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一种致白血病的鼠逆转录病毒的组织嗜性由长末端重复序列之外的序列决定。

Tissue tropism of a leukemogenic murine retrovirus is determined by sequences outside of the long terminal repeats.

作者信息

Wolff L, Ruscetti S

出版信息

Proc Natl Acad Sci U S A. 1986 May;83(10):3376-80. doi: 10.1073/pnas.83.10.3376.

DOI:10.1073/pnas.83.10.3376
PMID:3010293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC323516/
Abstract

Although it has been previously determined that the long terminal repeat (LTR) sequences of several murine retroviruses specify the major tissue tropism of leukemias they induce, data reported here show that the LTR is not responsible for tissue tropism in the case of all leukemogenic viruses. In an effort to determine whether LTR sequences of the acute erythroleukemia-inducing spleen focus-forming virus (SFFV), like those of the other murine leukemia viruses, are uniquely required to confer tissue specificity to the virus, we prepared recombinant SFFVs in which the LTR region containing promoter and enhancer functions was replaced with analogous LTR regions from Friend and Moloney ecotropic and mink cell focus-inducing viruses. It was found that all of the SFFV constructs, even those with a LTR derived from lymphoma-inducing viruses such as Moloney murine leukemia virus, transformed erythroid cells in vitro and induced exclusively an erythroid disease. These results demonstrate that sequences in SFFV that determine the tissue-specific nature of the disease reside outside the LTR.

摘要

尽管先前已确定几种鼠逆转录病毒的长末端重复序列(LTR)决定了它们所诱导白血病的主要组织嗜性,但此处报告的数据表明,并非所有致白血病病毒的组织嗜性都由LTR决定。为了确定诱导急性红白血病的脾集落形成病毒(SFFV)的LTR序列是否像其他鼠白血病病毒的LTR序列一样,是赋予病毒组织特异性所唯一必需的,我们制备了重组SFFV,其中包含启动子和增强子功能的LTR区域被来自Friend病毒、莫洛尼嗜亲性病毒和貂细胞集落形成病毒的类似LTR区域所取代。结果发现,所有SFFV构建体,即使是那些具有源自淋巴瘤诱导病毒(如莫洛尼鼠白血病病毒)的LTR的构建体,在体外都能转化红系细胞,并且仅诱导红系疾病。这些结果表明,SFFV中决定疾病组织特异性本质的序列位于LTR之外。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76b6/323516/5176d6c0c5c4/pnas00314-0336-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76b6/323516/7e920f9f9d42/pnas00314-0336-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76b6/323516/ff66c055c208/pnas00314-0336-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76b6/323516/5176d6c0c5c4/pnas00314-0336-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76b6/323516/7e920f9f9d42/pnas00314-0336-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76b6/323516/ff66c055c208/pnas00314-0336-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76b6/323516/5176d6c0c5c4/pnas00314-0336-c.jpg

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本文引用的文献

1
Analysis of the env gene of a molecularly cloned and biologically active Moloney mink cell focus-forming proviral DNA.对分子克隆且具有生物活性的莫洛尼貂细胞病灶形成前病毒DNA的env基因进行分析。
J Virol. 1982 Oct;44(1):19-31. doi: 10.1128/JVI.44.1.19-31.1982.
2
Function of the retrovirus long terminal repeat.逆转录病毒长末端重复序列的功能。
Cell. 1982 Jan;28(1):3-5. doi: 10.1016/0092-8674(82)90367-1.
3
Envelope gene sequences which encode the gp52 protein of spleen focus-forming virus are required for the induction of erythroid cell proliferation.
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J Virol. 1997 Sep;71(9):6323-31. doi: 10.1128/JVI.71.9.6323-6331.1997.
4
A Friend virus mutant that overcomes Fv-2rr host resistance encodes a small glycoprotein that dimerizes, is processed to cell surfaces, and specifically activates erythropoietin receptors.一种克服Fv - 2rr宿主抗性的Friend病毒突变体编码一种小糖蛋白,该糖蛋白会二聚化,被加工到细胞表面,并特异性激活促红细胞生成素受体。
J Virol. 1993 May;67(5):2611-20. doi: 10.1128/JVI.67.5.2611-2620.1993.
5
Selectable retrovirus vectors encoding Friend virus gp55 or erythropoietin induce polycythemia with different phenotypic expression and disease progression.编码弗氏病毒gp55或促红细胞生成素的可选择逆转录病毒载体可诱导具有不同表型表达和疾病进展的红细胞增多症。
J Virol. 1994 Nov;68(11):7235-43. doi: 10.1128/JVI.68.11.7235-7243.1994.
6
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J Mol Med (Berl). 1995 Mar;73(3):113-20. doi: 10.1007/BF00198238.
7
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8
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9
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10
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4
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J Virol. 1983 Nov;48(2):542-6. doi: 10.1128/JVI.48.2.542-546.1983.
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Proc Natl Acad Sci U S A. 1983 Jul;80(14):4408-11. doi: 10.1073/pnas.80.14.4408.
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J Virol. 1983 Mar;45(3):1004-16. doi: 10.1128/JVI.45.3.1004-1016.1983.