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Article: Induction of proinflammatory cytokines in human macrophages by influenza A (H5N1) viruses: A mechanism for the unusual severity of human disease?

TitleInduction of proinflammatory cytokines in human macrophages by influenza A (H5N1) viruses: A mechanism for the unusual severity of human disease?
Authors
Issue Date2002
PublisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/locate/lancet
Citation
Lancet, 2002, v. 360 n. 9348, p. 1831-1837 How to Cite?
AbstractBackground: In 1997, the first documented instance of human respiratory disease and death associated with a purely avian H5N1 influenza virus resulted in an overall case-fatality rate of 33%. The biological basis for the severity of human H5N1 disease has remained unclear. We tested the hypothesis that virus-induced cytokine dysregulation has a role. Methods: We used cDNA arrays and quantitative RT-PCR to compare the profile of cytokine gene expression induced by viruses A/HK/486/97 and A/HK/483/97 (both H5N1/97) with that of human H3N2 and H1N1 viruses in human primary monocyte-derived macrophages in vitro. Secretion of tumour necrosis factor α (TNF α) from macrophages infected with the viruses was compared by ELISA. By use of naturally occurring viral reassortants and recombinant viruses generated by reverse genetic techniques, we investigated the viral genes associated with the TNF-α response. Findings: The H5N1/97 viruses induced much higher gene transcription of proinflammatory cytokines than did H3N2 or H1N1 viruses, particularly TNF α and interferon beta. The concentration of TNF-α protein in culture supernatants of macrophages infected with these viruses was similar to that induced by stimulation with Escherichia coli lipopolysaccharide. The non-structural (NS) gene-segment of H5N1/97 viruses contributed to the increase in TNF α induced by the virus. Interpretation: The H5N1/97 viruses are potent inducers of proinflammatory cytokines in macrophages, the most notable being TNF α. This characteristic may contribute to the unusual severity of human H5N1 disease.
Persistent Identifierhttp://hdl.handle.net/10722/78926
ISSN
2015 Impact Factor: 44.002
2015 SCImago Journal Rankings: 14.638
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorPoon, LLMen_HK
dc.contributor.authorLau, ASen_HK
dc.contributor.authorLuk, Wen_HK
dc.contributor.authorLau, YLen_HK
dc.contributor.authorShortridge, KFen_HK
dc.contributor.authorGordon, Sen_HK
dc.contributor.authorGuan, Yen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.date.accessioned2010-09-06T07:48:28Z-
dc.date.available2010-09-06T07:48:28Z-
dc.date.issued2002en_HK
dc.identifier.citationLancet, 2002, v. 360 n. 9348, p. 1831-1837en_HK
dc.identifier.issn0140-6736en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78926-
dc.description.abstractBackground: In 1997, the first documented instance of human respiratory disease and death associated with a purely avian H5N1 influenza virus resulted in an overall case-fatality rate of 33%. The biological basis for the severity of human H5N1 disease has remained unclear. We tested the hypothesis that virus-induced cytokine dysregulation has a role. Methods: We used cDNA arrays and quantitative RT-PCR to compare the profile of cytokine gene expression induced by viruses A/HK/486/97 and A/HK/483/97 (both H5N1/97) with that of human H3N2 and H1N1 viruses in human primary monocyte-derived macrophages in vitro. Secretion of tumour necrosis factor α (TNF α) from macrophages infected with the viruses was compared by ELISA. By use of naturally occurring viral reassortants and recombinant viruses generated by reverse genetic techniques, we investigated the viral genes associated with the TNF-α response. Findings: The H5N1/97 viruses induced much higher gene transcription of proinflammatory cytokines than did H3N2 or H1N1 viruses, particularly TNF α and interferon beta. The concentration of TNF-α protein in culture supernatants of macrophages infected with these viruses was similar to that induced by stimulation with Escherichia coli lipopolysaccharide. The non-structural (NS) gene-segment of H5N1/97 viruses contributed to the increase in TNF α induced by the virus. Interpretation: The H5N1/97 viruses are potent inducers of proinflammatory cytokines in macrophages, the most notable being TNF α. This characteristic may contribute to the unusual severity of human H5N1 disease.en_HK
dc.languageengen_HK
dc.publisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/locate/lanceten_HK
dc.relation.ispartofLanceten_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshCytokines - biosynthesis - geneticsen_HK
dc.subject.meshGene Expression Regulationen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInfluenza, Human - immunology - virologyen_HK
dc.subject.meshInfluenzavirus A - genetics - immunology - pathogenicityen_HK
dc.subject.meshMacrophages - immunologyen_HK
dc.subject.meshRNA, Messenger - analysisen_HK
dc.subject.meshSeverity of Illness Indexen_HK
dc.subject.meshTumor Necrosis Factor-alpha - biosynthesis - geneticsen_HK
dc.titleInduction of proinflammatory cytokines in human macrophages by influenza A (H5N1) viruses: A mechanism for the unusual severity of human disease?en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0140-6736&volume=360&spage=1831&epage=1837&date=2002&atitle=Induction+of+proinflammatory+cytokines+in+human+macrophages+by+influenza+A+(H5N1)+viruses:+a+mechanism+for+the+unusual+severity+of+human+disease?en_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailPoon, LLM: llmpoon@hkucc.hku.hken_HK
dc.identifier.emailLau, AS: asylau@hku.hken_HK
dc.identifier.emailLau, YL: lauylung@hku.hken_HK
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.identifier.authorityPoon, LLM=rp00484en_HK
dc.identifier.authorityLau, AS=rp00474en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.identifier.authorityGuan, Y=rp00397en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0140-6736(02)11772-7en_HK
dc.identifier.pmid12480361-
dc.identifier.scopuseid_2-s2.0-0037038866en_HK
dc.identifier.hkuros75694en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037038866&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume360en_HK
dc.identifier.issue9348en_HK
dc.identifier.spage1831en_HK
dc.identifier.epage1837en_HK
dc.identifier.isiWOS:000179706100011-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridCheung, CY=7202061836en_HK
dc.identifier.scopusauthoridPoon, LLM=7005441747en_HK
dc.identifier.scopusauthoridLau, AS=7202626202en_HK
dc.identifier.scopusauthoridLuk, W=7005237837en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK
dc.identifier.scopusauthoridShortridge, KF=7005677034en_HK
dc.identifier.scopusauthoridGordon, S=35391350600en_HK
dc.identifier.scopusauthoridGuan, Y=7202924055en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK

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