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MAVS promotes interferon signaling in RNA virus infection by ZUFSP-mediated chromatin regulation

Tongyu Li1, Siji Li2

  • 1Department of Hematology, The First Affiliated Hospital of Ningbo University, No. 59, Liuting Street, Ningbo 315010, Zhejiang Province, China; Zhejiang University School of Medicine, Hangzhou, Zhejiang 310000, China.

International Immunopharmacology
|March 9, 2024
PubMed

Insights

Zinc finger-containing ubiquitin peptidase 1 (ZUFSP) promotes antiviral immunity by regulating interferon signaling. ZUFSP deficiency impairs the host response to RNA viruses, highlighting its crucial role in innate immunity.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Mitochondria are key platforms for innate immune signaling.
  • Mitochondrial antiviral signaling protein (MAVS) is crucial for antiviral immunity against RNA viruses.
  • Interferon-beta (IFN-β) production is vital for controlling viral infections.

Purpose of the Study:

  • To identify novel MAVS-interacting proteins.
  • To investigate the role of ZUFSP in the retinoic acid-inducible gene-I (RIG-I)-like receptor (RLR) pathway.
  • To elucidate the mechanism by which ZUFSP regulates antiviral gene expression.

Main Methods:

  • Proximity-based labeling technology in HEK293T cells.
  • Identification of ZUFSP as a MAVS-interacting protein.
  • Analysis of RNA virus-triggered antiviral gene induction in ZUFSP-deficient cells and mice.

Main Results:

  • ZUFSP positively regulates RIG-I-like receptors (RLRs), including RIG-I and MDA5.
  • ZUFSP deficiency significantly inhibits RNA virus-induced antiviral gene expression.
  • Zufsp-deficient mice exhibit increased susceptibility to RNA virus infection.
  • ZUFSP translocates to the nucleus upon viral infection and interacts with chromatin remodeling complexes.

Conclusions:

  • ZUFSP is a critical positive regulator of the MAVS-mediated antiviral signaling pathway.
  • ZUFSP facilitates interferon-stimulated gene (ISG) transcription through chromatin remodeling.
  • This study reveals a novel mechanism for MAVS-regulated chromatin remodeling in promoting interferon signaling.
Keywords:
Antiviral immune responseChromatinSMARCA5ZUFSP

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