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细小病毒同种异型决定簇对基因表达的发育调控控制是由病毒颗粒介导的证据。

Evidence that developmentally regulated control of gene expression by a parvoviral allotropic determinant is particle mediated.

作者信息

Gardiner E M, Tattersall P

机构信息

Department of Human Genetics, Yale University School of Medicine, New Haven, Connecticut 06510.

出版信息

J Virol. 1988 May;62(5):1713-22. doi: 10.1128/JVI.62.5.1713-1722.1988.

Abstract

An infectious molecular clone of the immunosuppressive strain of the autonomous parvovirus minute virus of mice [MVM(i)] was constructed deriving left-hand terminal sequences from a rare encapsidated plus strand. Progeny virus was shown to package the same proportions of plus and minus strands as did authentic MVM(i) virions. Rescue of virus from this clone also resulted in the repair of a 21-base truncation at the junction between the right-hand end of the viral insert and the vector and generated the same heterogeneous 5' end as is present in standard MVM(i) DNA. Progeny virus rescued by transfection of this clone into mouse cell lines displayed the lymphotropic phenotype characteristic of the parental MVM(i) virus from which it was derived. However, analysis of viral RNA from transfected mouse fibroblasts revealed that the MVM(i) and MVM(p) genomic clones are transcribed at the same low level. Furthermore, transfected fibroblasts yielded similar numbers of infectious centers regardless of which MVM clone was introduced. These results contrast markedly with the different infectivities of MVM(i) and MVM(p) particles and with the observation that viral transcription in fibroblasts productively infected with MVM(p) virions is 100-fold greater than that seen in the restrictive MVM(i) particle-mediated infection. These results suggest that the developmentally regulated intracellular factors controlling host cell susceptibility at the level of viral transcription interact with a component of the incoming viral capsid, rather than with a sequence within the viral DNA.

摘要

构建了小鼠自主细小病毒免疫抑制株[MVM(i)]的感染性分子克隆,其左手末端序列源自一条罕见的被包裹的正链。结果显示,子代病毒包装的正链和负链比例与正宗的MVM(i)病毒粒子相同。从该克隆中拯救病毒还导致病毒插入片段右手末端与载体连接处的21个碱基截短得到修复,并产生了与标准MVM(i) DNA中相同的异质5'末端。通过将该克隆转染到小鼠细胞系中拯救的子代病毒表现出其来源的亲本MVM(i)病毒特有的嗜淋巴细胞表型。然而,对转染的小鼠成纤维细胞中的病毒RNA分析表明,MVM(i)和MVM(p)基因组克隆的转录水平相同。此外,无论引入哪种MVM克隆,转染的成纤维细胞产生的感染中心数量相似。这些结果与MVM(i)和MVM(p)颗粒的不同感染性以及在被MVM(p)病毒粒子有效感染的成纤维细胞中病毒转录比在限制性MVM(i)颗粒介导的感染中高100倍的观察结果形成鲜明对比。这些结果表明,在病毒转录水平上控制宿主细胞易感性的发育调控细胞内因子与进入的病毒衣壳成分相互作用,而不是与病毒DNA内的序列相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef4f/253210/584734799d7d/jvirol00084-0253-a.jpg

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