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The Zinc-Finger Domain Was Essential for Porcine Reproductive and Respiratory Syndrome Virus Nonstructural Protein-1 alpha to Inhibit the Production of Interferon-beta

文献类型： 外文期刊

作者： Shi, Xibao 1 ; Zhang, Xiaozhuan 3 ; Wang, Fangyu 1 ; Wang, Li 1 ; Qiao, Songlin 1 ; Guo, Junqing 1 ; Luo, Chunhui 4 ; Wan 1 ;

作者机构： 1.Henan Acad Agr Sci, Henan Prov Key Lab Anim Immunol, Zhengzhou 450002, Peoples R China

2.Henan Agr Univ, Coll Anim Sci & Vet Med, Zhengzhou, Peoples R China

3.Henan Acad Sci, Henan Inst Chem, Zhengzhou, Peoples R China

4.Henan Prov Hosp Infect Dis, Dept Lab Med, Zhengzhou, Peoples R China

5.Jilin Univ, Coll Anim Sci & Vet Med, Changchun 1300

期刊名称：JOURNAL OF INTERFERON AND CYTOKINE RESEARCH （ 影响因子：2.607； 五年影响因子：2.941 ）

ISSN： 1079-9907

年卷期： 2013 年 33 卷 6 期

页码：

收录情况： SCI

摘要： Porcine reproductive and respiratory syndrome virus (PRRSV) has caused one of the most economically devastating and pandemic diseases of swine. Previous studies have documented that PRRSV nonstructural protein-1 alpha (nsp1 alpha) was an interferon antagonist, but the mechanism by which nsp1 alpha inhibited the interferon (IFN)-beta production was unclear. Here, by site-directed mutagenesis of the predicted zinc-coordinating residues of the zinc-finger (ZF) domain of nsp1 alpha or by deletion of the ZF domain of nsp1 alpha, we explored whether the ZF domain was required for nsp1 alpha to disrupt the IFN-beta production. The results showed that both mutagenesis of the predicted zinc-coordinating residues of the ZF domain and deletion of the ZF domain made nsp1 alpha lose its interferon antagonism activity. In conclusion, our present work indicated that the ZF domain of nsp1 alpha was necessary for nsp1 alpha to inhibit the IFN-beta induction.

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