ACSL1 Inhibits ALV-J Replication by IFN-I Signaling and PI3K/Akt Pathway

文献类型： 外文期刊

第一作者： Zhang, Qihong

作者： Zhang, Qihong;Xie, Tingting;Mo, Guodong;Zhang, Zihao;Lin, Ling;Zhang, Xiquan;Zhang, Qihong;Xie, Tingting;Mo, Guodong;Zhang, Zihao;Lin, Ling;Zhang, Xiquan;Zhang, Qihong;Xie, Tingting;Mo, Guodong;Zhang, Zihao;Lin, Ling;Zhang, Xiquan

作者机构：

关键词： ACSL1; ALV-J; IFN-I; PI3K; Akt; apoptosis

期刊名称：FRONTIERS IN IMMUNOLOGY （ 影响因子：7.561； 五年影响因子：7.624 ）

ISSN： 1664-3224

年卷期： 2021 年 12 卷

页码：

收录情况： SCI

摘要： J subgroup avian leukosis virus (ALV-J) infection causes serious immunosuppression problems, leading to hematopoietic malignancy tumors in chicken. It has been demonstrated that interferon-stimulated genes (ISGs) could limit ALV-J replication; nevertheless, the underlying mechanisms remain obscure. Here, we demonstrate that Long-chain Acyl-CoA synthetase 1 (ACSL1) is an interferon (IFN)-stimulated gene that specifically restricts the replication of ALV-J due to the higher IFN-I production. More importantly, ACSL1 induces primary monocyte-derived macrophages (MDMs) to pro-inflammatory phenotypic states during ALV-J infection, and ACSL1 mediates apoptosis through the PI3K/Akt signaling pathway in ALV-J-infected primary monocyte-derived macrophages (MDMs). Overall, these results provide evidence that ACSL1 contributes to the antiviral response against ALV-J.

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