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Poly(I:C) inhibits porcine reproductive and respiratory syndrome virus replication in MARC-145 cells via activation of IFIT3

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文献类型：外文期刊

作者： Zhang, Lili ¹ ; Liu, Jie ¹ ; Bai, Juan ¹ ; Du, Yijun ² ; Wang, Xiaoye ¹ ; Liu, Xing ¹ ; Jiang, Ping ¹ ;

作者机构： 1.Nanjing Agr Univ, Key Lab Anim Dis Diagnost & Immunol, Minist Agr, Coll Vet Med, Nanjing 210095, Jiangsu, Peoples R China

2.Shandong Acad Agr Sci, Inst Anim Sci & Vet Med, Shandong Key Lab Anim Dis Control & Breeding, Jinan, Peoples R China

关键词： PRRSV;IFN-beta;Poly(I:C);IFIT3;Antivirus

期刊名称：ANTIVIRAL RESEARCH （影响因子：5.97；五年影响因子：5.801 ）

ISSN： 0166-3542

年卷期： 2013 年 99 卷 3 期

页码：

收录情况： SCI

摘要： Porcine reproductive and respiratory syndrome virus (PRRSV) is a major cause of heavy economic losses in many swine-producing regions. Current vaccination strategies and antiviral drugs provide only limited protection. Interferon (IFN)-induced protein with tetratricopeptide repeats 3 (IFIT3) has been characterized as the product of a novel antiviral gene and as an important modulator in innate immunity. However, the role of IFIT3 in PRRSV infection is scarcely understood. In this study, polyinosinic-polycytidylic acid (poly(I:C)) inhibited PRRSV replication in MARC-145 cells, following the appearance of increased IFIT3. Overexpression of porcine IFIT3 resulted in a decrease of PRRSV. Knockdown of IFIT3 in MARC-145 cells increased PRRSV replication and impaired the antiviral activity mediated by poly(I:C). Moreover, in the presence or absence of IFIT3, poly(I:C)-induced IFN-beta promoter activity was significantly boosted or crippled, respectively. IFIT3, TBK1 and phosphorylation of IRF3 were activated in poly(I:C)-transfected MARC-145 cells. It demonstrated that IFIT3 plays an important role in IFN-beta induction in MARC-145 cells, and, when activated, it can inhibit PRRSV replication. (C) 2013 Elsevier B.V. All rights reserved.

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意 见 箱

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意见箱