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多瘤病毒在弗氏红白血病细胞中的生长与持续存在

Polyomavirus growth and persistence in Friend erythroleukemic cells.

作者信息

Delli Bovi P, De Simone V, Giordano R, Amati P

出版信息

J Virol. 1984 Feb;49(2):566-71. doi: 10.1128/JVI.49.2.566-571.1984.

DOI:10.1128/JVI.49.2.566-571.1984
PMID:6319756
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC255498/
Abstract

Infection of Friend erythroleukemic (FL) cells by polyomavirus (Py) invariably results in the selection of persistently infected FL-Py cell lines and clones. Anti-Py serum treatment of FL-Py lines and clones leads to the loss of Py genome and consequent cell cure. Conversely, cure has not been obtained in FL-PytsA cell lines (isolated after infection by a Py thermosensitive early mutant) and their derivative clones cultivated for a long time at nonpermissive temperature (39 degrees C), where viral large-T protein is inactive. Rescue of viral particles has always been obtained after shifting cells to 32 degrees C. Integrated viral genomes were detected by blot hybridization in an FL-PytsA clone at 39 degrees C. Long-term observation of FL-Py cell lines and their derivative clones reveals a reciprocal selection mechanism (coevolution) between the viral and the cellular populations, resulting in either a completely virus-free Py-resistant FL cell line (cure) or in a continuously Py-shedding line bearing Py genome variants. Structural analysis of these viral populations has been carried out, and some viral variants have been isolated and characterized. On the basis of the results obtained, the possible mechanisms of Py persistence in FL cells will be discussed.

摘要

多瘤病毒(Py)感染弗氏红白血病(FL)细胞总会导致选择出持续感染的FL-Py细胞系和克隆。用抗Py血清处理FL-Py细胞系和克隆会导致Py基因组丢失,从而使细胞治愈。相反,在FL-PytsA细胞系(感染Py温度敏感早期突变体后分离得到)及其在非允许温度(39℃)长期培养的衍生克隆中未实现治愈,在该温度下病毒大T蛋白无活性。将细胞转移至32℃后总能拯救出病毒颗粒。在39℃时通过印迹杂交在一个FL-PytsA克隆中检测到整合的病毒基因组。对FL-Py细胞系及其衍生克隆的长期观察揭示了病毒群体与细胞群体之间的相互选择机制(共同进化),导致要么产生完全无病毒的抗Py FL细胞系(治愈),要么产生携带Py基因组变体的持续释放Py的细胞系。已对这些病毒群体进行了结构分析,并且分离和鉴定了一些病毒变体。基于所获得的结果,将讨论Py在FL细胞中持续存在的可能机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f59c/255498/3e6d887e771e/jvirol00137-0276-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f59c/255498/0f06990e31a1/jvirol00137-0276-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f59c/255498/6b3ed35b224a/jvirol00137-0276-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f59c/255498/3e6d887e771e/jvirol00137-0276-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f59c/255498/0f06990e31a1/jvirol00137-0276-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f59c/255498/6b3ed35b224a/jvirol00137-0276-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f59c/255498/3e6d887e771e/jvirol00137-0276-c.jpg

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引用本文的文献

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Replicative cis-advantage of polyomavirus regulatory region mutants in different murine cell lines.多瘤病毒调控区突变体在不同小鼠细胞系中的复制顺式优势
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Polyomavirus mutation that confers a cell-specific cis advantage for viral DNA replication.

本文引用的文献

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Trans-complementable copy-number mutants of plasmid ColE1.质粒ColE1的反式可互补拷贝数突变体
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Ultrastructural observations of polyoma infected Friend erythroleukemic cells.多瘤病毒感染的Friend红白血病细胞的超微结构观察
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A small segment of polyoma virus DNA enhances the expression of a cloned beta-globin gene over a distance of 1400 base pairs.多瘤病毒DNA的一小段在1400个碱基对的距离上增强了一个克隆的β-珠蛋白基因的表达。
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