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Related Concept Videos

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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Vaccinia Virus Infection & Temporal Analysis of Virus Gene Expression: Part 2
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AIM2 drives inflammatory cell death and monkeypox pathogenesis.

Jueun Oh1, Yun-Ho Hwang2, Jihye Lee1

  • 1Department of Biological Science, Ulsan National Institute of Science and Technology (UNIST), Ulsan, Republic of Korea.

Cellular & Molecular Immunology
|November 12, 2025
PubMed
Summary
This summary is machine-generated.

Researchers identified AIM2 as a key sensor in the innate immune response to monkeypox virus (MPXV). Targeting AIM2 inflammasome activation offers a potential therapeutic strategy against MPXV infection.

Keywords:
AIM2InflammasomeInflammationInflammatory cell deathInnate immunityMonkeypox virus

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Area of Science:

  • Immunology and Virology
  • Innate Immunity and Host-Pathogen Interactions

Background:

  • Monkeypox virus (MPXV) poses significant global health risks.
  • Inflammasomes are critical for innate immunity but their role in MPXV infection is unclear.
  • Understanding MPXV-induced inflammasome activation is crucial for developing countermeasures.

Purpose of the Study:

  • To elucidate the molecular mechanisms of inflammasome activation during MPXV infection.
  • To identify the specific sensor responsible for detecting MPXV within the inflammasome.
  • To evaluate the therapeutic potential of targeting AIM2-mediated pathways against MPXV.

Main Methods:

  • CRISPR-knockout screening to identify cytosolic innate immune sensors.
  • Co-immunoprecipitation assays to determine protein-protein interactions.
  • In vivo studies using AIM2-deficient mice and pharmacological inhibitors.

Main Results:

  • AIM2 was identified as the primary sensor for MPXV, triggering inflammasome activation and pyroptosis.
  • AIM2 interacts with ASC and caspase-1 (CASP1), but not RIPK3 or CASP8.
  • AIM2 deficiency or inhibition in mice led to increased viral spread and pathology, while inhibition improved survival.

Conclusions:

  • AIM2-mediated inflammasome activation is a critical component of the innate immune response to MPXV.
  • Targeting AIM2 and associated programmed cell death pathways presents a promising therapeutic avenue for monkeypox.
  • IRF1 acts as an upstream regulator of AIM2, influencing MPXV-induced cell death.