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Article: p38 mitogen-activated protein kinase-dependent hyperinduction of tumor necrosis factor alpha expression in response to avian influenza virus H5N1

Titlep38 mitogen-activated protein kinase-dependent hyperinduction of tumor necrosis factor alpha expression in response to avian influenza virus H5N1
Authors
Issue Date2005
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal Of Virology, 2005, v. 79 n. 16, p. 10147-10154 How to Cite?
AbstractAvian influenza A virus subtype H5N1 can infect humans to cause a severe viral pneumonia with mortality rates of more than 30%. The biological basis for this unusual disease severity is not fully understood. We previously demonstrated that in contrast to human influenza A virus subtypes including H1N1 or H3N2, the H5N1 virus associated with the "bird flu" outbreak in Hong Kong in 1997 (H5N1/97) hyperinduces proinflammatory cytokines, including tumor necrosis factor alpha (TNF-α), in primary human macrophages in vitro. To delineate the molecular mechanisms involved, we analyzed the role of transcription factor NF-κB and cellular kinases in TNF-α dysregulation. H5N1 and H1N1 viruses did not differ in the activation of NF-κB or degradation of IκB-α in human macrophages. However, we demonstrated that unlike H1N1 virus, H5N1/97 strongly activates mitogen-activated protein kinase (MAPK), including p38 MAPK and extracellular signal-regulated kinases 1 and 2. Specific inhibitors of p38 MAPK significantly reduced the H5N1/97-induced TNF-α expression in macrophages. Taken together, our findings suggest that H5N1/97-mediated hyperinduction of cytokines involves the p38 MAPK signaling pathway. These results may provide insights into the pathogenesis of H5N1 disease and rationales for the development of novel therapeutic strategies. Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/49163
ISSN
2015 Impact Factor: 4.606
2015 SCImago Journal Rankings: 3.347
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, DCWen_HK
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorLaw, AHYen_HK
dc.contributor.authorMok, CKPen_HK
dc.contributor.authorPeiris, Men_HK
dc.contributor.authorLau, ASYen_HK
dc.date.accessioned2008-06-12T06:35:51Z-
dc.date.available2008-06-12T06:35:51Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Virology, 2005, v. 79 n. 16, p. 10147-10154en_HK
dc.identifier.issn0022-538Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/49163-
dc.description.abstractAvian influenza A virus subtype H5N1 can infect humans to cause a severe viral pneumonia with mortality rates of more than 30%. The biological basis for this unusual disease severity is not fully understood. We previously demonstrated that in contrast to human influenza A virus subtypes including H1N1 or H3N2, the H5N1 virus associated with the "bird flu" outbreak in Hong Kong in 1997 (H5N1/97) hyperinduces proinflammatory cytokines, including tumor necrosis factor alpha (TNF-α), in primary human macrophages in vitro. To delineate the molecular mechanisms involved, we analyzed the role of transcription factor NF-κB and cellular kinases in TNF-α dysregulation. H5N1 and H1N1 viruses did not differ in the activation of NF-κB or degradation of IκB-α in human macrophages. However, we demonstrated that unlike H1N1 virus, H5N1/97 strongly activates mitogen-activated protein kinase (MAPK), including p38 MAPK and extracellular signal-regulated kinases 1 and 2. Specific inhibitors of p38 MAPK significantly reduced the H5N1/97-induced TNF-α expression in macrophages. Taken together, our findings suggest that H5N1/97-mediated hyperinduction of cytokines involves the p38 MAPK signaling pathway. These results may provide insights into the pathogenesis of H5N1 disease and rationales for the development of novel therapeutic strategies. Copyright © 2005, American Society for Microbiology. All Rights Reserved.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/en_HK
dc.relation.ispartofJournal of Virologyen_HK
dc.rightsJournal of Virology. Copyright © American Society for Microbiology.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsCopyright © American Society for Microbiology, Journal of Virology, 2005, v. 79 n. 16, p. 10147-10154en_HK
dc.subject.meshInfluenza A Virus, H5N1 Subtypeen_HK
dc.subject.meshInfluenza A virus - pathogenicityen_HK
dc.subject.meshTumor Necrosis Factor-alpha - biosynthesisen_HK
dc.subject.meshp38 Mitogen-Activated Protein Kinases - antagonists & inhibitors - physiologyen_HK
dc.subject.meshExtracellular Signal-Regulated MAP Kinases - metabolismen_HK
dc.titlep38 mitogen-activated protein kinase-dependent hyperinduction of tumor necrosis factor alpha expression in response to avian influenza virus H5N1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-538X&volume=79&issue=16&spage=10147&epage=10154&date=2005&atitle=p38+mitogen-activated+protein+kinase-dependent+hyperinduction+of+tumor+necrosis+factor+alpha+expression+in+response+to+avian+influenza+virus+H5N1en_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailMok, CKP: ch02mkp@hkucc.hku.hken_HK
dc.identifier.emailPeiris, M: malik@hkucc.hku.hken_HK
dc.identifier.emailLau, ASY: asylau@hku.hken_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.identifier.authorityMok, CKP=rp01805en_HK
dc.identifier.authorityPeiris, M=rp00410en_HK
dc.identifier.authorityLau, ASY=rp00474en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1128/JVI.79.16.10147-10154.2005en_HK
dc.identifier.pmid16051807-
dc.identifier.pmcidPMC1182678en_HK
dc.identifier.scopuseid_2-s2.0-23244461479en_HK
dc.identifier.hkuros109109-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23244461479&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume79en_HK
dc.identifier.issue16en_HK
dc.identifier.spage10147en_HK
dc.identifier.epage10154en_HK
dc.identifier.isiWOS:000230884700005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, DCW=15751156000en_HK
dc.identifier.scopusauthoridCheung, CY=7202061836en_HK
dc.identifier.scopusauthoridLaw, AHY=8692488400en_HK
dc.identifier.scopusauthoridMok, CKP=36159732100en_HK
dc.identifier.scopusauthoridPeiris, M=7005486823en_HK
dc.identifier.scopusauthoridLau, ASY=7202626202en_HK

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