Ibrutinib inhibits the replication of multiple poxviruses by targeting the Bruton tyrosine kinase

Kang Niu1, Xiru Wang1, Qiwei Jiang2

  • 1National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing, China.

Journal of Virology
|August 20, 2025
PubMed

Insights

Ibrutinib effectively combats mpox and other poxviruses by inhibiting viral replication. This Bruton tyrosine kinase (BTK) inhibitor shows promise as a broad-spectrum antiviral agent against emerging zoonotic threats.

Area of Science:

  • Virology
  • Drug Discovery
  • Immunology

Background:

  • Global outbreaks of monkeypox (mpox) underscore the urgent need for effective orthopoxvirus antiviral therapies.
  • Existing treatments for poxvirus infections are limited, particularly for diseases like lumpy skin disease (LSD) impacting livestock.
  • High-throughput screening identified ibrutinib, a Bruton tyrosine kinase (BTK) inhibitor, as a potential antiviral agent against vaccinia virus (VACV).

Purpose of the Study:

  • To evaluate the antiviral efficacy of ibrutinib against multiple poxviruses, including mpox virus (MPXV), VACV, and lumpy skin disease virus (LSDV).
  • To investigate the mechanism of action of ibrutinib's antiviral activity.
  • To determine the role of Bruton tyrosine kinase (BTK) in poxvirus replication.

Main Methods:

  • In vitro antiviral assays were performed across multiple cell lines to assess ibrutinib's effect on VACV, MPXV, and LSDV replication.
  • In vivo studies utilized VACV-infected BALB/c mice to evaluate ibrutinib's therapeutic potential, monitoring survival, weight, lesions, and viral load.
  • Mechanistic studies examined the impact of ibrutinib on viral protein synthesis and DNA replication, alongside BTK manipulation (knockdown and overexpression).

Main Results:

  • Ibrutinib demonstrated significant inhibition of VACV, MPXV, and LSDV replication in vitro.
  • In vivo, ibrutinib treatment improved survival rates, reduced disease severity, and lowered viral loads in VACV-infected mice.
  • Ibrutinib's mechanism involves inhibiting viral protein synthesis and DNA replication; BTK was identified as a pro-viral host factor.

Conclusions:

  • Ibrutinib is a potent antiviral agent effective against a range of poxviruses, including MPXV and LSDV.
  • The study identifies BTK as a critical host factor supporting poxvirus replication, making it a viable therapeutic target.
  • Ibrutinib represents a promising candidate for developing broad-spectrum antiviral therapies against emerging and re-emerging poxvirus infections.

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