ArticleCell reports2022
Macrophages activated by hepatitis B virus have distinct metabolic profiles and suppress the virus via IL-1β to downregulate PPARα and FOXO3.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 37 citations in OpenAlex.
- Review
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- 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
- Article
- Review
- TLR9 decreases FOXO3 expression to prevent excessive inflammation in macrophage activation syndrome.iScience · 2025Article
- Hepatitis B Virus e Antigen in Mother-to-Child Transmission and Clinical Management of Hepatitis B.Viruses · 2025Review
- HBV and host metabolic crosstalk: Reprogramming pathways for viral replication and pathogenesis.Virologica Sinica · 2025Review
- The role of liver macrophages in viral liver pathogenesis.Journal of leukocyte biology · 2025Review
- IL-1b-Bearing NETs: Bridging Inflammation to Early Cirrhosis in Hepatitis B.International journal of molecular sciences · 2025Article
- Mitochondrial oxidative stress inhibited Sirt3/Foxo3/PPARα pathway and aggravated copper and zinc co-deficiency-induced hepatic lipotoxicity in a fish model.Cellular and molecular life sciences : CMLS · 2025Article
- Synergy between pluripotent stem cell-derived macrophages and self-renewing macrophages: Envisioning a promising avenue for the modelling and cell therapy of infectious diseases.Cell proliferation · 2025Review
- Metabolic hijacking styles: a review of how viral life cycles dictate glucose metabolism reprogramming.Frontiers in microbiology · 2025Review
- Early boosting of p38 MAPK signaling pathway by lycorine hydrochloride potently inhibits PRRSV proliferation in primary and established cells.Frontiers in microbiology · 2025Article
- Circulating plasma derived exosomes from systemic lupus erythematosus aggravate lupus nephritis through miR-122-5p/FOXO3-mediated macrophage activation.Journal of nanobiotechnology · 2024Article
- Effective protection of biological tissues from severe blunt force injury by engineered nanoscale liquid flow.Scientific reports · 2024Article
- Hepatitis B virus e antigen induces atypical metabolism and differentially regulates programmed cell deaths of macrophages.PLoS pathogens · 2024Article
- The novel mechanism facilitating chronic hepatitis B infection: immunometabolism and epigenetic modification reprogramming.Frontiers in immunology · 2024Review
- Inflammaging and fatty acid oxidation in monocytes and macrophages.Immunometabolism (Cobham, Surrey) · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Macrophages display phenotypic plasticity and can be induced by hepatitis B virus (HBV) to undergo either M1-like pro-inflammatory or M2-like anti-inflammatory polarization. Here, we report that M1-like macrophages stimulated by HBV exhibit a strong HBV-suppressive effect, which is diminished in M2-like macrophages. Transcriptomic analysis reveals that HBV induces the expression of interleukin-1β (IL-1β) in M1-like macrophages, which display a high oxidative phosphorylation (OXPHOS) activity distinct from that of conventional M1-like macrophages. Further analysis indicates that OXPHOS attenuates the expression of IL-1β, which suppresses the expression of peroxisome proliferator-activated receptor α (PPARα) and forkhead box O3 (FOXO3) in hepatocytes to suppress HBV gene expression and replication. Moreover, multiple HBV proteins can induce the expression of IL-1β in macrophages. Our results thus indicate that macrophages can respond to HBV by producing IL-1β to suppress HBV replication. However, HBV can also metabolically reprogram macrophages to enhance OXPHOS to minimize this host antiviral response.
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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.