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脾脏病灶形成病毒变体之间的生物学和生化差异可定位于包含包膜基因3'端的区域。

Biological and biochemical differences between variants of spleen focus-forming virus can be localized to a region containing the 3' end of the envelope gene.

作者信息

Ruscetti S, Wolff L

出版信息

J Virol. 1985 Dec;56(3):717-22. doi: 10.1128/JVI.56.3.717-722.1985.

DOI:10.1128/JVI.56.3.717-722.1985
PMID:2999427
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC252641/
Abstract

Two variants of the spleen focus-forming virus (SFFV), SFFVP and SFFVA, induce acute erythroleukemia in mice but differ in their effects on erythroid cells as well as in the posttranslational modification of the product of their envelope genes. To localize the region of the SFFV envelope gene responsible for these differences, we utilized a recombinant virus containing the 3' half of the SFFVP env gene, where the vast majority of the differences between SFFVP and SFFVA reside, and the SFFVP long terminal repeat (LTR) on an SFFVA background. Analysis of the recombinant virus indicates that it is capable of inducing all of the biological effects previously associated with SFFVP, including the ability to proliferate and differentiate without the need for erythropoietin. In addition, the env gene product of the recombinant virus can be detected on the cell surface, a property previously associated only with SFFVP. Although the recombinant virus also contains LTR sequences from SFFVP, we do not believe it is likely that the four LTR nucleotides that are unique to SFFVP are responsible for the biological or biochemical differences observed. These results strengthen the argument that the SFFVP env gene product acts at the cell surface to alter the hormonal requirements for erythroid cell growth and differentiation.

摘要

脾集落形成病毒(SFFV)的两个变体,即SFFVP和SFFVA,可在小鼠中诱发急性红白血病,但它们对红系细胞的影响以及包膜基因产物的翻译后修饰有所不同。为了定位SFFV包膜基因中导致这些差异的区域,我们利用了一种重组病毒,该病毒在SFFVA背景上含有SFFVP env基因的3' 半段,SFFVP和SFFVA之间的绝大多数差异都存在于此,以及SFFVP长末端重复序列(LTR)。对该重组病毒的分析表明,它能够诱导所有先前与SFFVP相关的生物学效应,包括无需促红细胞生成素即可增殖和分化的能力。此外,重组病毒的env基因产物可以在细胞表面检测到,这是一种先前仅与SFFVP相关的特性。尽管重组病毒还含有来自SFFVP的LTR序列,但我们认为SFFVP特有的四个LTR核苷酸不太可能是观察到的生物学或生化差异的原因。这些结果进一步证明,SFFVP env基因产物在细胞表面起作用,以改变红系细胞生长和分化的激素需求。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5377/252641/78fe617baa52/jvirol00117-0076-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5377/252641/78fe617baa52/jvirol00117-0076-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5377/252641/78fe617baa52/jvirol00117-0076-a.jpg

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1
Biological and biochemical differences between variants of spleen focus-forming virus can be localized to a region containing the 3' end of the envelope gene.脾脏病灶形成病毒变体之间的生物学和生化差异可定位于包含包膜基因3'端的区域。
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本文引用的文献

1
Plasma membrane glycoproteins encoded by cloned Rauscher and Friend spleen focus-forming viruses.由克隆的劳舍尔和弗瑞德脾脏集落形成病毒编码的质膜糖蛋白。
J Virol. 1980 Sep;35(3):844-53. doi: 10.1128/JVI.35.3.844-853.1980.
2
Polycythaemia- and anaemia-inducing strains of spleen focus-forming virus differ in post-translational processing of envelope-related glycoproteins.引起红细胞增多症和贫血症的脾集落形成病毒毒株在包膜相关糖蛋白的翻译后加工方面存在差异。
Nature. 1981 Dec 17;294(5842):663-5. doi: 10.1038/294663a0.
3
Envelope gene sequences which encode the gp52 protein of spleen focus-forming virus are required for the induction of erythroid cell proliferation.
弗瑞德脾集落形成病毒的红细胞增多症诱导株和贫血症诱导株均可诱导Raf-1/丝裂原活化蛋白激酶信号转导途径的组成性激活。
J Virol. 1998 Feb;72(2):919-25. doi: 10.1128/JVI.72.2.919-925.1998.
4
Increased hematopoiesis in mice soon after infection by Friend murine leukemia virus.感染弗氏鼠白血病病毒后不久,小鼠的造血作用增强。
J Virol. 1993 Jun;67(6):3665-70. doi: 10.1128/JVI.67.6.3665-3670.1993.
5
Erythropoietin receptor (EpoR)-dependent mitogenicity of spleen focus-forming virus correlates with viral pathogenicity and processing of env protein but not with formation of gp52-EpoR complexes in the endoplasmic reticulum.红细胞生成素受体(EpoR)依赖性脾集落形成病毒的促有丝分裂活性与病毒致病性和env蛋白的加工有关,但与内质网中gp52-EpoR复合物的形成无关。
J Virol. 1993 Mar;67(3):1322-7. doi: 10.1128/JVI.67.3.1322-1327.1993.
6
The membrane glycoprotein of Friend spleen focus-forming virus: evidence that the cell surface component is required for pathogenesis and that it binds to a receptor.弗瑞德脾脏灶形成病毒的膜糖蛋白:细胞表面成分是发病机制所必需且其与受体结合的证据
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7
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8
A tagged helper-free Friend virus causes clonal erythroblast immortality by specific proviral integration in the cellular genome.一种标记的无辅助病毒的弗氏病毒通过在细胞基因组中的特异性前病毒整合导致克隆性成红细胞永生。
J Virol. 1988 Nov;62(11):4129-35. doi: 10.1128/JVI.62.11.4129-4135.1988.
9
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J Virol. 1988 Feb;62(2):511-8. doi: 10.1128/JVI.62.2.511-518.1988.
10
A nonimmunosuppressive helper virus allows high efficiency induction of B cell lymphomas by reticuloendotheliosis virus strain T.一种非免疫抑制性辅助病毒可使网状内皮组织增生症病毒T株高效诱导B细胞淋巴瘤。
J Exp Med. 1988 Jan 1;167(1):89-108. doi: 10.1084/jem.167.1.89.
编码脾集落形成病毒gp52蛋白的包膜基因序列是诱导红细胞增殖所必需的。
J Virol. 1982 Jul;43(1):223-33. doi: 10.1128/JVI.43.1.223-233.1982.
4
Polycythemia- and anemia-inducing erythroleukemia viruses exhibit differential erythroid transforming effects in vitro.引起红细胞增多症和贫血的红白血病病毒在体外表现出不同的红系转化作用。
Cell. 1980 Dec;22(3):693-9. doi: 10.1016/0092-8674(80)90545-0.
5
Anemia- and polycythemia-inducing isolates of Friend spleen focus-forming virus. Biological and molecular evidence for two distinct viral genomes.弗氏脾脏灶形成病毒的贫血和红细胞增多诱导分离株。两种不同病毒基因组的生物学和分子证据。
J Exp Med. 1980 Jun 1;151(6):1477-92. doi: 10.1084/jem.151.6.1477.
6
A simple microassay for erythropoietin based on 3H-thymidine incorporation into spleen cells from phenylhydrazine treated mice.一种基于将3H-胸腺嘧啶核苷掺入经苯肼处理的小鼠脾细胞的促红细胞生成素简易微量测定法。
Exp Hematol. 1983 Aug;11(7):649-60.
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Glycosylation and intracellular transport of spleen focus-forming virus glycoproteins.脾脏集落形成病毒糖蛋白的糖基化与细胞内运输
Virology. 1983 Mar;125(2):274-86. doi: 10.1016/0042-6822(83)90201-5.
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Structural analysis of the spleen focus-forming virus envelope gene product.脾集落形成病毒包膜基因产物的结构分析。
Virology. 1984 Mar;133(2):376-85. doi: 10.1016/0042-6822(84)90403-3.
9
Transformation of adult and fetal hemopoietic tissues with RNA tumor viruses.
Prog Clin Biol Res. 1983;134:245-61.
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Studies with inhibitors of oligosaccharide processing indicate a functional role for complex sugars in the transport and proteolysis of Friend mink cell focus-inducing murine leukemia virus envelope proteins.对寡糖加工抑制剂的研究表明,复合糖在Friend水貂细胞集落诱导型小鼠白血病病毒包膜蛋白的转运和蛋白水解过程中发挥功能性作用。
Virology. 1984 Jul 15;136(1):196-210. doi: 10.1016/0042-6822(84)90259-9.