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Article: Viral replication and innate host responses in primary human alveolar epithelial cells and alveolar macrophages infected with influenza H5N1 and H1N1 viruses

TitleViral replication and innate host responses in primary human alveolar epithelial cells and alveolar macrophages infected with influenza H5N1 and H1N1 viruses
Authors
Issue Date2011
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal Of Virology, 2011, v. 85 n. 14, p. 6844-6855 How to Cite?
AbstractHighly pathogenic influenza H5N1 virus continues to pose a threat to public health. Although the mechanisms underlying the pathogenesis of the H5N1 virus have not been fully defined, it has been suggested that cytokine dysregulation plays an important role. As the human respiratory epithelium is the primary target cell for influenza viruses, elucidating the viral tropism and innate immune responses of influenza H5N1 virus in the alveolar epithelium may help us to understand the pathogenesis of the severe pneumonia associated with H5N1 disease. Here we used primary cultures of differentiated human alveolar type II cells, alveolar type I-like cells, and alveolar macrophages isolated from the same individual to investigate viral replication competence and host innate immune responses to influenza H5N1 (A/HK/483/97) and H1N1 (A/HK/54/98) virus infection. The viral replication kinetics and cytokine and chemokine responses were compared by quantitative PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA). We demonstrated that influenza H1N1 and H5N1 viruses replicated productively in type II cells and type I-like cells although with different kinetics. The H5N1 virus replicated productively in alveolar macrophages, whereas the H1N1 virus led to an abortive infection. The H5N1 virus was a more potent inducer of proinflammatory cytokines and chemokines than the H1N1 virus in all cell types. However, higher levels of cytokine expression were observed for peripheral blood monocytederived macrophages than for alveolar macrophages in response to H5N1 virus infection. Our findings provide important insights into the viral tropisms and host responses of different cell types found in the lung and are relevant to an understanding of the pathogenesis of severe human influenza disease. © 2011, American Society for Microbiology.
Persistent Identifierhttp://hdl.handle.net/10722/135252
ISSN
2015 Impact Factor: 4.606
2015 SCImago Journal Rankings: 3.347
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong SAR Government06060552
Research Grants Council, Hong Kong SAR GovernmentHKU 761009 M
University Grants Committee, Hong Kong SAR GovernmentAoE/M-12/06
U.S. National Institutes of Health
Department of DefenseAI082982
W81XWH-07-1-0550
Parker B. Francis Foundation
Funding Information:

This work was supported by a Research Fund for Control of Infectious Disease (RFCID) grant (reference no. 06060552) from the Research Fund for Control of Infectious Disease, Health, Welfare, and Food Bureau, Hong Kong SAR Government; the General Research Fund (HKU 761009 M), Research Grants Council, Hong Kong SAR Government (to M. C. W. C.); AoE funding (AoE/M-12/06) from the Area of Excellence Scheme of the University Grants Committee, Hong Kong SAR Government; and funding from the U.S. National Institutes of Health and Department of Defense (grants AI082982 and W81XWH-07-1-0550) as well as the Parker B. Francis Foundation.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorYu, WCLen_HK
dc.contributor.authorChan, RWYen_HK
dc.contributor.authorWang, Jen_HK
dc.contributor.authorTravanty, EAen_HK
dc.contributor.authorNicholls, JMen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.contributor.authorMason, RJen_HK
dc.contributor.authorChan, MCWen_HK
dc.date.accessioned2011-07-27T01:30:41Z-
dc.date.available2011-07-27T01:30:41Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Virology, 2011, v. 85 n. 14, p. 6844-6855en_HK
dc.identifier.issn0022-538Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/135252-
dc.description.abstractHighly pathogenic influenza H5N1 virus continues to pose a threat to public health. Although the mechanisms underlying the pathogenesis of the H5N1 virus have not been fully defined, it has been suggested that cytokine dysregulation plays an important role. As the human respiratory epithelium is the primary target cell for influenza viruses, elucidating the viral tropism and innate immune responses of influenza H5N1 virus in the alveolar epithelium may help us to understand the pathogenesis of the severe pneumonia associated with H5N1 disease. Here we used primary cultures of differentiated human alveolar type II cells, alveolar type I-like cells, and alveolar macrophages isolated from the same individual to investigate viral replication competence and host innate immune responses to influenza H5N1 (A/HK/483/97) and H1N1 (A/HK/54/98) virus infection. The viral replication kinetics and cytokine and chemokine responses were compared by quantitative PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA). We demonstrated that influenza H1N1 and H5N1 viruses replicated productively in type II cells and type I-like cells although with different kinetics. The H5N1 virus replicated productively in alveolar macrophages, whereas the H1N1 virus led to an abortive infection. The H5N1 virus was a more potent inducer of proinflammatory cytokines and chemokines than the H1N1 virus in all cell types. However, higher levels of cytokine expression were observed for peripheral blood monocytederived macrophages than for alveolar macrophages in response to H5N1 virus infection. Our findings provide important insights into the viral tropisms and host responses of different cell types found in the lung and are relevant to an understanding of the pathogenesis of severe human influenza disease. © 2011, American Society for Microbiology.en_HK
dc.languageengen_US
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.-
dc.titleViral replication and innate host responses in primary human alveolar epithelial cells and alveolar macrophages infected with influenza H5N1 and H1N1 virusesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-538X&volume=85&issue=14&spage=6844&epage=6855&date=2011&atitle=Viral+replication+and+innate+host+responses+in+primary+human+alveolar+epithelial+cells+and+alveolar+macrophages+infected+with+influenza+H5N1+and+H1N1+viruses-
dc.identifier.emailChan, RWY: reneewy@hku.hken_HK
dc.identifier.emailNicholls, JM: jmnichol@hkucc.hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.emailChan, MCW: mchan@hku.hken_HK
dc.identifier.authorityChan, RWY=rp01596en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.identifier.authorityChan, MCW=rp00420en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.02200-10en_HK
dc.identifier.pmid21543489-
dc.identifier.pmcidPMC3126566-
dc.identifier.scopuseid_2-s2.0-79960418204en_HK
dc.identifier.hkuros186633en_US
dc.identifier.hkuros202486-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79960418204&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume85en_HK
dc.identifier.issue14en_HK
dc.identifier.spage6844en_HK
dc.identifier.epage6855en_HK
dc.identifier.eissn1098-5514-
dc.identifier.isiWOS:000291932400003-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectControl of Pandemic and Inter-pandemic Influenza-
dc.relation.projectReplication and pathogenesis of avian influenza A (H5N1) viruses in polarized human bronchial and alveolar epithelium-
dc.identifier.scopusauthoridYu, WCL=26324133100en_HK
dc.identifier.scopusauthoridChan, RWY=26661379100en_HK
dc.identifier.scopusauthoridWang, J=7701309561en_HK
dc.identifier.scopusauthoridTravanty, EA=6507096634en_HK
dc.identifier.scopusauthoridNicholls, JM=7201463077en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK
dc.identifier.scopusauthoridMason, RJ=7403491658en_HK
dc.identifier.scopusauthoridChan, MCW=26654715500en_HK

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