• 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

水泡性口炎病毒基因组在允许性和非允许性宿主细胞中的复制。

Replication of the vesicular stomatitis virus genome in permissive and nonpermissive host cells.

作者信息

Piwnica-Worms H, Keene J D

出版信息

J Biol Chem. 1985 Sep 5;260(19):10503-11.

PMID:2993276
Abstract

Permissive infections of BHK cells and nonpermissive infections of Raji cells were probed for the accumulation of vesicular stomatitis virus intracellular RNAs. In Raji cells, the onset of vesicular stomatitis virus transcription and replication was delayed when compared to BHK cells, and the accumulation of plus and minus sense leader RNAs was significantly reduced. In contrast, full length plus and minus strand replicative RNAs accumulated in Raji cells to levels approximately equivalent to those in BHK cells. In both cell types, approximately four times as many minus strands as plus strands were detected late in the infections. At 16 h postinfection, 12% of the total genomic RNA synthesized in BHK cells was packaged and released whereas only 0.8% was released from Raji cells. In addition, of those particles released by Raji cells, only 1% were infectious whereas 77% of those released by BHK cells were infectious. The virions released from both cell types contained similar amounts of the five viral proteins, however. Analysis of virions from Raji cells revealed a faster electrophoretic mobility of the glycoprotein than the glycoprotein in virions released from BHK cells. These results suggest that Raji cells may be restricted in their ability to support a complete infection at the level of virus assembly rather than at the level of RNA replication.

摘要

研究了水泡性口炎病毒在BHK细胞中的允许性感染以及在Raji细胞中的非允许性感染,以检测细胞内RNA的积累情况。与BHK细胞相比,Raji细胞中水泡性口炎病毒转录和复制的起始延迟,正链和负链前导RNA的积累显著减少。相比之下,全长正链和负链复制性RNA在Raji细胞中的积累水平与BHK细胞中的大致相当。在两种细胞类型中,感染后期检测到的负链数量约为正链的四倍。感染后16小时,BHK细胞中合成的总基因组RNA中有12%被包装并释放,而Raji细胞中只有0.8%被释放。此外,Raji细胞释放的颗粒中只有1%具有感染性,而BHK细胞释放的颗粒中有77%具有感染性。然而,两种细胞类型释放的病毒粒子所含的五种病毒蛋白量相似。对Raji细胞释放的病毒粒子分析显示,其糖蛋白的电泳迁移率比BHK细胞释放的病毒粒子中的糖蛋白更快。这些结果表明,Raji细胞在支持完整感染方面的能力可能在病毒组装水平而非RNA复制水平受到限制。

相似文献

1
Replication of the vesicular stomatitis virus genome in permissive and nonpermissive host cells.水泡性口炎病毒基因组在允许性和非允许性宿主细胞中的复制。
J Biol Chem. 1985 Sep 5;260(19):10503-11.
2
Characterization of the infections of permissive and nonpermissive cells by host range mutants of vesicular stomatitis virus defective in RNA methylation.由RNA甲基化缺陷的水泡性口炎病毒宿主范围突变体对允许细胞和非允许细胞感染的特征分析
Virology. 1984 Oct 15;138(1):1-15. doi: 10.1016/0042-6822(84)90142-9.
3
Nonpermissive infection of lymphoblastoid cells by vesicular stomatitis virus. II. Effect on viral morphogenesis.水泡性口炎病毒对淋巴母细胞的非允许感染。II. 对病毒形态发生的影响。
Virus Res. 1985 Jun;2(4):345-58. doi: 10.1016/0168-1702(85)90030-9.
4
Base mutations in the terminal noncoding regions of the genome of vesicular stomatitis virus isolated from persistent infections of L cells.
Virology. 1985 Jan 30;140(2):249-56. doi: 10.1016/0042-6822(85)90363-0.
5
RNA synthesis of vesicular stomatitis virus-infected cells: in vivo regulation of replication.水泡性口炎病毒感染细胞的RNA合成:复制的体内调节
J Virol. 1979 Jul;31(1):124-32. doi: 10.1128/JVI.31.1.124-132.1979.
6
Effect of defective interfering particles on plus- and minus- strand leader RNAs in vesicular stomatitis virus-infected cells.缺陷干扰颗粒对感染水疱性口炎病毒的细胞中正链和负链前导RNA的影响。
J Virol. 1980 Sep;35(3):704-9. doi: 10.1128/JVI.35.3.704-709.1980.
7
Rapid and transient localization of the leader RNA of vesicular stomatitis virus in the nuclei of infected cells.水疱性口炎病毒前导RNA在受感染细胞核中的快速瞬时定位
Proc Natl Acad Sci U S A. 1982 Sep;79(17):5240-4. doi: 10.1073/pnas.79.17.5240.
8
A host protein (La) binds to a unique species of minus-sense leader RNA during replication of vesicular stomatitis virus.在水疱性口炎病毒复制过程中,一种宿主蛋白(La)与一种独特的负义前导RNA结合。
Proc Natl Acad Sci U S A. 1983 Oct;80(19):5827-31. doi: 10.1073/pnas.80.19.5827.
9
Replicative RNA synthesis and nucleocapsid assembly in vesicular stomatitis virus-infected permeable cells.水泡性口炎病毒感染的可渗透细胞中的复制性RNA合成与核衣壳组装。
J Virol. 1980 Dec;36(3):796-804. doi: 10.1128/JVI.36.3.796-804.1980.
10
Nonpermissive infection of lymphoblastoid cells by vesicular stomatitis virus. I. Synthesis and function of the viral transcripts.
Virus Res. 1984;1(3):259-74. doi: 10.1016/0168-1702(84)90043-1.

引用本文的文献

1
Cell-type-specific growth restriction of vesicular stomatitis virus polR mutants is linked to defective viral polymerase function.水泡性口炎病毒polR突变体的细胞类型特异性生长限制与病毒聚合酶功能缺陷有关。
J Virol. 2007 Jan;81(2):492-502. doi: 10.1128/JVI.01217-06. Epub 2006 Oct 25.
2
Stimulation of vesicular stomatitis virus in vitro RNA synthesis by microtubule-associated proteins.微管相关蛋白对水泡性口炎病毒体外RNA合成的刺激作用。
Proc Natl Acad Sci U S A. 1986 Aug;83(15):5410-3. doi: 10.1073/pnas.83.15.5410.
3
Vesicular stomatitis virus in Drosophila melanogaster cells: regulation of viral transcription and replication.
黑腹果蝇细胞中的水泡性口炎病毒:病毒转录与复制的调控
J Virol. 1988 Jan;62(1):277-84. doi: 10.1128/JVI.62.1.277-284.1988.
4
Viral transcription is necessary and sufficient for vesicular stomatitis virus to inhibit maturation of small nuclear ribonucleoproteins.水泡性口炎病毒抑制小核核糖核蛋白成熟,病毒转录是必要且充分的条件。
J Virol. 1989 Oct;63(10):4172-80. doi: 10.1128/JVI.63.10.4172-4180.1989.