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野生型麻疹病毒适应Vero细胞并不需要其受体结合血凝素蛋白发生变化。

Changes in the receptorbinding haemagglutinin protein of wild-type morbilliviruses are not required for adaptation to Vero cells.

作者信息

Nielsen Line, Andersen Mads Klindt, Jensen Tove Dannemann, Blixenkrone-Møller Merete, Bolt Gert

机构信息

Laboratory of Virology and Immunology, Royal Veterinary and Agricultural University, Copenhagen, Denmark.

出版信息

Virus Genes. 2003 Oct;27(2):157-62. doi: 10.1023/a:1025724526378.

DOI:10.1023/a:1025724526378
PMID:14501193
Abstract

We examined the consequences of isolation and adaptation to Vero cells for the receptorbinding haemagglutinin (H) gene of four syncytia-forming isolates of canine distemper virus (CDV) and of a dolphin morbillivirus isolate. A Vero-adapted CDV isolate exhibited biased hypermutation, since 11 out of 12 nucleotide differences to other isolates from the same epidemic were U-C transitions. Most of these transitions appeared to have taken place during in vitro cultivation. Previously, biased hypermutation in morbilliviruses has almost exclusively been described for subacute sclerosing panencephalitis and measles inclusion body encephalitis, which are rare measles virus brain infections. Amino acid changes in the H proteins were not required for Vero cell adaptation, suggesting that Vero cells express receptors for wild-type morbilliviruses. This strongly indicate the existence of other morbillivirus receptors than CD46 and CDw150.

摘要

我们研究了犬瘟热病毒(CDV)的四种形成合胞体的分离株以及一种海豚麻疹病毒分离株的受体结合血凝素(H)基因在适应Vero细胞及分离过程中的变化情况。一株适应Vero细胞的CDV分离株表现出偏向性超突变,因为与同一流行毒株的其他分离株相比,12个核苷酸差异中有11个是U-C转换。这些转换大多似乎发生在体外培养过程中。此前,偏向性超突变几乎仅在亚急性硬化性全脑炎和麻疹包涵体脑炎中被描述过,这两种都是罕见的麻疹病毒脑部感染。Vero细胞适应过程中H蛋白的氨基酸变化并非必需,这表明Vero细胞表达野生型麻疹病毒的受体。这有力地表明,除了CD46和CDw150之外,还存在其他麻疹病毒受体。

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本文引用的文献

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CD46- and CD150-independent endothelial cell infection with wild-type measles viruses.野生型麻疹病毒对内皮细胞的感染不依赖CD46和CD150
J Gen Virol. 2003 May;84(Pt 5):1189-1197. doi: 10.1099/vir.0.18877-0.
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Efficiency of measles virus entry and dissemination through different receptors.麻疹病毒通过不同受体进入和传播的效率。
J Virol. 2002 Aug;76(15):7460-7. doi: 10.1128/jvi.76.15.7460-7467.2002.
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SLAM (CD150)-independent measles virus entry as revealed by recombinant virus expressing green fluorescent protein.表达绿色荧光蛋白的重组病毒揭示的不依赖信号淋巴细胞激活分子(CD150)的麻疹病毒进入机制
建立用于犬瘟热病毒研究的表达犬信号淋巴细胞激活分子的犬猫细胞系。
Vet Microbiol. 2009 Jan 1;133(1-2):179-83. doi: 10.1016/j.vetmic.2008.06.016. Epub 2008 Jul 4.
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Genetically distant American Canine distemper virus lineages have recently caused epizootics with somewhat different characteristics in raccoons living around a large suburban zoo in the USA.基因上有差异的美洲犬瘟热病毒谱系最近在美国一个大型郊区动物园周边的浣熊中引发了具有不同特征的 epizootics。
Virol J. 2004 Sep 2;1:2. doi: 10.1186/1743-422X-1-2.
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4
Recombinant wild-type and edmonston strain measles viruses bearing heterologous H proteins: role of H protein in cell fusion and host cell specificity.携带异源H蛋白的重组野生型和埃德蒙斯顿株麻疹病毒:H蛋白在细胞融合和宿主细胞特异性中的作用。
J Virol. 2002 May;76(10):4891-900. doi: 10.1128/jvi.76.10.4891-4900.2002.
5
An immunohistochemical study of the distribution of the measles virus receptors, CD46 and SLAM, in normal human tissues and subacute sclerosing panencephalitis.麻疹病毒受体CD46和信号淋巴细胞激活分子(SLAM)在正常人体组织及亚急性硬化性全脑炎中分布的免疫组化研究
Lab Invest. 2002 Apr;82(4):403-9. doi: 10.1038/labinvest.3780434.
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J Virol. 2002 Feb;76(3):1505-9. doi: 10.1128/jvi.76.3.1505-1509.2002.
7
Morbilliviruses use signaling lymphocyte activation molecules (CD150) as cellular receptors.麻疹病毒利用信号淋巴细胞激活分子(CD150)作为细胞受体。
J Virol. 2001 Jul;75(13):5842-50. doi: 10.1128/JVI.75.13.5842-5850.2001.
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Adaptation of wild-type measles virus to CD46 receptor usage.野生型麻疹病毒对CD46受体利用的适应性
Arch Virol. 2001;146(2):197-208. doi: 10.1007/s007050170169.
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CD150 (SLAM) is a receptor for measles virus but is not involved in viral contact-mediated proliferation inhibition.CD150(信号淋巴细胞激活分子)是麻疹病毒的一种受体,但不参与病毒接触介导的增殖抑制。
J Virol. 2001 May;75(10):4499-505. doi: 10.1128/JVI.75.10.4499-4505.2001.
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CDw150(SLAM) is a receptor for a lymphotropic strain of measles virus and may account for the immunosuppressive properties of this virus.CDw150(信号淋巴细胞激活分子)是一种嗜淋巴细胞性麻疹病毒株的受体,可能是该病毒免疫抑制特性的原因所在。
Virology. 2001 Jan 5;279(1):9-21. doi: 10.1006/viro.2000.0711.