Avian Tembusu virus infection effectively triggers host innate immune response through MDA5 and TLR3-dependent signaling pathways
文献类型： 外文期刊
作者： Chen, Shilong 1 ; Luo, Guifeng 1 ; Yang, Zhou 1 ; Lin, Shuncheng 1 ; Chen, Shaoying 4 ; Wang, Song 1 ; Goraya, Mohsan 1 ;
作者机构： 1.Fujian Agr & Forestry Univ, Coll Anim Sci, Fuzhou 350002, Peoples R China
2.Fujian Agr & Forestry Univ, Coll Life Sci, Fuzhou 350002, Peoples R China
3.Chinese Acad Sci, Inst Microbiol, CAS Key Lab Pathogen Microbiol & Immunol, Beijing 100101, Peoples R China
4.Fujian Acad Agr Sci, Inst Anim Husb & Vet Med, Fuzhou 350002, Peoples R China
期刊名称：VETERINARY RESEARCH （ 影响因子：3.683； 五年影响因子：4.106 ）
ISSN： 0928-4249
年卷期： 2016 年 47 卷
页码：
收录情况： SCI
摘要： Avian Tembusu virus (ATMUV) is a newly emerged flavivirus that belongs to the Ntaya virus group. ATMUV is a highly pathogenic virus causing significant economic loss to the Chinese poultry industry. However, little is known about the role of host innate immune mechanism in defending against ATMUV infection. In this study, we found that ATMUV infection significantly up-regulated the expression of type I and type III interferons (IFN) and some critical IFN-stimulated genes (ISG) in vivo and in vitro. This innate immune response was induced by genomic RNA of ATMUV. Furthermore, we observed that ATMUV infection triggered IFN response mainly through MDA5 and TLR3-dependent signaling pathways. Strikingly, shRNA-based disruption of IPS-1, IRF3 or IRF7 expression significantly reduced the production of IFN in the 293T cell model. Moreover, NF-kappa B was shown to be activated in both chicken and human cells during the ATMUV infection. Inhibition of NF-kappa B signaling also resulted in a clear decrease in expression of IFN. Importantly, experiments revealed that treatment with IFN significantly impaired ATMUV replication in the chicken cell. Consistently, type I IFN also exhibited promising antiviral activity against ATMUV replication in the human cell. Together, these data indicate that ATMUV infection triggers host innate immune response through MDA5 and TLR3-dependent signaling that controls IFN production, and thereby induces an effective antiviral immunity.
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