Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking I kappa B Phosphorylation

文献类型： 外文期刊

第一作者： Lin, Wencheng

作者： Lin, Wencheng;Xu, Zhouyi;Yan, Yiming;Li, Hongxin;Chen, Weiguo;Chen, Feng;Xie, Qingmei;Lin, Wencheng;Xu, Zhouyi;Yan, Yiming;Li, Hongxin;Chen, Weiguo;Chen, Feng;Xie, Qingmei;Lin, Wencheng;Li, Hongxin;Chen, Weiguo;Chen, Feng;Xie, Qingmei;Lin, Wencheng;Li, Hongxin;Chen, Weiguo;Chen, Feng;Xie, Qingmei;Zhang, Huanmin

作者机构：

关键词： ALV-J; immunosuppression; macrophage; type I interferon; NF-kappa B

期刊名称：FRONTIERS IN MICROBIOLOGY （ 影响因子：5.64； 五年影响因子：6.32 ）

ISSN： 1664-302X

年卷期： 2018 年 9 卷

页码：

收录情况： SCI

摘要： Avian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that causes immunosuppression and enhances susceptibility to secondary infection, resulting in great economic losses. Although ALV-J-induced immunosuppression has been well established, the underlying molecular mechanism for such induction is still unclear. Here, we report that the inhibitory effect of ALV-J infection on type I interferon expression is associated with the down-regulation of transcriptional regulator NF-kappa B in host cells. We found that ALV-J possess the inhibitory effect on type I interferon production in HD11 cells and that ALV-J causes the up-regulation of I kappa B alpha a and down-regulation of NF-kappa B p65, and that ALV-J blocks the phosphorylation of I kappa B alpha a on Ser32/36 amino acid residues. Collectively, our findings provide insights into the pathogenesis of ALV-J.

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