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水泡性口炎病毒频繁产生新的3'缺陷干扰颗粒。

Frequent generation of new 3'-defective interfering particles of vesicular stomatitis virus.

作者信息

Kang C Y, Schubert M, Lazzarini R A

出版信息

Virology. 1985 Jun;143(2):630-5. doi: 10.1016/0042-6822(85)90403-9.

DOI:10.1016/0042-6822(85)90403-9
PMID:2998029
Abstract

We have isolated and partially characterized a number of different genome types of defective interfering (DI) particles newly generated by a highly heat-resistant strain of vesicular stomatitis virus in either Rat(B77) or Vero cells. Northern blot analyses revealed that many of these DI genomes contain N gene sequences and/or sequences of the NS, M, and G genes. One type contains NS sequences without any indication for the presence of either N, M, or G sequences. Another type of DI particle genomes did not contain any detectable sequences of N, NS, M, or G, but contain panhandle-type sequences and, thus, most likely resembles the 5'-panhandle-type DI particles. Unlike previously assumed, these data demonstrate that DI genomes which have the 3'-terminal N, NS, M, and G genes or portions of these genes conserved do frequently arise together with 5'-DI particle genomes after serial undiluted passages of the heat-resistant strain of vesicular stomatitis virus.

摘要

我们已经分离并部分鉴定了由水疱性口炎病毒的一种高度耐热菌株在大鼠(B77)或非洲绿猴肾细胞(Vero细胞)中新产生的多种不同基因组类型的缺陷干扰(DI)颗粒。Northern印迹分析表明,这些DI基因组中的许多都包含N基因序列和/或NS、M和G基因的序列。一种类型包含NS序列,但没有任何迹象表明存在N、M或G序列。另一种类型的DI颗粒基因组不包含N、NS、M或G的任何可检测序列,但包含柄型序列,因此很可能类似于5'-柄型DI颗粒。与之前的假设不同,这些数据表明,在水疱性口炎病毒耐热菌株连续未稀释传代后,具有3'-末端N、NS、M和G基因或这些基因部分保守的DI基因组确实经常与5'-DI颗粒基因组一起出现。

相似文献

1
Frequent generation of new 3'-defective interfering particles of vesicular stomatitis virus.水泡性口炎病毒频繁产生新的3'缺陷干扰颗粒。
Virology. 1985 Jun;143(2):630-5. doi: 10.1016/0042-6822(85)90403-9.
2
Continuing coevolution of virus and defective interfering particles and of viral genome sequences during undiluted passages: virus mutants exhibiting nearly complete resistance to formerly dominant defective interfering particles.在未稀释传代过程中病毒与缺陷干扰颗粒以及病毒基因组序列的持续协同进化:表现出对先前占主导地位的缺陷干扰颗粒几乎完全抗性的病毒突变体。
J Virol. 1987 Feb;61(2):454-64. doi: 10.1128/JVI.61.2.454-464.1987.
3
Sites of copy choice replication involved in generation of vesicular stomatitis virus defective-interfering particle RNAs.参与水疱性口炎病毒缺陷干扰颗粒RNA产生的复制选择位点。
J Virol. 1984 Aug;51(2):515-21. doi: 10.1128/JVI.51.2.515-521.1984.
4
Vesicular stomatitis virus defective interfering particles can contain extensive genomic sequence rearrangements and base substitutions.水泡性口炎病毒缺陷干扰颗粒可包含广泛的基因组序列重排和碱基替换。
Cell. 1984 Apr;36(4):915-24. doi: 10.1016/0092-8674(84)90041-2.
5
Structure and origin of a novel class of defective interfering particle of vesicular stomatitis virus.水泡性口炎病毒一类新型缺陷干扰颗粒的结构与起源
Nucleic Acids Res. 1984 Mar 26;12(6):2775-90. doi: 10.1093/nar/12.6.2775.
6
RNA polymerase-associated interactions near template promoter sequences of defective interfering particles of vesicular stomatitis virus.水疱性口炎病毒缺陷干扰颗粒模板启动子序列附近的RNA聚合酶相关相互作用。
J Virol. 1982 Jul;43(1):241-9. doi: 10.1128/JVI.43.1.241-249.1982.
7
Isolation of vesicular stomatitis virus defective interfering genomes with different amounts of 5'-terminal complementarity.具有不同5'-末端互补量的水疱性口炎病毒缺陷干扰基因组的分离
J Virol. 1982 Feb;41(2):566-74. doi: 10.1128/JVI.41.2.566-574.1982.
8
Internal genome deletions in two distinct classes of defective interfering particles of vesicular stomatitis virus.水泡性口炎病毒两类缺陷干扰颗粒中的内部基因组缺失
Proc Natl Acad Sci U S A. 1979 Dec;76(12):6191-5. doi: 10.1073/pnas.76.12.6191.
9
Oligonucleotide sequence analyses indicate that vesicular stomatitis virus large defective interfering virus particle RNA is made by internal deletion: evidence for similar transcription polyadenylation signals for the synthesis of all vesicular stomatitis virus mRNA species.寡核苷酸序列分析表明,水泡性口炎病毒大型缺陷干扰病毒颗粒RNA是通过内部缺失产生的:合成所有水泡性口炎病毒mRNA种类的转录多聚腺苷酸化信号相似的证据。
J Virol. 1980 Feb;33(2):807-17. doi: 10.1128/JVI.33.2.807-817.1980.
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Vesicular stomatitis virus defective interfering particle containing a muted internal leader RNA gene.含有沉默内部引导RNA基因的水疱性口炎病毒缺陷干扰颗粒。
Proc Natl Acad Sci U S A. 1981 Apr;78(4):2090-4. doi: 10.1073/pnas.78.4.2090.

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