Further studies of the RNA synthesis phenotype selected during persistent infection with vesicular stomatitis virus.
Further studies of the RNA synthesis phenotype selected during persistent infection with vesicular stomatitis virus.
复制标题
水泡性口炎病毒持续感染期间选择的RNA合成表型的进一步研究。
DOI：
10.1016/0042-6822(84)90260-5
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发表时间：
1984
期刊：
影响因子：
3.7
通讯作者：
Youngner,JS
中科院分区：
文献类型：
--
作者：
Frey,TK;Youngner,JS
水泡性口炎病毒分离自两个独立建立的小鼠L细胞系，在37°时，RNA合成的表型发生了变化，这是持续感染的培养物保持的温度(T.K.Frey和J.S.Young，1982，J.Viro.44,167-174)。与野生型(Wt)VSV和ts-0-23(ts−，rna+互补组III)相比，表达该rna表型的vsv合成的mRNA量少得多，但相当于或更多的40株S基因组rna(rt-rna表型)。在wt-VSV启动的品系中，在启动后第17天，当85%的克隆为ts−时，36%的ts−克隆为RT−。到63天时，VSV-PI群体的−和RT-−都是一致的，这种表型至少持续了2年。在ts-0-23启动的品系中，RT-−表型至少稳定了3年。为了研究在持续期间共选择的ts-−和RT-−表型之间的关系，分离了ts-−RT-−vsv-PI克隆的ts+回复株。所有ts+回复株均表达37°(RT+)的wt-VSV RNA合成表型，表明这两个表型标记可能是同一突变的多效性表现。RT-−病毒抑制宿主细胞核糖核酸和蛋白质合成的速度比wt-VSV慢。然而，与wt-VSV相比，RT-−vsv合成了等量或更多的所有病毒蛋白，尽管mRNA量减少了。RT−病毒对宿主细胞大分子合成的弱阻断，以及伴随而来的40 S基因组复制和病毒蛋白合成，可能部分解释了RT−突变在持续期间的选择性优势。RT−的表型不是持续性感染所特有的；TS−RT−突变体也是在wt-vsv在L细胞中连续传代过程中进化的，从wt-vsv群体中分离的一组自发突变株中发现了一个ts−RT−突变体。
Vesicular stomatitis virus (VSV) isolated from two independently established lines of persistently infected mouse L cells expressed an altered phenotype of RNA synthesis at 37°, the temperature at which the persistently infected cultures were maintained (T. K. Frey and J. S. Youngner, 1982,J. Virol.44, 167–174). In comparison to the viruses used to initiate the two lines, wild-type (wt) VSV and ts-0–23 (ts−, RNA+complementation group III), the VSV expressing this RNA phenotype synthesized much less mRNA but equal or greater amounts of 40 S genomic RNA (rt−phenotype). In the line initiated with wt-VSV, at 17 days after initiation, when 85% of the clones were ts−, 36% of the ts−clones were rt−. By 63 days the VSV-PI population was uniformly ts−and rt−and this phenotype prevailed for at least 2 years of persistence. In the line initiated with ts-0–23, the rt−phenotype was stable for at least 3 years of persistence. To study the relationship of the ts−and rt−phenotypes which were coselected during persistence, ts+revertants of a ts−rt−VSV-PI clone were isolated. All of the ts+revertants expressed a wt-VSV phenotype of RNA synthesis at 37° (rt+), indicating that the two phenotypic markers may be pleiotropic manifestations of the same mutation. rt−VSV inhibited host cell RNA and protein synthesis more slowly than did wt-VSV. However, rt−VSV synthesized equivalent or greater amounts of all the virus proteins, compared to wt-VSV, despite the reduced amount of mRNA transcription. The attenuated shutoff of host cell macromolecular synthesis by rt−VSV and the concomitant efficient 40 S genome replication and virus protein synthesis may in part explain the selective advantage of the rt−mutation during persistence. The rt−phenotype was not unique to persistent infection; ts−rt−mutants also evolved during serial undiluted passages of wt-VSV in L cells and one ts−rt−mutant was identified in a group of spontaneous mutants isolated from a wt-VSV stock.