Chicken PRMT3 facilitates IBDV replication

Zhixuan Xiong1, Jingjing Cao2, Mengchen Xiu3

  • 1Department of Veterinary Preventive Medicine, College of Animal Science and Technology, Jiangxi Agricultural University, Qingshan Lake, Nanchang, 330045, PR China; College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, 430070, PR China.

Poultry Science
|July 9, 2024
PubMed

Insights

Chicken protein arginine methyltransferases (PRMTs) inhibit interferon production, aiding viral replication. PRMT3 specifically supports infectious bursal disease virus (IBDV) replication by suppressing interferon signaling, offering new therapeutic targets.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Protein arginine methyltransferases (PRMTs) are crucial in mammalian signaling pathways, including antiviral responses.
  • The specific roles of chicken PRMTs in interferon production and viral interactions are not well understood.

Purpose of the Study:

  • To investigate the function of chicken PRMTs in interferon production and their role in infectious bursal disease virus (IBDV) replication.
  • To elucidate the involvement of PRMTs in the MDA5-MAVS-TBK1 signaling pathway.

Main Methods:

  • Investigated chicken PRMTs' function in interferon production upon dsRNA or MDA5 stimulation.
  • Analyzed PRMT colocalization with IBDV viral protein VP3.
  • Examined PRMT3 expression, its role in IBDV replication using ectopic expression and SGC-707 inhibition, and the effects of PRMT3 silencing.

Main Results:

  • Chicken PRMTs inhibit interferon production induced by dsRNA or MDA5.
  • PRMTs participate at different stages of the MDA5-MAVS-TBK1 interferon induction pathway.
  • PRMT3 is upregulated during IBDV infection, colocalizes with VP3, and supports IBDV replication.
  • PRMT3 silencing enhances interferon production and inhibits IBDV replication.

Conclusions:

  • Chicken PRMTs, particularly PRMT3, suppress interferon signaling to promote IBDV replication.
  • PRMT3 is a key factor in IBDV pathogenesis, representing a potential target for antiviral strategies.