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Area of Science:

  • Virology
  • Immunology
  • Epigenetics

Background:

  • Kaposi sarcoma-associated herpesvirus (KSHV) inflammatory cytokine syndrome (KICS) is a chronic inflammatory disease linked to KSHV infection.
  • KICS is characterized by high KSHV viral load and elevated serum levels of viral IL-6 (vIL-6) and human IL-6 (hIL-6).
  • Prolonged vIL-6 exposure is suspected to drive disease progression, but its precise biological effects are not fully understood.

Purpose of the Study:

  • To investigate the impact of prolonged vIL-6 exposure on the chromatin landscape and subsequent cytokine production.
  • To elucidate the molecular mechanisms by which vIL-6 influences inflammatory responses in monocytes.
  • To assess the therapeutic potential of BRD4 inhibitors in mitigating vIL-6-driven inflammation.

Main Methods:

  • Utilized thiol(SH)-linked alkylation for metabolic sequencing (SLAM) and Cleavage Under Target & Release Using Nuclease (CUT&RUN) analyses.
  • Examined chromatin modifications, including histone acetylation and transcription factor binding (BRD4, NF-κB p65).
  • Assessed cytokine production (hIL-6, IL-10) and the effect of BRD4 inhibitors (OTX015, MZ1).

Main Results:

  • Prolonged vIL-6 exposure increased co-occupancy of BRD4 and acetylated histone H3K27 on chromatin, often colocalizing with poised RNA polymerase II.
  • Enhanced BRD4 recruitment led to increased and sustained NF-κB p65 binding after stimulation, promoting rapid and prolonged transcription bursts.
  • This resulted in elevated hIL-6 and IL-10 production, which was reversed by BRD4 inhibitors.

Conclusions:

  • Persistent vIL-6 exposure establishes a permissive chromatin landscape for inflammatory responses in monocytes.
  • This epigenetic memory, driven by BRD4 and NF-κB, may explain the heightened risk of chronic inflammatory diseases in KSHV-infected individuals.
  • BRD4 inhibition offers a potential therapeutic strategy for KICS by blocking vIL-6-induced inflammatory cytokine production.