ArticleHepatology (Baltimore, Md.)2014
Activated macrophages promote hepatitis C virus entry in a tumor necrosis factor-dependent manner.
Article in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Enhanced hepatitis E virus infection of polarised hepatocytes in vitro.Scientific reports · 2025Article
- HCV-induced autophagy and innate immunity.Frontiers in immunology · 2024Review
- Hepatitis C virus and intracellular antiviral response.Current opinion in virology · 2022Review
- Control of HCV Infection by Natural Killer Cells and Macrophages.Cold Spring Harbor perspectives in medicine · 2020Review
- IFN-I Independent Antiviral Immune Response to Vesicular Stomatitis Virus Challenge in Mouse Brain.Vaccines · 2020Article
- Review
- IL-4/IL-13 polarization of macrophages enhances Ebola virus glycoprotein-dependent infection.PLoS neglected tropical diseases · 2019Article
- Bacterial flagellin promotes viral entry via an NF-kB and Toll Like Receptor 5 dependent pathway.Scientific reports · 2019Article
- Mononuclear phagocyte system in hepatitis C virus infection.World journal of gastroenterology · 2018Review
- Tumor Necrosis Factor-Mediated Survival of CD169Journal of virology · 2018Article
- Cytokine-Mediated Tissue Injury in Non-human Primate Models of Viral Infections.Frontiers in immunology · 2018Review
- Reversing immune dysfunction and liver damage after direct-acting antiviral treatment for hepatitis C.Canadian liver journal · 2018Review
- Tumor Necrosis Factor Inhibits Spread of Hepatitis C Virus Among Liver Cells, Independent From Interferons.Gastroenterology · 2017Article
- Regulated Entry of Hepatitis C Virus into Hepatocytes.Viruses · 2017Review
- TNF superfamily members promote hepatitis C virus entry via an NF-κB and myosin light chain kinase dependent pathway.The Journal of general virology · 2017Article
- Organ system view of the hepatic innate immunity in HCV infection.Journal of medical virology · 2016Review
- Deep sequencing of hepatitis C virus reveals genetic compartmentalization in cerebrospinal fluid from cognitively impaired patients.Liver international : official journal of the International Association for the Study of the Liver · 2016Article
- Role of apoptotic hepatocytes in HCV dissemination: regulation by acetaldehyde.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Inflammatory status in human hepatic cirrhosis.World journal of gastroenterology · 2015Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
unlabelledMacrophages are critical components of the innate immune response in the liver. Chronic hepatitis C is associated with immune infiltration and the infected liver shows a significant increase in total macrophage numbers; however, their role in the viral life cycle is poorly understood. Activation of blood-derived and intrahepatic macrophages with a panel of Toll-like receptor agonists induce soluble mediators that promote hepatitis C virus (HCV) entry into polarized hepatoma cells. We identified tumor necrosis factor α (TNF-α) as the major cytokine involved in this process. Importantly, this effect was not limited to HCV; TNF-α increased the permissivity of hepatoma cells to infection by Lassa, measles and vesicular stomatitis pseudoviruses. TNF-α induced a relocalization of tight junction protein occludin and increased the lateral diffusion speed of HCV receptor tetraspanin CD81 in polarized HepG2 cells, providing a mechanism for their increased permissivity to support HCV entry. High concentrations of HCV particles could stimulate macrophages to express TNF-α, providing a direct mechanism for the virus to promote infection.
conclusionThis study shows a new role for TNF-α to increase virus entry and highlights the potential for HCV to exploit existing innate immune responses in the liver to promote de novo infection events.
Indexed as
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What OpenQuestion holds
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.