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IFI16 Inhibits Porcine Reproductive and Respiratory Syndrome Virus 2 Replication in a MAVS-Dependent Manner in MARC-145 Cells

文献类型： 外文期刊

作者： Chang, Xiaobo 1 ; Shi, Xibao 2 ; Zhang, Xiaozhuan 3 ; Wang, Li 2 ; Li, Xuewu 2 ; Wang, Aiping 4 ; Deng, Ruiguang 2 ; Zhou 1 ;

作者机构： 1.Northwest A&F Univ, Coll Vet Med, Yangling 712100, Shaanxi, Peoples R China

2.Henan Acad Agr Sci, Henan Prov Key Lab Anim Immunol, Zhengzhou 450002, Peoples R China

3.Henan Normal Univ, Coll Life Sci, Xinxiang 453007, Henan, Peoples R China

4.Zhengzhou Univ, Dept Bioengn, Zhengzhou 450000, Peoples R China

5.Henan Agr Univ, Coll Anim Sci & Vet Med, Zhengzhou 450002, Peoples R China

6.Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Jiangsu, Peoples R China

关键词： PRRSV; IFI16; antiviral protein; MAVS

期刊名称：VIRUSES-BASEL （ 影响因子：5.048； 五年影响因子：5.127 ）

ISSN：

年卷期： 2019 年 11 卷 12 期

页码：

收录情况： SCI

摘要： Porcine reproductive and respiratory syndrome virus (PRRSV) is a single-stranded positive-sense RNA virus, and the current strategies for controlling PRRSV are limited. Interferon gamma-inducible protein 16 (IFI16) has been reported to have a broader role in the regulation of the type I interferons (IFNs) response to RNA and DNA viruses. However, the function of IFI16 in PRRSV infection is unclear. Here, we revealed that IFI16 acts as a novel antiviral protein against PRRSV-2. IFI16 could be induced by interferon-beta (IFN-beta). Overexpression of IFI16 could significantly suppress PRRSV-2 replication, and silencing the expression of endogenous IFI16 by small interfering RNAs led to the promotion of PRRSV-2 replication in MARC-145 cells. Additionally, IFI16 could promote mitochondrial antiviral signaling protein (MAVS)-mediated production of type I interferon and interact with MAVS. More importantly, IFI16 exerted anti-PRRSV effects in a MAVS-dependent manner. In conclusion, our data demonstrated that IFI16 has an inhibitory effect on PRRSV-2, and these findings contribute to understanding the role of cellular proteins in regulating PRRSV replication and may have implications for the future antiviral strategies.

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