ArticleCell death & disease2025
IFN-β production promotes metabolic rewiring and protection against oxidative stress in hepatitis delta virus-infected hepatocyte cultures.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Immunometabolic reprogramming in multiple sclerosis: from pathogenic amplifier to therapeutic target in neuroinflammation and remyelination.Inflammopharmacology · 2026Review
- Selenium-enriched probiotics improve growth performance in PCV2-infected weaned piglets by regulating antioxidant systems and immune responses.Veterinary research communications · 2026Article
- Chronic hepatitis D infection is associated with distinguishing microbial and functional features in the gut microbiome.Frontiers in microbiology · 2026Article
- Metabolic Imprint of Poliovirus on Glioblastoma Cells and Its Role in Virus Replication and Cytopathic Activity.International journal of molecular sciences · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
Type I interferons are secreted in response to various stimuli and are used as a treatment for many diseases, including infections with the hepatitis B virus (HBV) and its satellite virus, hepatitis delta (HDV). HDV significantly aggravates HBV-mediated liver damage and is - in contrast to HBV - a strong inducer of interferon responses, including IFN-β. As the role of IFN- β in liver metabolism is so far ill explored, we studied its impact on hepatocyte metabolism in HDV-infected cultures. Transcriptome analysis, isotope tracing and functional tests on differentiated, HDV-infected hepatocytes showed reduction of mitochondrial TCA cycle and respiratory activity and increases in serine, asparagine and glutathione synthesis. Furthermore, the stress-response factor ATF4 was activated by IFN-β via yet unidentified non-canonical mechanisms and mediated resistance to oxidants. IFN-β furthermore reduced the expression and activity of liver differentiation markers. Thus, IFN-β-mediated dedifferentiation and stress-resistance may contribute to HDV-associated liver pathology.
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