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Conference Paper: Pathogenesis of avian flu H5N1 and SARS

TitlePathogenesis of avian flu H5N1 and SARS
Authors
Issue Date2006
Citation
Novartis Foundation Symposium, 2006, v. 279, p. 56-60 How to Cite?
AbstractAvian influenza A (H5N1) and severe acute respiratory syndrome (SARS) coronavirus are infections that cause a severe viral pneumonia leading to acute respiratory dysfunction syndrome and carry a high case-fatality rate. We have investigated innate immune responses to both viruses using primary human macrophages and respiratory epithelial cells as in vitro models. In contrast to human influenza A H1N1 viruses, the H5N1 viruses hyper-induce cytokines (tumour necrosis factor [TNF]α, interferon β) and chemokines (IP10, MIP1α, MCP) in in vitro cultures of primary human macrophages. A similar differential effect is observed in primary human bronchial epithelial cells and in type 2 pneumocytes although TNFα is not induced in respiratory epithelial cells. The cell signalling pathways responsible for this differential effect remain to be explored. Preliminary data suggest that such differential signalling involves p38 MAP kinase rather than NF-κB. SARS coronavirus infection of primary human macrophages is associated with a strong induction of chemokines without an associated type 1 interferon response. These observations may be relevant in disease pathogenesis. Copyright © Novartis Foundation 2006.
Persistent Identifierhttp://hdl.handle.net/10722/179846
ISSN
2004 Impact Factor: 1.879
2011 SCImago Journal Rankings: 0.267
References

 

DC FieldValueLanguage
dc.contributor.authorPeiris, Men_US
dc.date.accessioned2012-12-19T10:06:03Z-
dc.date.available2012-12-19T10:06:03Z-
dc.date.issued2006en_US
dc.identifier.citationNovartis Foundation Symposium, 2006, v. 279, p. 56-60en_US
dc.identifier.issn1528-2511en_US
dc.identifier.urihttp://hdl.handle.net/10722/179846-
dc.description.abstractAvian influenza A (H5N1) and severe acute respiratory syndrome (SARS) coronavirus are infections that cause a severe viral pneumonia leading to acute respiratory dysfunction syndrome and carry a high case-fatality rate. We have investigated innate immune responses to both viruses using primary human macrophages and respiratory epithelial cells as in vitro models. In contrast to human influenza A H1N1 viruses, the H5N1 viruses hyper-induce cytokines (tumour necrosis factor [TNF]α, interferon β) and chemokines (IP10, MIP1α, MCP) in in vitro cultures of primary human macrophages. A similar differential effect is observed in primary human bronchial epithelial cells and in type 2 pneumocytes although TNFα is not induced in respiratory epithelial cells. The cell signalling pathways responsible for this differential effect remain to be explored. Preliminary data suggest that such differential signalling involves p38 MAP kinase rather than NF-κB. SARS coronavirus infection of primary human macrophages is associated with a strong induction of chemokines without an associated type 1 interferon response. These observations may be relevant in disease pathogenesis. Copyright © Novartis Foundation 2006.en_US
dc.languageengen_US
dc.relation.ispartofNovartis Foundation Symposiumen_US
dc.subject.meshAnimalsen_US
dc.subject.meshHumansen_US
dc.subject.meshInfluenza A Virus, H5n1 Subtype - Pathogenicity - Physiologyen_US
dc.subject.meshInfluenza, Human - Pathology - Virologyen_US
dc.subject.meshSars Virus - Pathogenicity - Physiologyen_US
dc.subject.meshSevere Acute Respiratory Syndrome - Pathology - Virologyen_US
dc.titlePathogenesis of avian flu H5N1 and SARSen_US
dc.typeConference_Paperen_US
dc.identifier.emailPeiris, M: malik@hkucc.hku.hken_US
dc.identifier.authorityPeiris, M=rp00410en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid17278385-
dc.identifier.scopuseid_2-s2.0-33847694909en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33847694909&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume279en_US
dc.identifier.spage56en_US
dc.identifier.epage60en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridPeiris, M=7005486823en_US

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