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Related Concept Videos

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Related Experiment Video

Updated: Jul 15, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

HBV pgRNA induces chronic inflammation in an IL-1β-dependent manner.

Aikaterini Skeva1, Konstantinos Marmanis2, Maria Ntinopoulou3

  • 1Laboratory of Microbiology, Department of Medicine, School of Health Sciences, Democritus University of Thrace, Alexandroupolis, Greece.

Frontiers in Immunology
|July 13, 2026
PubMed
Summary

Hepatitis B virus pregenomic RNA (pgRNA) activates platelets, leading to inflammation. This study reveals pgRNA

Keywords:
HBeAg negativeLL-37chronic hepatitis Bchronic inflammationinterleukin-1b (IL-1β)pregenomic RNA

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Last Updated: Jul 15, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
09:01

An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection

Published on: December 10, 2013

Area of Science:

  • Immunology
  • Hepatology
  • Molecular Biology

Background:

  • Chronic hepatitis B (CHB) is a significant global health concern.
  • Pregenomic RNA (pgRNA) is an indicator of HBV transcriptional activity.
  • Understanding CHB's impact on innate immunity is crucial for treatment.

Purpose of the Study:

  • To investigate the transcriptomic profile of pgRNA-positive CHB patients.
  • To compare pgRNA-positive and pgRNA-negative CHB patients.
  • To evaluate the role of pgRNA in innate immunity and inflammation.

Main Methods:

  • Analysis of 88 CHB patients on nucleoside analogs.
  • Detection of viral load, genotype, and HBV pgRNA.
  • Transcriptomic sequencing and bioinformatic analysis of pgRNA-positive and negative samples.
  • Examination of platelet activation, platelet-neutrophil interactions, and cytokine expression (IL-1β, IL-17A, LL-37).

Main Results:

  • 18.1% of CHB patients were pgRNA-positive.
  • Transcriptomic analysis identified shared pathways: platelet activation and neutrophil degranulation.
  • HBV pgRNA stimulated platelets, inducing autophagy and LL-37 synthesis.
  • Platelet-neutrophil interactions resulted in a proinflammatory phenotype with IL-1β overexpression and limited NET formation.

Conclusions:

  • HBV pgRNA activates platelets via autophagy.
  • The platelet-neutrophil axis drives a proinflammatory state with elevated IL-1β.
  • Findings highlight the role of pgRNA in CHB pathogenesis and innate immune response.