دورية أكاديمية
أعرض في EDS

Hepatitis B virus e antigen induces atypical metabolism and differentially regulates programmed cell deaths of macrophages.

التفاصيل البيبلوغرافية
العنوان: Hepatitis B virus e antigen induces atypical metabolism and differentially regulates programmed cell deaths of macrophages.
المؤلفون: Li Y; Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America., Wu C; Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America., Lee J; Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America., Ning Q; Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America., Lim J; Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America., Eoh H; Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America., Wang S; Michael Amini Transfusion Medicine Center, City of Hope, Duarte, California, United States of America., Hurrell BP; Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America., Akbari O; Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America., Ou JJ; Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
المصدر: PLoS pathogens [PLoS Pathog] 2024 Mar 11; Vol. 20 (3), pp. e1012079. Date of Electronic Publication: 2024 Mar 11 (Print Publication: 2024).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101238921 Publication Model: eCollection Cited Medium: Internet ISSN: 1553-7374 (Electronic) Linking ISSN: 15537366 NLM ISO Abbreviation: PLoS Pathog Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science, c2005-
مواضيع طبية MeSH: Hepatitis B virus*/genetics , Hepatitis B*, Humans ; Hepatitis B e Antigens/metabolism ; Macrophages/metabolism ; Apoptosis
مستخلص: 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.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2024 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
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معلومات مُعتمدة: R01 AI129540 United States AI NIAID NIH HHS; R01 AI169687 United States AI NIAID NIH HHS; R37 AI129540 United States AI NIAID NIH HHS; R01 HL151493 United States HL NHLBI NIH HHS; R01 AI148304 United States AI NIAID NIH HHS; R01 AI145813 United States AI NIAID NIH HHS
المشرفين على المادة: 0 (Hepatitis B e Antigens)
تواريخ الأحداث: Date Created: 20240311 Date Completed: 20240325 Latest Revision: 20240612
رمز التحديث: 20240612
مُعرف محوري في PubMed: PMC10957081
DOI: 10.1371/journal.ppat.1012079
PMID: 38466743
قاعدة البيانات: MEDLINE
الوصف
تدمد:1553-7374
DOI:10.1371/journal.ppat.1012079