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Cytokine inducible SH2-containing protein potentiate J subgroup avian leukosis virus replication and suppress antiviral responses in DF-1 chicken fibroblast cells

文献类型: 外文期刊

作者: Ruan, Zhuohao 1 ; Chen, Genghua 1 ; Xie, Tingting 1 ; Mo, Guodong 1 ; Wang, Guiyan 1 ; Luo, Wen 1 ; Li, Hongmei 1 ; Shi, 1 ;

作者机构: 1.South China Agr Univ, Coll Anim Sci, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Guangzhou 510642, Peoples R China

2.Minist Agr, Key Lab Chicken Genet Breeding & Reprod, Guangzhou 510642, Peoples R China

3.Univ Maryland, Div Immunol, Virginia Maryland Reg Coll Vet Med, College Pk, MD 20742 USA

4.South China Agr Univ, Coll Marine Sci, Guangzhou, Peoples R China

5.South China Agr Univ, Guangdong Prov Engn Res Ctr Aquat Immunizat & Aqu, Guangzhou, Peoples R China

关键词: Chicken; CIS; IFN; ISG; ALV-J

期刊名称:VIRUS RESEARCH ( 影响因子:2.934; 五年影响因子:2.775 )

ISSN: 0168-1702

年卷期: 2021 年 296 卷

页码:

收录情况: SCI

摘要: Cytokine-inducible Srchomology2 (SH2)-containing protein (CIS) belongs to the suppressors of cytokine signaling (SOCS) protein family function as a negative feedback loop inhibiting cytokine signal transduction. J subgroup avian leukosis virus (ALV-J), a commonly-seen avian virus with a feature of immunosuppression, poses an unmeasurable threat to the poultry industry across the world. However, commercial medicines or vaccines are still no available for this virus. This study aims to evaluate the potential effect of chicken CIS in antiviral response and its role on ALV-J replication. The results showed that ALV-J strain SCAU-HN06 infection induced CIS expression in DF-1 cells, which was derived from chicken embryo free of endogenous avian sarcoma-leukosis virus (ASLV) like sequences. By overexpressing CIS, the expression of chicken type I interferon (IFN-I) and interferon-stimulated genes (ISGs; PKR, ZAP, CH25H, CCL4, IFIT5, and ISG12) were both suppressed. Meanwhile, data showed that CIS overexpression also increased viral yield. Interestingly, knockdown of CIS enhanced induction of IFN-I and ISGs and inhibited viral replication. Collectively, we proved that modulation of CIS expression not only affected SCAU-HN06 replication in vitro but also altered the expression of IFN-I and ISGs that act as an essential part of antiviral innate immune system. Our data provide a potential target for developing antiviral agents for ALV-J.

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