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Article: Differential onset of apoptosis in influenza A virus H5N1- and H1N1-infected human blood macrophages

TitleDifferential onset of apoptosis in influenza A virus H5N1- and H1N1-infected human blood macrophages
Authors
Issue Date2007
PublisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.org
Citation
Journal Of General Virology, 2007, v. 88 n. 4, p. 1275-1280 How to Cite?
AbstractPathogenesis of the highly pathogenic avian influenza virus A/Hong Kong/ 483/97 (H5N1/97) remains to be investigated. It was demonstrated recently that H5N1 dysregulation of proinflammatory cytokines in human macrophages is a p38-kinase-dependent process. The results indicated that macrophages may play a role in disease severity. To investigate cellular responses to H5N1 infection further, apoptosis and its related pathways were studied in primary blood macrophages. Here, it is shown that the H5N1/97 virus triggered apoptosis, including caspases and PARP activation, in infected macrophages with a delayed onset compared with H1N1 counterparts. Similar results were also found in human macrophages infected by precursors of the H5N1/97 virus. Thus, these results showed that the delay in apoptosis onset in macrophages infected by H5N1/97 and its related precursor subtypes may be a means for the pathogens to have longer survival in the cells; this may contribute to the pathogenesis of H5N1 disease in humans. © 2007 SGM.
Persistent Identifierhttp://hdl.handle.net/10722/78838
ISSN
2015 Impact Factor: 3.192
2015 SCImago Journal Rankings: 1.741
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMok, CKPen_HK
dc.contributor.authorLee, DCWen_HK
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorPeiris, Men_HK
dc.contributor.authorLau, ASYen_HK
dc.date.accessioned2010-09-06T07:47:26Z-
dc.date.available2010-09-06T07:47:26Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of General Virology, 2007, v. 88 n. 4, p. 1275-1280en_HK
dc.identifier.issn0022-1317en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78838-
dc.description.abstractPathogenesis of the highly pathogenic avian influenza virus A/Hong Kong/ 483/97 (H5N1/97) remains to be investigated. It was demonstrated recently that H5N1 dysregulation of proinflammatory cytokines in human macrophages is a p38-kinase-dependent process. The results indicated that macrophages may play a role in disease severity. To investigate cellular responses to H5N1 infection further, apoptosis and its related pathways were studied in primary blood macrophages. Here, it is shown that the H5N1/97 virus triggered apoptosis, including caspases and PARP activation, in infected macrophages with a delayed onset compared with H1N1 counterparts. Similar results were also found in human macrophages infected by precursors of the H5N1/97 virus. Thus, these results showed that the delay in apoptosis onset in macrophages infected by H5N1/97 and its related precursor subtypes may be a means for the pathogens to have longer survival in the cells; this may contribute to the pathogenesis of H5N1 disease in humans. © 2007 SGM.en_HK
dc.languageengen_HK
dc.publisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.orgen_HK
dc.relation.ispartofJournal of General Virologyen_HK
dc.titleDifferential onset of apoptosis in influenza A virus H5N1- and H1N1-infected human blood macrophagesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1317&volume=88&issue=Pt 4&spage=1275&epage=1280&date=2007&atitle=Differential+onset+of+apoptosis+in+influenza+A+virus+H5N1+-+and+H1N1+-+infected+human+blood+macrophagesen_HK
dc.identifier.emailMok, CKP: ch02mkp@hkucc.hku.hken_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailPeiris, M: malik@hkucc.hku.hken_HK
dc.identifier.emailLau, ASY: asylau@hku.hken_HK
dc.identifier.authorityMok, CKP=rp01805en_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.identifier.authorityPeiris, M=rp00410en_HK
dc.identifier.authorityLau, ASY=rp00474en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1099/vir.0.82423-0en_HK
dc.identifier.pmid17374772-
dc.identifier.scopuseid_2-s2.0-34047156113en_HK
dc.identifier.hkuros126929en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34047156113&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume88en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1275en_HK
dc.identifier.epage1280en_HK
dc.identifier.isiWOS:000245493500023-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridMok, CKP=36159732100en_HK
dc.identifier.scopusauthoridLee, DCW=15751156000en_HK
dc.identifier.scopusauthoridCheung, CY=7202061836en_HK
dc.identifier.scopusauthoridPeiris, M=7005486823en_HK
dc.identifier.scopusauthoridLau, ASY=7202626202en_HK

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