ArticlePLoS pathogens2024
Hepatitis B virus e antigen induces atypical metabolism and differentially regulates programmed cell deaths of macrophages.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 9 citations in OpenAlex.
- Dysregulated BCR repertoire and metabolic state of HBsAg-specific B cells in chronic hepatitis B revealed by integrated single-cell analysis.Hepatology communications · 2026Article
- Macrophages in oncoviral infections: from immune regulators to therapeutic targets.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Bioenergetic-active hybrid nanovesicles empower tumor associated macrophages phagocytosis for cancer immunotherapy.Materials today. Bio · 2026Article
- The Landscape of Anti-HBV Activity in Essential Oils: A Machine Learning-Based Virtual Screening Framework and Anti-HBV Activity ofACS omega · 2026Article
- The clinical significance and optimization strategies of HBeAg seroclearance in chronic hepatitis B treatment.Frontiers in cellular and infection microbiology · 2026Review
- Review
- Hepatitis B Virus e Antigen in Mother-to-Child Transmission and Clinical Management of Hepatitis B.Viruses · 2025Review
- HBV p22-interacting protein C1QBP inhibits viral replication through impeding nucleocapsid formation and nuclear import.PLoS pathogens · 2025Article
- The role of liver macrophages in viral liver pathogenesis.Journal of leukocyte biology · 2025Review
- Pyroptosis, a double-edged sword during pathogen infection: a review.Cell death discovery · 2025Review
- [Progress in clinical research related to viral hepatitis in 2024].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Macrophages can undergo M1-like proinflammatory polarization with low oxidative phosphorylation (OXPHOS) and high glycolytic activities or M2-like anti-inflammatory polarization with the opposite metabolic activities. Here we show that M1-like macrophages induced by hepatitis B virus (HBV) display high OXPHOS and low glycolytic activities. This atypical metabolism induced by HBV attenuates the antiviral response of M1-like macrophages and is mediated by HBV e antigen (HBeAg), which induces death receptor 5 (DR5) via toll-like receptor 4 (TLR4) to induce death-associated protein 3 (DAP3). DAP3 then induces the expression of mitochondrial genes to promote OXPHOS. HBeAg also enhances the expression of glutaminases and increases the level of glutamate, which is converted to α-ketoglutarate, an important metabolic intermediate of the tricarboxylic acid cycle, to promote OXPHOS. The induction of DR5 by HBeAg leads to apoptosis of M1-like and M2-like macrophages, although HBeAg also induces pyroptosis of the former. These findings reveal novel activities of HBeAg, which can reprogram mitochondrial metabolism and trigger different programmed cell death responses of macrophages depending on their phenotypes to promote HBV persistence.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.