Please use this identifier to cite or link to this item: https://doi.org/10.1002/hep.26911
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dc.titleActivated macrophages promote hepatitis C virus entry in a tumor necrosis factor-dependent manner
dc.contributor.authorFletcher, N.F
dc.contributor.authorSutaria, R
dc.contributor.authorJo, J
dc.contributor.authorBarnes, A
dc.contributor.authorBlahova, M
dc.contributor.authorMeredith, L.W
dc.contributor.authorCosset, F.-L
dc.contributor.authorCurbishley, S.M
dc.contributor.authorAdams, D.H
dc.contributor.authorBertoletti, A
dc.contributor.authorMckeating, J.A
dc.date.accessioned2020-10-27T04:40:28Z
dc.date.available2020-10-27T04:40:28Z
dc.date.issued2014
dc.identifier.citationFletcher, 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.issn0270-9139
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/180764
dc.description.abstractMacrophages 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.publisherJohn Wiley and Sons Ltd
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectCD81 antigen
dc.subjectgamma interferon
dc.subjectinterleukin 10
dc.subjectinterleukin 17
dc.subjectinterleukin 18
dc.subjectinterleukin 1beta
dc.subjectinterleukin 4
dc.subjectinterleukin 6
dc.subjectinterleukin 8
dc.subjectmessenger RNA
dc.subjectoccludin
dc.subjecttight junction protein
dc.subjecttumor necrosis factor alpha
dc.subjectarticle
dc.subjectcell differentiation
dc.subjectcell membrane permeability
dc.subjectcell strain HepG2
dc.subjectcontrolled study
dc.subjectdiffusion coefficient
dc.subjecthepatitis C
dc.subjectHepatitis C virus
dc.subjecthepatoma cell
dc.subjecthuman
dc.subjecthuman cell
dc.subjectHuman immunodeficiency virus
dc.subjectinnate immunity
dc.subjectKupffer cell
dc.subjectLassa virus
dc.subjectliver cell
dc.subjectmacrophage activation
dc.subjectMeasles virus
dc.subjectnonhuman
dc.subjectpolarization
dc.subjectpriority journal
dc.subjectvesicular stomatitis
dc.subjectVesicular stomatitis virus
dc.subjectvirus entry
dc.subjectAntigens, CD81
dc.subjectCarcinoma, Hepatocellular
dc.subjectCell Line, Tumor
dc.subjectCell Polarity
dc.subjectHep G2 Cells
dc.subjectHepacivirus
dc.subjectHepatitis C
dc.subjectHumans
dc.subjectImmunity, Innate
dc.subjectInterleukin-1beta
dc.subjectLiver Neoplasms
dc.subjectMacrophage Activation
dc.subjectMacrophages
dc.subjectOccludin
dc.subjectTight Junctions
dc.subjectTumor Necrosis Factor-alpha
dc.subjectVirus Internalization
dc.typeArticle
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1002/hep.26911
dc.description.sourcetitleHepatology
dc.description.volume59
dc.description.issue4
dc.description.page1320-1330
dc.published.statePublished
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