IFN-Inducible SerpinA5 Triggers Antiviral Immunity by Regulating STAT1 Phosphorylation and Nuclear Translocation

Int J Mol Sci. 2023 Mar 13;24(6):5458. doi: 10.3390/ijms24065458.

Abstract

Deeply understanding virus-host interactions is a prerequisite for developing effective strategies to control frequently emerging infectious diseases, which have become a serious challenge for global public health. The type I interferon (IFN)-mediated JAK/STAT pathway is well known for playing an essential role in host antiviral immunity, but the exact regulatory mechanisms of various IFN-stimulated genes (ISGs) are not yet fully understood. We herein reported that SerpinA5, as a novel ISG, played a previously unrecognized role in antiviral activity. Mechanistically, SerpinA5 can upregulate the phosphorylation of STAT1 and promote its nuclear translocation, thus effectively activating the transcription of IFN-related signaling pathways to impair viral infections. Our data provide insights into SerpinA5-mediated innate immune signaling during virus-host interactions.

Keywords: STAT1 phosphorylation; SerpinA5; innate immunity; interferon-stimulated genes (ISGs).

MeSH terms

  • Active Transport, Cell Nucleus
  • Antiviral Agents* / pharmacology
  • Immunity, Innate
  • Interferon Type I / metabolism
  • Janus Kinases* / metabolism
  • Phosphorylation
  • STAT Transcription Factors / metabolism
  • STAT1 Transcription Factor / metabolism
  • Signal Transduction

Substances

  • Antiviral Agents
  • Janus Kinases
  • STAT Transcription Factors
  • STAT1 Transcription Factor
  • Interferon Type I