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莫洛尼鼠白血病病毒包膜蛋白中的点突变:对感染性、病毒体结合及超感染抗性的影响。

Point mutations in Moloney murine leukemia virus envelope protein: effects on infectivity, virion association, and superinfection resistance.

作者信息

Berkowitz R D, Goff S P

机构信息

Howard Hughes Medical Institute, Columbia University College of Physicians and Surgeons, New York, New York 10032.

出版信息

Virology. 1993 Oct;196(2):748-57. doi: 10.1006/viro.1993.1532.

DOI:10.1006/viro.1993.1532
PMID:8372445
Abstract

Retroviral envelope proteins are synthesized in the infected cell and targetted to the assembling virion; during infection, they mediate receptor binding and fusion of the virion and cell membranes. We have generated a series of mutants of the Moloney murine leukemia virus (M-MuLV) with alterations in the TM protein, p15E, and determined whether the mutants are defective for replication and where the defects lie. Twenty-one point mutants were assessed for infectivity, virion-associated envelope protein levels, and the ability to confer resistance to superinfection. Only one mutant was specifically defective in a post-receptor binding step. Three other mutants encoded virion-associated envelope proteins that could not confer resistance to superinfection, implying that they could not bind to the receptor. These mutants demonstrate that in M-MuLV, receptor binding and early events such as membrane fusion can be affected by amino acid changes in the TM protein.

摘要

逆转录病毒包膜蛋白在受感染细胞中合成,并靶向组装中的病毒体;在感染过程中,它们介导病毒体与细胞膜的受体结合和融合。我们构建了一系列莫洛尼氏鼠白血病病毒(M-MuLV)的突变体,这些突变体的跨膜蛋白p15E发生了改变,并确定了这些突变体在复制方面是否存在缺陷以及缺陷所在位置。对21个点突变体的感染性、病毒体相关包膜蛋白水平以及赋予对超感染抗性的能力进行了评估。只有一个突变体在受体结合后的步骤中存在特异性缺陷。另外三个突变体编码的病毒体相关包膜蛋白不能赋予对超感染的抗性,这意味着它们不能与受体结合。这些突变体表明,在M-MuLV中,受体结合和诸如膜融合等早期事件可受跨膜蛋白中氨基酸变化的影响。

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Point mutations in Moloney murine leukemia virus envelope protein: effects on infectivity, virion association, and superinfection resistance.莫洛尼鼠白血病病毒包膜蛋白中的点突变:对感染性、病毒体结合及超感染抗性的影响。
Virology. 1993 Oct;196(2):748-57. doi: 10.1006/viro.1993.1532.
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引用本文的文献

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J Virol. 2006 Jul;80(13):6706-11. doi: 10.1128/JVI.00273-06.
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Linkage of reduced receptor affinity and superinfection to pathogenesis of TR1.3 murine leukemia virus.受体亲和力降低和双重感染与TR1.3小鼠白血病病毒发病机制的关联。
J Virol. 2006 May;80(9):4601-9. doi: 10.1128/JVI.80.9.4601-4609.2006.
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The envelope glycoprotein of human endogenous retrovirus type W uses a divergent family of amino acid transporters/cell surface receptors.
人内源性逆转录病毒W型的包膜糖蛋白利用一类不同的氨基酸转运蛋白/细胞表面受体。
J Virol. 2002 Jul;76(13):6442-52. doi: 10.1128/jvi.76.13.6442-6452.2002.
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Mapping full-length porcine endogenous retroviruses in a large white pig.绘制大白猪中全长猪内源性逆转录病毒图谱。
J Virol. 2001 Dec;75(24):12252-65. doi: 10.1128/JVI.75.24.12252-12265.2001.
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Second-site changes affect viability of amphotropic/ecotropic chimeric enveloped murine leukemia viruses.第二位点变化影响双嗜性/亲嗜性嵌合包膜鼠白血病病毒的生存能力。
J Virol. 2000 Jan;74(2):899-913. doi: 10.1128/jvi.74.2.899-913.2000.
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Receptor-mediated Moloney murine leukemia virus entry can occur independently of the clathrin-coated-pit-mediated endocytic pathway.受体介导的莫洛尼鼠白血病病毒进入过程可独立于网格蛋白包被小窝介导的内吞途径发生。
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Tumor cells expressing a retroviral envelope escape immune rejection in vivo.表达逆转录病毒包膜的肿瘤细胞在体内逃避免疫排斥。
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