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<p>In August 2024, mpox was declared a public health emergency. However, little is known about how the proteins of the mpox virus (MPXV) interact with host innate immunity. This study identified that the D8L protein of MPXV inhibited the interferon (IFN)-mediated antiviral innate immune response and suppressed the mRNA transcription and protein expression of several IFN-stimulated genes, including <i>Cig5</i>, <i>MX2</i>, <i>ISG56</i>, <i>IFITM1</i>, <i>OAS1</i>, and <i>ISG15</i>. Mechanistically, D8L prevented antiviral immune responses by interacting with signal transducer and activator of transcription 1 (STAT1). Furthermore, D8L interacted with the SH2 structural domain of the STAT1 protein but not with other regions. The point-mutant plasmids capable of binding STAT1 were D8L-9–11, D8L-13, and D8L-18. In addition, D8L attenuated IFN responses by inhibiting the phosphorylation and nuclear translocation of STAT1. These findings provide valuable information for the development of novel antiviral therapies.</p>

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Mpox virus D8L protein binds to STAT1 and inhibits its phosphorylation to antagonize IFN-induced signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月14日

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  • Hao Zhou,
  • Zixuan Yang,
  • Qiwei Jiang,
  • Chao Shang,
  • Yang Wang,
  • Jinlin Guo,
  • Xiao Li,
  • Ping Leng

摘要

In August 2024, mpox was declared a public health emergency. However, little is known about how the proteins of the mpox virus (MPXV) interact with host innate immunity. This study identified that the D8L protein of MPXV inhibited the interferon (IFN)-mediated antiviral innate immune response and suppressed the mRNA transcription and protein expression of several IFN-stimulated genes, including Cig5, MX2, ISG56, IFITM1, OAS1, and ISG15. Mechanistically, D8L prevented antiviral immune responses by interacting with signal transducer and activator of transcription 1 (STAT1). Furthermore, D8L interacted with the SH2 structural domain of the STAT1 protein but not with other regions. The point-mutant plasmids capable of binding STAT1 were D8L-9–11, D8L-13, and D8L-18. In addition, D8L attenuated IFN responses by inhibiting the phosphorylation and nuclear translocation of STAT1. These findings provide valuable information for the development of novel antiviral therapies.