9-SFV-infected SJL mice. M9-SFV multiplied to a similar titre in primary cultures of glial cells derived from either BALB/c or SJL mice. Following infection with M9-SFV, small plaques of demyelination in the CNS and occasional small aggregates of mononuclear leukocytes in the leptomeninges persisted for up to 12 months in SJL mice but not BALB/c mice. This was not associated with detectable persistence of infectious virus, viral antigen or viral RNA in the CNS.

摘要

利用BALB/c和SJL小鼠品系,确定了塞姆利基森林病毒(SFV)的强毒株L10和L10衍生的脱髓鞘M9突变体在小鼠中枢神经系统(CNS)中的增殖部位。使用针对SFV非结构序列的cRNA探针进行原位杂交(ISH),以及使用多克隆抗SFV兔IgG进行免疫金银染色(IGSS),是所采用的技术。对于L10 - SFV,在两种小鼠品系的神经元和胶质细胞中均检测到病毒RNA和抗原。对于感染M9 - SFV的BALB/c小鼠,神经元和胶质细胞感染的范围均不如L10感染时广泛。ISH或IGSS通常不够灵敏,无法分别在感染M9 - SFV的SJL小鼠中检测到病毒RNA和抗原。M9 - SFV在源自BALB/c或SJL小鼠的胶质细胞原代培养物中增殖至相似滴度。感染M9 - SFV后,SJL小鼠中枢神经系统中的小脱髓鞘斑块和软脑膜中偶尔出现的小单核白细胞聚集可持续长达12个月,而BALB/c小鼠则不会出现这种情况。这与中枢神经系统中可检测到的传染性病毒、病毒抗原或病毒RNA的持续存在无关。

相似文献

1
Multiplication of virulent and demyelinating Semliki Forest virus in the mouse central nervous system: consequences in BALB/c and SJL mice.强毒株和脱髓鞘性塞姆利基森林病毒在小鼠中枢神经系统中的增殖:对BALB/c和SJL小鼠的影响
J Gen Virol. 1990 Nov;71 ( Pt 11):2575-83. doi: 10.1099/0022-1317-71-11-2575.
2
The pathogenicity of the A7, M9 and L10 strains of Semliki Forest virus for weanling mice and primary mouse brain cell cultures.
J Gen Virol. 1985 Nov;66 ( Pt 11):2365-73. doi: 10.1099/0022-1317-66-11-2365.
3
Two mutations in the envelope glycoprotein E2 of Semliki Forest virus affecting the maturation and entry patterns of the virus alter pathogenicity for mice.
Virology. 1991 Dec;185(2):741-8. doi: 10.1016/0042-6822(91)90545-m.
4
Virulent and avirulent strains of Semliki Forest virus show similar cell tropism for the murine central nervous system but differ in the severity and rate of induction of cytolytic damage.塞姆利基森林病毒的强毒株和无毒株对小鼠中枢神经系统表现出相似的细胞嗜性,但在溶细胞损伤的严重程度和诱导速率方面存在差异。
Neuropathol Appl Neurobiol. 1993 Jun;19(3):233-9. doi: 10.1111/j.1365-2990.1993.tb00433.x.
5
Long-term effects of Semliki Forest virus infection in the mouse central nervous system.
Neuropathol Appl Neurobiol. 1997 Jun;23(3):235-41.
6
Persistence of virulent Semliki Forest virus in mouse brain following co-inoculation with defective interfering particles.与缺陷干扰颗粒共同接种后,强毒株塞姆利基森林病毒在小鼠脑中的持续存在。
J Gen Virol. 1986 Jun;67 ( Pt 6):1189-94. doi: 10.1099/0022-1317-67-6-1189.
7
Replication of the A7(74) strain of Semliki Forest virus is restricted in neurons.
Virology. 1993 Aug;195(2):627-37. doi: 10.1006/viro.1993.1414.
8
Pathogenicity of Semliki Forest virus for the rat central nervous system and primary rat neural cell cultures: possible implications for the pathogenesis of multiple sclerosis.Semliki森林病毒对大鼠中枢神经系统及原代大鼠神经细胞培养物的致病性:对多发性硬化症发病机制的可能影响
Neuropathol Appl Neurobiol. 1990 Feb;16(1):57-68. doi: 10.1111/j.1365-2990.1990.tb00932.x.
9
The pathogenicity of the M9 mutant of Semliki Forest virus in immune-compromised mice.塞姆利基森林病毒M9突变体在免疫受损小鼠中的致病性。
J Gen Virol. 1984 Jan;65 ( Pt 1):73-80. doi: 10.1099/0022-1317-65-1-73.
10
Semliki Forest virus induced, immune mediated demyelination: the effect of irradiation.塞姆利基森林病毒诱导的免疫介导性脱髓鞘:辐射的影响
Br J Exp Pathol. 1987 Feb;68(1):101-13.

引用本文的文献

1
Corpus callosum: a favorable target for rSFV-mediated gene transfer to rat brain with broad and efficient expression.胼胝体:rSFV 介导的基因转移到大鼠脑内的有利靶标,具有广泛而高效的表达。
J Mol Neurosci. 2010 Oct;42(2):255-60. doi: 10.1007/s12031-010-9386-1. Epub 2010 May 12.
2
Initiation and exacerbation of autoimmune demyelination of the central nervous system via virus-induced molecular mimicry: implications for the pathogenesis of multiple sclerosis.通过病毒诱导的分子模拟引发和加剧中枢神经系统的自身免疫性脱髓鞘:对多发性硬化症发病机制的影响
J Virol. 2005 Jul;79(13):8581-90. doi: 10.1128/JVI.79.13.8581-8590.2005.
3
A single amino acid change in the nuclear localization sequence of the nsP2 protein affects the neurovirulence of Semliki Forest virus.
nsP2蛋白核定位序列中的单个氨基酸变化会影响塞姆利基森林病毒的神经毒力。
J Virol. 2002 Jan;76(1):392-6. doi: 10.1128/jvi.76.1.392-396.2002.
4
Transient virus infection and multiple sclerosis.短暂性病毒感染与多发性硬化症
Rev Med Virol. 2000 Sep-Oct;10(5):291-303. doi: 10.1002/1099-1654(200009/10)10:5<291::aid-rmv278>3.0.co;2-u.
5
Replicase complex genes of Semliki Forest virus confer lethal neurovirulence.塞姆利基森林病毒的复制酶复合体基因赋予致命神经毒力。
J Virol. 2000 May;74(10):4579-89. doi: 10.1128/jvi.74.10.4579-4589.2000.
6
bcl-2 acts early to restrict Semliki Forest virus replication and delays virus-induced programmed cell death.bcl-2早期发挥作用,限制Semliki森林病毒复制,并延缓病毒诱导的程序性细胞死亡。
J Virol. 1997 Feb;71(2):1583-90. doi: 10.1128/JVI.71.2.1583-1590.1997.
7
Analysis of the molecular basis of neuropathogenesis of RNA viruses in experimental animals: relevance for human disease?实验动物中RNA病毒神经发病机制的分子基础分析:与人类疾病的相关性?
Neuropathol Appl Neurobiol. 1994 Apr;20(2):91-102. doi: 10.1111/j.1365-2990.1994.tb01167.x.
8
Multiplication of rubella and measles viruses in primary rat neural cell cultures: relevance to a postulated triggering mechanism for multiple sclerosis.风疹病毒和麻疹病毒在原代大鼠神经细胞培养物中的增殖:与多发性硬化症假定触发机制的相关性。
Neuropathol Appl Neurobiol. 1991 Aug;17(4):299-308. doi: 10.1111/j.1365-2990.1991.tb00727.x.