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Interferon regulatory factors inhibit TiLV replication by activating interferon-a3 in tilapia (Oreochromis niloticus)

文献类型： 外文期刊

作者： Ke, Zishan 1 ; Wen, Jing 1 ; Wang, Yingying 1 ; Li, Bo 1 ; Wu, Siyu 4 ; Zhang, Defeng 1 ; Mo, Xubing 1 ; Li, Yingying 1 ; Ren, Yan 1 ; Yin, Jiyuan 1 ; Shi, Cunbin 1 ; Wang, Qing 1 ; Zheng, Shucheng 1 ;

作者机构： 1.Chinese Acad Fishery Sci, Key Lab Fishery Drug Dev, Guangdong Prov Key Lab Aquat Anim Immunol & Sustai, Minist Agr & Rural Affairs,Pearl River Fisheries R, Guangzhou 510380, Peoples R China

2.Shanghai Ocean Univ, Coll Fisheries & Life Sci, Shanghai 201306, Peoples R China

3.City Univ Hong Kong, Dept Infect Dis & Publ Hlth, State Key Lab Marine Pollut, Jockey Club,Coll Vet Med & Life Sci, Hong Kong, Peoples R China

4.Guangdong Acad Agr Sci, Agrobiol Gene Res Ctr, Guangzhou 510640, Peoples R China

5.Chinese Acad Fishery Sci, Key Lab Fishery Drug Dev, Guangdong Prov Key Lab Aquat Anim Immunol & Sustai, Minist Agr & Rural Affairs,Pearl River Fishery Res, Guangzhou 510380, Peoples R China

关键词： Interferon regulatory factor; Interferon; Innate immunity; Tilapia; Tilapia lake virus

期刊名称：DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY （ 影响因子：2.9； 五年影响因子：3.1 ）

ISSN： 0145-305X

年卷期： 2024 年 155 卷

页码：

收录情况： SCI

摘要： Tilapia lake virus (TiLV) is an emerging virus that seriously threatens the tilapia industries worldwide. Interferon regulatory factors (IRFs), which are the crucial mediators regulating the response of interferon (IFN) to combat invading viruses, have not yet been reported in tilapia during TiLV infection. Here, six IRF (IRF1, IRF2, IRF4, IRF7, IRF8, and IRF9) homologs from tilapia were characterized and analyzed. These IRFs typically shared the conserved domains and phylogenetic relationship with IRF homologs of other species. Tissue distribution analysis showed that all six IRF genes were expressed in various tissues, with the highest expression in immunerelated tissues. Furthermore, overexpression of IRFs in tilapia brain (TiB) cells significantly inhibited TiLV propagation, as evidenced by decreased viral segment 8 gene transcripts and copy numbers of viral segment 1. More importantly, all six IRF genes significantly enhanced the promoter activity of type I interferon -a3 (IFNa3) in TiB cells, suggesting that tilapia IRF genes serve as positive regulators in activating IFNa3. Surprisingly, the promoter activity of IFNa3 mediated by IRF genes was markedly inhibited post-TiLV infection, indicating that TiLV antagonized IRF-mediated IFN immune response. Taken together, six IRF genes of tilapia are highly conserved transcription factors that inhibit TiLV infection by activating the promoter of IFNa3, which is in turn restrained by TiLV. These findings broaden our knowledge about the functionality of IRF-mediated antiviral immunity in tilapia against TiLV infection and host-TiLV interaction, which lays a foundation for developing antiviral strategies in tilapia cultural industries.

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