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小鼠微小病毒对转化大鼠细胞的选择性杀伤并不需要产生感染性病毒。

Selective killing of transformed rat cells by minute virus of mice does not require infectious virus production.

作者信息

Guetta E, Mincberg M, Mousset S, Bertinchamps C, Rommelaere J, Tal J

机构信息

Biology Department, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

出版信息

J Virol. 1990 Jan;64(1):458-62. doi: 10.1128/JVI.64.1.458-462.1990.

DOI:10.1128/JVI.64.1.458-462.1990
PMID:2293669
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC249127/
Abstract

Fischer rat fibroblasts, naturally resistant to killing by the fibrotropic strain of minute virus of mice [(parvovirus MVM(p)], became sensitive to MVM when transformed by polyomavirus. This sensitization did not involve an increase in the percentage of cells which synthesized viral capsid antigens or in the percentage of cells which produced infectious virus. The addition of anti-MVM antiserum to the growth medium of MVM-infected cells had only a small effect on their survival rates, indicating that the majority of the killing effect of MVM occurs in a single cycle of infection. The data indicate that cell killing by MVM is independent of infectious virus production and thus support the notion that the preferential cytolytic effect is affected by viral cytotoxic gene products which accumulate to intolerable levels in transformed cells but not in normal ones. Finally, using cells transformed with polyomavirus and genomic and subgenomic clones of polyomavirus, we showed that the extent of sensitization to killing by MVM depended on the transforming agent used.

摘要

费舍尔大鼠成纤维细胞对亲纤维性小鼠微小病毒株[细小病毒MVM(p)]的杀伤作用天然具有抗性,当被多瘤病毒转化后,它们对MVM变得敏感。这种致敏作用并不涉及合成病毒衣壳抗原的细胞百分比增加,也不涉及产生感染性病毒的细胞百分比增加。向感染MVM的细胞生长培养基中添加抗MVM抗血清对其存活率只有很小的影响,这表明MVM的大部分杀伤作用发生在单个感染周期内。数据表明,MVM对细胞的杀伤作用与感染性病毒的产生无关,因此支持这样一种观点,即优先的溶细胞作用受病毒细胞毒性基因产物的影响,这些产物在转化细胞中积累到无法忍受的水平,而在正常细胞中则不会。最后,使用用多瘤病毒以及多瘤病毒的基因组和亚基因组克隆转化的细胞,我们表明对MVM杀伤作用的致敏程度取决于所使用的转化剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c84/249127/040ee2fe255e/jvirol00056-0475-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c84/249127/040ee2fe255e/jvirol00056-0475-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c84/249127/040ee2fe255e/jvirol00056-0475-a.jpg

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本文引用的文献

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Inhibition of 7,12-dimethylbenz(a)anthracene-induced tumors in Syrian hamsters by prior infection with H-1 parvovirus.H-1细小病毒预先感染对叙利亚仓鼠7,12-二甲基苯并(a)蒽诱导肿瘤的抑制作用。
Cancer Res. 1982 Jul;42(7):2552-5.
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Interaction of minute virus of mice with differentiated cells: strain-dependent target cell specificity is mediated by intracellular factors.小鼠微小病毒与分化细胞的相互作用:毒株依赖性靶细胞特异性由细胞内因子介导。
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Minute virus of mice inhibits cell transformation by simian virus 40.
定位于非结构基因的基因组复制和衣壳化后功能限制了鼠细小病毒在人细胞中的宿主范围。
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Neoplastic transformation-associated stimulation of the in vitro resolution of concatemer junction fragments from minute virus of mice DNA.小鼠微小病毒DNA串联体连接片段体外切割的肿瘤转化相关刺激作用
J Virol. 1999 Mar;73(3):2552-8. doi: 10.1128/JVI.73.3.2552-2558.1999.
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The cytotoxicity of the parvovirus minute virus of mice nonstructural protein NS1 is related to changes in the synthesis and phosphorylation of cell proteins.小鼠细小病毒非结构蛋白NS1的细胞毒性与细胞蛋白质合成及磷酸化的变化有关。
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Virus Genes. 1995;11(2-3):239-57. doi: 10.1007/BF01728663.
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The cytotoxicity of the autonomous parvovirus minute virus of mice nonstructural proteins in FR3T3 rat cells depends on oncogene expression.小鼠自主细小病毒非结构蛋白在FR3T3大鼠细胞中的细胞毒性取决于癌基因表达。
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Selective killing of carcinogen-treated SV40-transformed Chinese hamster cells by a defective parvovirus.
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Virology. 1968 Jul;35(3):475-8. doi: 10.1016/0042-6822(68)90226-2.