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Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
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Related Experiment Video

Updated: Oct 4, 2025

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle
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Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle

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Inducers of the NF-κB pathways impair hepatitis delta virus replication and strongly decrease progeny infectivity

Maud Michelet1, Dulce Alfaiate2, Brieux Chardès1

  • 1INSERM, U1052, Cancer Research Center of Lyon (CRCL), University of Lyon (UCBL1), CNRS UMR_5286, Centre Léon Bérard, Lyon, France.

JHEP Reports : Innovation in Hepatology
|February 10, 2022
PubMed
Summary

Hepatitis delta virus (HDV) infection, the most severe hepatitis, can be inhibited by immune stimulators. These novel therapies targeting NF-κB pathways show promise for treating chronic HBV/HDV infections.

Keywords:
HDV-AG(s), HDV anti-genome(s)HDV-G(s), HDV genome(s)Hepatitis B virusHepatitis D virusIFN, interferonIL-, interleukin-L-HDAg, large HDV antigenLTβR, lymphotoxin-β receptorNF-κBNTCP, Na+-taurocholate cotransporting polypeptidePHH, primary human hepatocytePeg-IFN-α, pegylated interferon-αRNP, ribonucleoproteinS-HDAg, small HDV antigenTLR, Toll-like receptorTNF, tumor necrosis factorantiviral activitydHepaRG, differentiated HepaRG cellshepatocyteslymphotoxin beta receptorrh, recombinant humantoll-like receptorvge, viral genome equivalent

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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Area of Science:

  • Hepatology
  • Virology
  • Immunology

Background:

  • Hepatitis delta virus (HDV) causes severe chronic viral hepatitis with poor treatment options.
  • HDV superinfection accelerates liver disease progression and increases mortality risk.
  • Current therapies for HDV are limited, with suboptimal responses to interferon-α.

Purpose of the Study:

  • To investigate the potential of innate immune stimulators as a novel therapeutic strategy against HDV replication.
  • To analyze the effects of TLR-1/2 and LTβR agonists on HDV infection in relevant cellular models.

Main Methods:

  • Utilized in vitro models of HDV and HBV infection using primary human hepatocytes (PHHs).
  • Employed the HepaRG cell line for exploring innate immune therapies against viral hepatitis.
  • Assessed the impact of Pam3CSK4 and BS1 agonists on viral RNA and protein levels.

Main Results:

  • Pam3CSK4 and BS1 agonists demonstrated significant anti-HDV effects in infected hepatocytes.
  • These immune modulators reduced viral RNA and protein levels without causing cellular toxicity.
  • Agonists also inhibited HDV progeny release and decreased viral infectivity.

Conclusions:

  • Immune modulators activating NF-κB pathways show potent inhibition of HDV replication.
  • These findings suggest a promising therapeutic avenue for chronic HBV/HDV-infected patients.
  • Further evaluation of these immune-modulating agents is warranted for clinical application.