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Article: Innate immune responses to influenza A H5N1: friend or foe?

TitleInnate immune responses to influenza A H5N1: friend or foe?
Authors
Issue Date2009
PublisherElsevier Ltd, Trends Journals. The Journal's web site is located at http://www.elsevier.com/locate/it
Citation
Trends In Immunology, 2009, v. 30 n. 12, p. 574-584 How to Cite?
AbstractAvian influenza A H5N1 remains unusual in its virulence for humans. Although infection of humans remains inefficient, many of those with H5N1 disease have a rapidly progressing viral pneumonia that leads to acute respiratory distress syndrome and death, but its pathogenesis remains an enigma. Comparison of the virology and pathogenesis of human seasonal influenza viruses (H3N2 and H1N1) and H5N1 in patients, animal models and relevant primary human cell cultures is instructive. Although the direct effects of viral replication and differences in the tropism of the virus for cells in the lower respiratory tract clearly contribute to pathogenesis, we focus here on the possible contribution of the host innate immune response in the pathogenesis of this disease. © 2009 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/148613
ISSN
2015 Impact Factor: 11.433
2015 SCImago Journal Rankings: 7.306
ISI Accession Number ID
Funding AgencyGrant Number
National Institutes of Health (NIAID)HHSN26620070005C
University Grants CommitteeAoE/M-12/06
Central AllocationHKU1/05C
Research Grants Council of the Hong KongHKU77370M
Funding Information:

We acknowledge research funding from the National Institutes of Health (NIAID Contract HHSN26620070005C), the Area of Excellence Scheme of the University Grants Committee (Grant AoE/M-12/06), the Central Allocation Grant HKU1/05C and General Research Fund (HKU77370M) from the Research Grants Council of the Hong Kong Special Administrative Region.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorPeiris, JSMen_US
dc.contributor.authorCheung, CYen_US
dc.contributor.authorLeung, CYHen_US
dc.contributor.authorNicholls, JMen_US
dc.date.accessioned2012-05-29T06:14:07Z-
dc.date.available2012-05-29T06:14:07Z-
dc.date.issued2009en_US
dc.identifier.citationTrends In Immunology, 2009, v. 30 n. 12, p. 574-584en_US
dc.identifier.issn1471-4906en_US
dc.identifier.urihttp://hdl.handle.net/10722/148613-
dc.description.abstractAvian influenza A H5N1 remains unusual in its virulence for humans. Although infection of humans remains inefficient, many of those with H5N1 disease have a rapidly progressing viral pneumonia that leads to acute respiratory distress syndrome and death, but its pathogenesis remains an enigma. Comparison of the virology and pathogenesis of human seasonal influenza viruses (H3N2 and H1N1) and H5N1 in patients, animal models and relevant primary human cell cultures is instructive. Although the direct effects of viral replication and differences in the tropism of the virus for cells in the lower respiratory tract clearly contribute to pathogenesis, we focus here on the possible contribution of the host innate immune response in the pathogenesis of this disease. © 2009 Elsevier Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Ltd, Trends Journals. The Journal's web site is located at http://www.elsevier.com/locate/iten_US
dc.relation.ispartofTrends in Immunologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunity, Innateen_US
dc.subject.meshInfluenza A Virus, H1n1 Subtype - Immunology - Pathogenicityen_US
dc.subject.meshInfluenza A Virus, H3n2 Subtype - Immunology - Pathogenicityen_US
dc.subject.meshInfluenza A Virus, H5n1 Subtype - Immunology - Pathogenicityen_US
dc.subject.meshInfluenza, Human - Epidemiology - Immunology - Pathology - Physiopathologyen_US
dc.subject.meshInterferons - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshOrthomyxoviridae Infections - Immunology - Physiopathologyen_US
dc.subject.meshRespiratory Distress Syndrome, Adult - Immunologyen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Metabolismen_US
dc.titleInnate immune responses to influenza A H5N1: friend or foe?en_US
dc.typeArticleen_US
dc.identifier.emailPeiris, JSM:malik@hkucc.hku.hken_US
dc.identifier.emailCheung, CY:chungey@hkucc.hku.hken_US
dc.identifier.emailLeung, CYH:cyhleung@hkucc.hku.hken_US
dc.identifier.emailNicholls, JM:nicholls@pathology.hku.hken_US
dc.identifier.authorityPeiris, JSM=rp00410en_US
dc.identifier.authorityCheung, CY=rp00404en_US
dc.identifier.authorityLeung, CYH=rp00307en_US
dc.identifier.authorityNicholls, JM=rp00364en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.it.2009.09.004en_US
dc.identifier.pmid19864182-
dc.identifier.scopuseid_2-s2.0-70449854577en_US
dc.identifier.hkuros173495-
dc.identifier.hkuros172050-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70449854577&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume30en_US
dc.identifier.issue12en_US
dc.identifier.spage574en_US
dc.identifier.epage584en_US
dc.identifier.eissn1471-4981-
dc.identifier.isiWOS:000272643500004-
dc.publisher.placeUnited Kingdomen_US
dc.relation.projectControl of Pandemic and Inter-pandemic Influenza-
dc.identifier.scopusauthoridPeiris, JSM=7005486823-
dc.identifier.scopusauthoridCheung, CY=7202061836-
dc.identifier.scopusauthoridLeung, CYH=26531438300-
dc.identifier.scopusauthoridNicholls, JM=7201463077-
dc.identifier.citeulike6048417-

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