A single amino acid substitution controls DAF-dependent phenotype of echovirus 11 in rhabdomyosarcoma cells

A single amino acid substitution controls DAF-dependent phenotype of echovirus 11 in rhabdomyosarcoma cells
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DOI:
10.1016/j.virusres.2012.03.007
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发表时间:
2012-06-01
期刊:
影响因子:
5
通讯作者:
Sokolova, Zoya I.
Sokolova, Zoya I.
中科院分区:
医学3区
文献类型:
--
作者:
Novoselov, Alexey V.;Rezaykin, Alexey V.;Sokolova, Zoya I.

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衰减加速因子(DAF)CD 55)被埃可病毒11(EV 11)的OAF依赖性(Daf+)变体用作主要细胞受体。EV 11与DAF的相互作用是完全可逆的,因此DAF依赖性变体需要一个未鉴定的辅助受体来启动脱壳。EV 11的Daf-变体不与E11相互作用,使用替代的初级细胞受体。本研究的目的是检验这一假设是否辅受体,这是必要的DAF依赖性变体的脱壳,可以作为一个替代的主要受体的DAF-变异的EV 11。通过在横纹肌肉瘤(RD)细胞系中使用EV 11的两个密切相关的daf+和daf-克隆的模型,表明衣壳蛋白VP 2中的单个氨基酸取代可以控制DAF依赖性表型的表达。抗EV 11单克隆抗体能阻断依赖OAF的daf+克隆对RD细胞的感染,但不能阻断EV 11的daf-克隆对RD细胞的感染。由于这两个克隆的结构蛋白仅在受体结合位点上不同,因此daf-克隆的未鉴定的非cirrhosis初级受体可能具有与daf+克隆所需的未包被辅助受体相同的构象。尽管在初级受体的差异,daf+和daf-克隆同样抑制β 2-微球蛋白的单克隆抗体。抗I类人白细胞抗原分子的单克隆抗体B9.12.1对任一克隆均无抑制作用。讨论了EV 11的Daf+和Daf-变体的会聚细胞内交通的假设。(C)2012 Elsevier B. V.保留所有权利。
Decay accelerating factor (DAF. CD55) is used by OAF-dependent (Daf+) variants of echovirus 11 (EV11) as a primary cellular receptor. The interaction of EV11 with DAF is completely reversible, therefore DAF-dependent variants require an unidentified coreceptor to initiate uncoating. Daf- variants of EV11, which do not interact with DAF, use an alternative primary cellular receptor. The aim of this study was to test the hypothesis whether the coreceptor, which is necessary for the uncoating of DAF-dependent variants, may act as an alternative primary receptor for the Daf- variants of EV11. By using the model of the two closely related daf+ and daf- clones of EV11 in rhabdomyosarcoma (RD) cell line, it was shown that a single amino acid substitution in the capsid protein VP2 could control the expression of the DAF-dependent phenotype. Anti-DAF monoclonal antibody has blocked the infection of RD cells by the OAF-dependent daf+ clone, but not by the daf- clone of EV11. Since the structural proteins of the two clones differed only in the receptor binding site for DAF, the unidentified non-DAF primary receptor for the daf- clone might have the same conformation as the uncoating coreceptor required for the daf+ clone. Despite the difference in primary receptors, both daf+ and daf- clones were equally inhibited by a monoclonal antibody to beta2-microglobulin. The monoclonal antibody B9.12.1 to class I human leukocyte antigen molecules showed no inhibitory effect in regards to either clone. The hypothesis of convergent intracellular traffic of Daf+ and Daf- variants of EV11 is discussed. (C) 2012 Elsevier B.V. All rights reserved.