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Functional Imaging of Viral Transcription Factories Using 3D Fluorescence Microscopy
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KSHV vIL-6 Enhances Inflammatory Responses by Epigenetic Reprogramming.

Tomoki Inagaki1, Kang-Hsin Wang1, Ashish Kumar1

  • 1Department of Dermatology, School of Medicine, the University of California Davis (UC Davis), Sacramento, California USA.

Biorxiv : the Preprint Server for Biology
|July 28, 2023
PubMed
Summary
This summary is machine-generated.

Kaposi sarcoma-associated herpesvirus (KSHV) inflammatory cytokine syndrome (KICS) involves high viral load and elevated IL-6. Prolonged exposure to viral IL-6 (vIL-6) creates an epigenetic memory, increasing inflammation risk in KSHV-infected individuals.

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Area of Science:

  • Immunology
  • Epigenetics
  • Virology

Background:

  • Kaposi sarcoma-associated herpesvirus (KSHV) inflammatory cytokine syndrome (KICS) is a chronic inflammatory condition linked to KSHV infection, characterized by high viral loads and elevated serum levels of KSHV-encoded IL-6 (vIL-6) and human IL-6 (hIL-6).
  • KICS is associated with increased risks of malignancies and other complications, with prolonged vIL-6 exposure suspected to play a role in disease progression, though its precise biological effects remain unclear.

Approach:

  • Utilized thiol-linked alkylation for metabolic sequencing and cleavage under target & release using nuclease (TRAM-seq) to investigate the impact of prolonged vIL-6 exposure on chromatin and cytokine production.
  • Examined changes in chromatin landscape, including bromodomain-containing 4 (BRD4) and histone H3 lysine 27 acetylation (H3K27ac) co-occupancies, and their association with RNA polymerase II (RNAPII) and NF-κB p65 binding.
  • Assessed the effect of the BRD4 inhibitor OTX015 on cytokine production.

Key Points:

  • Prolonged vIL-6 exposure led to increased BRD4 and H3K27ac co-occupancies on chromatin, often colocalizing with poised RNAPII.
  • Enhanced BRD4 recruitment at promoters correlated with increased and sustained NF-κB p65 binding post-lipopolysaccharide stimulation.
  • This mechanism resulted in heightened production of hIL-6 and IL-10 in vitro, an effect reversed by the BRD4 inhibitor OTX015.

Conclusions:

  • Persistent vIL-6 exposure may induce an epigenetic memory in monocytes, establishing a chromatin state that favors inflammatory responses.
  • This epigenetic modification could explain the elevated risk of chronic inflammatory diseases observed in individuals with KSHV infection.
  • Targeting BRD4 offers a potential therapeutic strategy for mitigating KICS-associated inflammation.