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脊髓灰质炎病毒的缺陷干扰颗粒。IV. 富集机制。

Defective interfering particles of poliovirus. IV. Mechanisms of enrichment.

作者信息

Cole C N, Baltimore D

出版信息

J Virol. 1973 Dec;12(6):1414-26. doi: 10.1128/JVI.12.6.1414-1426.1973.

DOI:10.1128/JVI.12.6.1414-1426.1973
PMID:4357514
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC356783/
Abstract

Infection of HeLa cells by mixtures of standard poliovirus and defective, interfering (DI) poliovirus particles leads to a higher ratio of DI particles in the progeny than in the inoculum. The extent of this enrichment could be varied by various manipulations of the co-infected cells. At any time during the infection cycle, virions made within short times after addition of radioactive uridine were hyperenriched in DI particles; this transient hyperenrichment fell to the equilibrium enrichment level within 45 min after uridine addition. A shift of the temperature of infection from 37 to 31 C also led to a hyperenrichment of DI particles and pulse-labeling revealed a superimposed transient hyperenrichment. By contrast, cells continuously infected at 31 C showed a severe decrement in DI particles apparently because poliovirus DI particles behave as cold-sensitive mutants for RNA synthesis. Cycloheximide treatment early in the infection cycle also led to hyperenrichment. Study of the cycloheximide effect showed that the drug acted as if to change the input ratio of standard to DI particles. These effects on enrichment can be explained as aspects of two different phenomena: enrichment due to preferential DI RNA synthesis and enrichment due to preferential encapsidation of DI RNA. Both mechanisms probably play a role in the normal level of enrichment.

摘要

标准脊髓灰质炎病毒与缺陷干扰(DI)脊髓灰质炎病毒颗粒混合物感染HeLa细胞后,子代中DI颗粒的比例高于接种物中的比例。通过对共感染细胞的各种操作,可以改变这种富集程度。在感染周期的任何时候,添加放射性尿苷后短时间内产生的病毒粒子中DI颗粒高度富集;这种短暂的高度富集在添加尿苷后45分钟内降至平衡富集水平。将感染温度从37℃转变为31℃也会导致DI颗粒高度富集,脉冲标记显示有叠加的短暂高度富集。相比之下,在31℃持续感染的细胞中DI颗粒明显减少,这显然是因为脊髓灰质炎病毒DI颗粒在RNA合成方面表现为冷敏感突变体。在感染周期早期用环己酰亚胺处理也会导致高度富集。对环己酰亚胺作用的研究表明,该药物的作用似乎是改变标准颗粒与DI颗粒的输入比例。这些对富集的影响可以解释为两种不同现象的表现:由于DI RNA的优先合成导致的富集和由于DI RNA的优先包装导致的富集。这两种机制可能都在正常富集水平中发挥作用。

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本文引用的文献

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INHIBITION OF PROTEIN SYNTHESIS BY CYCLOHEXIMIDE IN RABBIT RETICULOCYTES.环己酰亚胺对兔网织红细胞蛋白质合成的抑制作用。
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Defective interfering particles of poliovirus. 3. Interference and enrichment.脊髓灰质炎病毒的缺陷干扰颗粒。3. 干扰与富集。
J Mol Biol. 1973 May 25;76(3):345-61. doi: 10.1016/0022-2836(73)90509-3.
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Defective interfering particles of poliovirus. II. Nature of the defect.脊髓灰质炎病毒的缺陷干扰颗粒。II. 缺陷的本质。
J Mol Biol. 1973 May 25;76(3):325-43. doi: 10.1016/0022-2836(73)90508-1.
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Defective interfering particles of poliovirus. I. Isolation and physical properties.脊髓灰质炎病毒的缺陷干扰颗粒。I. 分离与物理性质。
J Virol. 1971 Apr;7(4):478-85. doi: 10.1128/JVI.7.4.478-485.1971.
7
Morphogenesis of poliovirus. I. Association of the viral RNA with coat protein.脊髓灰质炎病毒的形态发生。I. 病毒RNA与衣壳蛋白的结合。
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Aspects of the synthesis of poliovirus RNA and the formation of virus particles.脊髓灰质炎病毒RNA的合成及病毒颗粒形成的相关方面。
Virology. 1966 Jun;29(2):179-89. doi: 10.1016/0042-6822(66)90024-9.