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Article: Functional tumor necrosis factor-related apoptosis-inducing ligand production by avian influenza virus-infected macrophages

TitleFunctional tumor necrosis factor-related apoptosis-inducing ligand production by avian influenza virus-infected macrophages
Authors
Issue Date2006
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
Journal Of Infectious Diseases, 2006, v. 193 n. 7, p. 945-953 How to Cite?
AbstractSevere human disease associated with influenza A H5N1 virus was first detected in Hong Kong in 1997. Its recent reemergence in Asia and high associated mortality highlight the need to understand its pathogenesis. We investigated the roles of death receptor ligands (DRLs) in H5N1 infection. Significant up-regulation of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and TNF-α, but not Fas ligand (FasL) mRNA, was detected in human monocyte-derived macrophages (MDMs) infected with avian influenza viruses A/Hong Kong/483/97 (H5N1/97) or its precursor, A/Quail/Hong Kong/G1/97. H5N1/97-infected MDMs exhibited the strongest induction of apoptosis in Jurkat T cells, and it could be reduced by TRAIL-receptor 2 blocking antibody. Furthermore, influenza virus infection enhanced the sensitivity of Jurkat T cells to apoptosis induced by TNF-α, TRAIL, and FasL. Our data suggested that functional TRAIL produced by influenza virus-infected MDMs was related to their cytotoxicity and that the enhanced sensitization to DRL-induced apoptosis detected in avian influenza may contribute to disease pathogenesis. © 2006 by the Infectious Diseases Society of America. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/45167
ISSN
2015 Impact Factor: 6.344
2015 SCImago Journal Rankings: 4.000
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhou, Jen_HK
dc.contributor.authorLaw, HKWen_HK
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorNg, IHYen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2007-10-30T06:18:52Z-
dc.date.available2007-10-30T06:18:52Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Infectious Diseases, 2006, v. 193 n. 7, p. 945-953en_HK
dc.identifier.issn0022-1899en_HK
dc.identifier.urihttp://hdl.handle.net/10722/45167-
dc.description.abstractSevere human disease associated with influenza A H5N1 virus was first detected in Hong Kong in 1997. Its recent reemergence in Asia and high associated mortality highlight the need to understand its pathogenesis. We investigated the roles of death receptor ligands (DRLs) in H5N1 infection. Significant up-regulation of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and TNF-α, but not Fas ligand (FasL) mRNA, was detected in human monocyte-derived macrophages (MDMs) infected with avian influenza viruses A/Hong Kong/483/97 (H5N1/97) or its precursor, A/Quail/Hong Kong/G1/97. H5N1/97-infected MDMs exhibited the strongest induction of apoptosis in Jurkat T cells, and it could be reduced by TRAIL-receptor 2 blocking antibody. Furthermore, influenza virus infection enhanced the sensitivity of Jurkat T cells to apoptosis induced by TNF-α, TRAIL, and FasL. Our data suggested that functional TRAIL produced by influenza virus-infected MDMs was related to their cytotoxicity and that the enhanced sensitization to DRL-induced apoptosis detected in avian influenza may contribute to disease pathogenesis. © 2006 by the Infectious Diseases Society of America. All rights reserved.en_HK
dc.format.extent703051 bytes-
dc.format.extent90580 bytes-
dc.format.extent2695 bytes-
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dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypetext/plain-
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dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org en_HK
dc.relation.ispartofJournal of Infectious Diseasesen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsJournal of Infectious Diseases. Copyright © University of Chicago Press.en_HK
dc.subject.meshApoptosis-en_HK
dc.subject.meshApoptosis-Regulatory-Proteins-biosynthesisen_HK
dc.subject.meshInfluenza-A-Virus,-H5N1-Subtype-pathogenicityen_HK
dc.subject.meshMacrophages-virologyen_HK
dc.subject.meshMembrane-Glycoproteins-biosynthesisen_HK
dc.titleFunctional tumor necrosis factor-related apoptosis-inducing ligand production by avian influenza virus-infected macrophagesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1899&volume=193&issue=7&spage=945&epage=953&date=2006&atitle=Functional+tumor+necrosis+factor-related+apoptosis-inducing+ligand+production+by+avian+influenza+virus-infected+macrophagesen_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.emailLau, YL: lauylung@hku.hken_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1086/500954en_HK
dc.identifier.pmid16518756-
dc.identifier.scopuseid_2-s2.0-33645332877en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645332877&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume193en_HK
dc.identifier.issue7en_HK
dc.identifier.spage945en_HK
dc.identifier.epage953en_HK
dc.identifier.eissn1537-6613-
dc.identifier.isiWOS:000235777000007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhou, J=34871165300en_HK
dc.identifier.scopusauthoridLaw, HKW=7101939394en_HK
dc.identifier.scopusauthoridCheung, CY=7202061836en_HK
dc.identifier.scopusauthoridNg, IHY=8671050800en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK

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