Nsp1 proteins of group I and SARS coronaviruses share structural and functional similarities

被引:31
|
作者
Wang, Yongjin [1 ]
Shi, Huiling [1 ]
Rigolet, Pascal [2 ]
Wu, Nannan [1 ]
Zhu, Lichen [1 ]
Xi, Xu-Guang [2 ]
Vabret, Astrid [3 ]
Wang, Xiaoming [1 ]
Wang, Tianhou [1 ]
机构
[1] E China Normal Univ, Lab Wildlife Epidem Dis, Shanghai 200062, Peoples R China
[2] Ctr Univ Orsay, CNRS, UMR 3348, Inst Curie,Sect Rech, F-91405 Orsay, France
[3] Univ Hosp Caen, Virol Lab, F-14033 Caen, France
关键词
Group I coronavirus; nsp1; Innate immunity; RESPIRATORY-SYNDROME CORONAVIRUS; DOUBLE-STRANDED-RNA; MOUSE HEPATITIS-VIRUS; HOST GENE-EXPRESSION; INFECTED-CELLS; NONSTRUCTURAL PROTEIN-1; INTERFERON-PRODUCTION; ALPHA-INTERFERON; RATIONAL DESIGN; VACCINIA VIRUS;
D O I
10.1016/j.meegid.2010.05.014
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
The nsp1 protein of the highly pathogenic SARS coronavirus suppresses host protein synthesis, including genes involved in the innate immune system. A bioinformatic analysis revealed that the nsp1 proteins of group I and SARS coronaviruses have similar structures. Nsp1 proteins of group I coronaviruses interacted with host ribosomal 40S subunit and did not inhibit IRF-3 activation. However, synthesis of host immune and non-immune proteins was inhibited by nsp1 proteins at both transcriptional and translational levels, similar to SARS coronavirus nsp1. These results indicate that different coronaviruses might employ the same nsp1 mechanism to antagonize host innate immunity and cell proliferation. However, nsp1 may not be the key determinant of viral pathogenicity, or the factor used by the SARS coronavirus to evade host innate immunity. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:919 / 924
页数:6
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