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Glucose-6-phosphate dehydrogenase deficiency facilitates hepatitis E virus entry and aggravates liver injury

Dongxue Chen1, Xiaoxia Hu1, Yuanwen Xue1

  • 1Medical School, The Academy for Cells and Life Health, Kunming University of Science and Technology, Kunming, PR China.

Virology Journal
|December 18, 2025
PubMed

Insights

Patients with Glucose-6-phosphate dehydrogenase (G6PD) deficiency are more susceptible to Hepatitis E virus (HEV) infection. G6PD deficiency facilitates HEV entry and increases disease severity, potentially due to oxidative stress.

Area of Science:

  • Hepatology and Virology
  • Enzyme Deficiencies
  • Infectious Diseases

Background:

  • Glucose-6-phosphate dehydrogenase (G6PD) deficiency affects 400 million people globally, causing hemolysis and liver dysfunction.
  • Individuals with G6PD deficiency exhibit increased susceptibility to viral infections.
  • The specific impact of G6PD deficiency on Hepatitis E virus (HEV) infection remains largely uncharacterized.

Purpose of the Study:

  • To investigate the prevalence and characteristics of HEV infection in patients with G6PD deficiency.
  • To elucidate the underlying mechanisms of HEV susceptibility and disease severity in G6PD-deficient individuals.

Main Methods:

  • Prevalence study comparing HEV infection rates in G6PD-deficient patients versus controls.
  • In vitro experiments using hepatoma cell lines with G6PD knockdown to assess HEV susceptibility.
  • Molecular assays including Co-immunoprecipitation (Co-IP) and colocation to analyze G6PD and HEV interactions.

Main Results:

  • HEV infection prevalence was significantly higher in G6PD-deficient patients (23.8%) compared to those with normal G6PD levels (0.65%).
  • G6PD deficiency was associated with increased rates of hyperbilirubinemia and pneumonia in HEV-infected patients.
  • G6PD knockdown facilitated HEV entry, exacerbated oxidative stress, and promoted viral replication, with HEV ORF3 interacting with G6PD.

Conclusions:

  • Patients with G6PD deficiency are demonstrably susceptible to HEV infection.
  • Facilitated HEV entry and heightened oxidative stress are key factors contributing to HEV susceptibility and severe outcomes in G6PD-deficient individuals.
Abstract

Keywords:
G6PDdHEV infectionOxidative stressSeveritySusceptibility

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