Porcine interferon-induced protein with tetratricopeptide repeats 3, poIFIT3, inhibits swine influenza virus replication and potentiates IFN-β production

被引：11

作者：

Li, Yongtao ^{[1
]}

Wen, Zhibin ^{[1
]}

Zhou, Hongbo ^{[1
]}

Wu, Shujuan ^{[1
]}

Jia, Guangmin ^{[1
]}

Qian, Wei ^{[1
]}

Jin, Meilin ^{[1
]}

机构：

[1] Huazhong Agr Univ, Coll Vet Med, State Key Lab Agr Microbiol, Wuhan, Peoples R China

来源：

DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY | 2015年 / 50卷 / 01期

关键词：

Porcine IFIT3; Antiviral; IFN-beta; Swine influenza virus; NF-KAPPA-B; ADAPTER PROTEIN; IDENTIFICATION; TRANSCRIPTION; RECOGNITION; TRANSDUCTION; PATHWAY; BINDING; FAMILY; CELLS;

D O I：

10.1016/j.dci.2014.10.008

中图分类号：

S9 [水产、渔业];

学科分类号：

0908 ;

摘要：

Porcine interferon-induced protein with tetratricopeptide repeats 3 (poIFIT3) is one of the genes most abundantly induced by IFN-alpha/beta and swine influenza virus (SIV). However, little information is available about the role of poIFIT3 in host defense among pigs. In this study, we detected the upregulation of poIFIT3 in porcine alveolar macrophages (PAM) infected with SIV and subsequently cloned poIFIT3 from poly(I:C)-treated PAM cells. The overexpression of poIFIT3 can efficiently suppress the replication of SIV, whereas knockdown of poIFIT3 increases SIV replication. Further experiments on the functional domains showed that the C-terminal of poIFIT3 plays the main role in the antiviral activity of poIFIT3. Moreover, poIFIT3 can significantly enhance poly(I:C)-induced IFN-beta promoter activity through both IRF3- and NF-kappa B-mediated signaling pathways. poIFIT3 potentiates IFN-beta production by targeting MAVS, which was further verified by co-immunoprecipitation. This study suggests that poIFIT3 plays a significant role in the clearance of SIV in pigs and potentiates IFN-beta production. (C) 2014 Published by Elsevier Ltd.

引用

页码：49 / 57

页数：9

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