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一种2.9千碱基的非编码核RNA在持久性Hz-1病毒感染的建立中发挥作用。

A 2.9-kilobase noncoding nuclear RNA functions in the establishment of persistent Hz-1 viral infection.

作者信息

Chao Y C, Lee S T, Chang M C, Chen H H, Chen S S, Wu T Y, Liu F H, Hsu E L, Hou R F

机构信息

Institute of Molecular Biology, Academia Sinica, Nankang, Taipei, Taiwan, Republic of China.

出版信息

J Virol. 1998 Mar;72(3):2233-45. doi: 10.1128/JVI.72.3.2233-2245.1998.

DOI:10.1128/JVI.72.3.2233-2245.1998
PMID:9499081
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC109520/
Abstract

Differential viral gene expression during both productive and persistent infections of Hz-1 virus in insect cells was elucidated. Despite more than 100 viral transcripts being expressed during productive viral infection, massive viral gene shutoff was observed during viral persistency, leaving the 2.9-kb persistence-associated transcript 1 (PAT1) as the only detectable viral RNA. Persistence-associated gene 1 (pag1), which encodes PAT1, was cloned and found to contain no significant open reading frames. PAT1 is not associated with the cellular translation machinery and is located exclusively in the nucleus. Further experiments showed that PAT1 is functional in the establishment of persistent Hz-1 viral infection in the cells. All the evidence collectively indicates that PAT1 is a novel nuclear transcript of viral origin. Our results showed that although PAT1 and XIST RNA, a mammalian X-inactive specific transcript, are transcribed by different genes, they have interesting similarities.

摘要

阐明了Hz-1病毒在昆虫细胞中生产性感染和持续性感染期间病毒基因的差异表达。尽管在生产性病毒感染期间有100多个病毒转录本被表达,但在病毒持续性感染期间观察到大量病毒基因关闭,仅留下2.9kb的持续性相关转录本1(PAT1)作为唯一可检测到的病毒RNA。克隆了编码PAT1的持续性相关基因1(pag1),发现其不包含明显的开放阅读框。PAT1与细胞翻译机制无关,仅位于细胞核中。进一步的实验表明,PAT1在细胞中建立持续性Hz-1病毒感染中起作用。所有证据共同表明,PAT1是一种新型的病毒来源的核转录本。我们的结果表明,尽管PAT1和哺乳动物X染色体失活特异性转录本XIST RNA由不同基因转录,但它们具有有趣的相似性。

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A 2.9-kilobase noncoding nuclear RNA functions in the establishment of persistent Hz-1 viral infection.一种2.9千碱基的非编码核RNA在持久性Hz-1病毒感染的建立中发挥作用。
J Virol. 1998 Mar;72(3):2233-45. doi: 10.1128/JVI.72.3.2233-2245.1998.
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