Nonstructural Protein A238L of the African Swine Fever Virus (ASFV) Enhances Antiviral Immune Responses by Activating the TBK1-IRF3 Pathway

文献类型： 外文期刊

第一作者： Liu, Wei

作者： Liu, Wei;Yang, Lanlan;Di, Chuanyuan;Sun, Jing;Liu, Penggang;Liu, Huisheng;Liu, Wei;Liu, Penggang;Liu, Huisheng

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关键词： African swine fever virus; A238L; TBK1; IRF3; NF-kappa B

期刊名称：VETERINARY SCIENCES （ 影响因子：2.0； 五年影响因子：2.2 ）

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年卷期： 2024 年 11 卷 6 期

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收录情况： SCI

摘要： Simple Summary A238L, a non-structural protein of the African swine fever virus (ASFV), inhibits the activation of NF-kappa B by suppressing the HAT activity of p300. Whether A238L also affects the transcriptional activity of IRF3 remains unexplored. Here we first confirmed the ability of A238L to suppress NF-kappa B-activity in L929 cells. In contrast, A238L did not inhibit but rather increased TBK1 and IRF3 phosphorylation and enhanced innate antiviral immunity in the absence or presence of poly d (A:T) or poly (I:C) stimulation, or herpes simplex virus type 1 (HSV-1) or Sendai virus (SeV) infection. This study reveals an unrecognized role for A238L in promoting antiviral immune responses by activating the TBK1-IRF3 pathway.Abstract African swine fever virus (ASFV) is a double-stranded DNA virus with an envelope. ASFV has almost the largest genome among all DNA viruses, and its mechanisms of immune evasion are complex. Better understanding of the molecular mechanisms of ASFV genes will improve vaccine design. A238L, a nonstructural protein of ASFV, inhibits NF-kappa B activation by suppressing the HAT activity of p300. Whether A238L also affects the transcriptional activity of IRF3 remains unexplored. Here we first confirmed the ability of A238L to suppress NF-kappa B-activity in L929 cells. A238L inhibits the expression of proinflammatory cytokine genes. In contrast, A238L increased the phosphorylation levels of TBK1 and IRF3 in three different cell lines. A238L increases the IRF3-driven promoter activity and induces IRF3 nuclear translocation. Furthermore, A238L enhanced innate antiviral immunity in the absence or presence of poly d (A:T) or poly (I:C) stimulation, or herpes simplex virus type 1 (HSV-1) or Sendai virus (SeV) infection. This study reveals a previously unrecognized role of A238L in promoting antiviral immune responses by TBK1-IRF3 pathway activation.

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