Please use this identifier to cite or link to this item:
https://doi.org/10.1002/hep.26911
DC Field | Value | |
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dc.title | Activated macrophages promote hepatitis C virus entry in a tumor necrosis factor-dependent manner | |
dc.contributor.author | Fletcher, N.F | |
dc.contributor.author | Sutaria, R | |
dc.contributor.author | Jo, J | |
dc.contributor.author | Barnes, A | |
dc.contributor.author | Blahova, M | |
dc.contributor.author | Meredith, L.W | |
dc.contributor.author | Cosset, F.-L | |
dc.contributor.author | Curbishley, S.M | |
dc.contributor.author | Adams, D.H | |
dc.contributor.author | Bertoletti, A | |
dc.contributor.author | Mckeating, J.A | |
dc.date.accessioned | 2020-10-27T04:40:28Z | |
dc.date.available | 2020-10-27T04:40:28Z | |
dc.date.issued | 2014 | |
dc.identifier.citation | Fletcher, N.F, Sutaria, R, Jo, J, Barnes, A, Blahova, M, Meredith, L.W, Cosset, F.-L, Curbishley, S.M, Adams, D.H, Bertoletti, A, Mckeating, J.A (2014). Activated macrophages promote hepatitis C virus entry in a tumor necrosis factor-dependent manner. Hepatology 59 (4) : 1320-1330. ScholarBank@NUS Repository. https://doi.org/10.1002/hep.26911 | |
dc.identifier.issn | 0270-9139 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/180764 | |
dc.description.abstract | Macrophages 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 ? (TNF-?) as the major cytokine involved in this process. Importantly, this effect was not limited to HCV; TNF-? increased the permissivity of hepatoma cells to infection by Lassa, measles and vesicular stomatitis pseudoviruses. TNF-? 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-?, providing a direct mechanism for the virus to promote infection. Conclusion: This study shows a new role for TNF-? 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. © 2014 The Authors. Hepatology published by Wiley on behalf of the American Association for the Study of Liver Diseases. | |
dc.publisher | John Wiley and Sons Ltd | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.source | Unpaywall 20201031 | |
dc.subject | CD81 antigen | |
dc.subject | gamma interferon | |
dc.subject | interleukin 10 | |
dc.subject | interleukin 17 | |
dc.subject | interleukin 18 | |
dc.subject | interleukin 1beta | |
dc.subject | interleukin 4 | |
dc.subject | interleukin 6 | |
dc.subject | interleukin 8 | |
dc.subject | messenger RNA | |
dc.subject | occludin | |
dc.subject | tight junction protein | |
dc.subject | tumor necrosis factor alpha | |
dc.subject | article | |
dc.subject | cell differentiation | |
dc.subject | cell membrane permeability | |
dc.subject | cell strain HepG2 | |
dc.subject | controlled study | |
dc.subject | diffusion coefficient | |
dc.subject | hepatitis C | |
dc.subject | Hepatitis C virus | |
dc.subject | hepatoma cell | |
dc.subject | human | |
dc.subject | human cell | |
dc.subject | Human immunodeficiency virus | |
dc.subject | innate immunity | |
dc.subject | Kupffer cell | |
dc.subject | Lassa virus | |
dc.subject | liver cell | |
dc.subject | macrophage activation | |
dc.subject | Measles virus | |
dc.subject | nonhuman | |
dc.subject | polarization | |
dc.subject | priority journal | |
dc.subject | vesicular stomatitis | |
dc.subject | Vesicular stomatitis virus | |
dc.subject | virus entry | |
dc.subject | Antigens, CD81 | |
dc.subject | Carcinoma, Hepatocellular | |
dc.subject | Cell Line, Tumor | |
dc.subject | Cell Polarity | |
dc.subject | Hep G2 Cells | |
dc.subject | Hepacivirus | |
dc.subject | Hepatitis C | |
dc.subject | Humans | |
dc.subject | Immunity, Innate | |
dc.subject | Interleukin-1beta | |
dc.subject | Liver Neoplasms | |
dc.subject | Macrophage Activation | |
dc.subject | Macrophages | |
dc.subject | Occludin | |
dc.subject | Tight Junctions | |
dc.subject | Tumor Necrosis Factor-alpha | |
dc.subject | Virus Internalization | |
dc.type | Article | |
dc.contributor.department | DUKE-NUS MEDICAL SCHOOL | |
dc.description.doi | 10.1002/hep.26911 | |
dc.description.sourcetitle | Hepatology | |
dc.description.volume | 59 | |
dc.description.issue | 4 | |
dc.description.page | 1320-1330 | |
dc.published.state | Published | |
Appears in Collections: | Staff Publications Elements |
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