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Article: Systems-level comparison of host responses induced by pandemic and seasonal influenza A H1N1 viruses in primary human type I-like alveolar epithelial cells in vitro

TitleSystems-level comparison of host responses induced by pandemic and seasonal influenza A H1N1 viruses in primary human type I-like alveolar epithelial cells in vitro
Authors
Issue Date2010
PublisherBioMed Central Ltd. The Journal's web site is located at http://respiratory-research.com/
Citation
Respiratory Research, 2010, v. 11 How to Cite?
AbstractBackground: Pandemic influenza H1N1 (pdmH1N1) virus causes mild disease in humans but occasionally leads to severe complications and even death, especially in those who are pregnant or have underlying disease. Cytokine responses induced by pdmH1N1 viruses in vitro are comparable to other seasonal influenza viruses suggesting the cytokine dysregulation as seen in H5N1 infection is not a feature of the pdmH1N1 virus. However a comprehensive gene expression profile of pdmH1N1 in relevant primary human cells in vitro has not been reported. Type I alveolar epithelial cells are a key target cell in pdmH1N1 pneumonia.Methods: We carried out a comprehensive gene expression profiling using the Affymetrix microarray platform to compare the transcriptomes of primary human alveolar type I-like alveolar epithelial cells infected with pdmH1N1 or seasonal H1N1 virus.Results: Overall, we found that most of the genes that induced by the pdmH1N1 were similarly regulated in response to seasonal H1N1 infection with respect to both trend and extent of gene expression. These commonly responsive genes were largely related to the interferon (IFN) response. Expression of the type III IFN IL29 was more prominent than the type I IFN IFNβ and a similar pattern of expression of both IFN genes was seen in pdmH1N1 and seasonal H1N1 infection. Genes that were significantly down-regulated in response to seasonal H1N1 but not in response to pdmH1N1 included the zinc finger proteins and small nucleolar RNAs. Gene Ontology (GO) and pathway over-representation analysis suggested that these genes were associated with DNA binding and transcription/translation related functions.Conclusions: Both seasonal H1N1 and pdmH1N1 trigger similar host responses including IFN-based antiviral responses and cytokine responses. Unlike the avian H5N1 virus, pdmH1N1 virus does not have an intrinsic capacity for cytokine dysregulation. The differences between pdmH1N1 and seasonal H1N1 viruses lay in the ability of seasonal H1N1 virus to down regulate zinc finger proteins and small nucleolar RNAs, which are possible viral transcriptional suppressors and eukaryotic translation initiation factors respectively. These differences may be biologically relevant and may represent better adaptation of seasonal H1N1 influenza virus to the host. © 2010 Lee et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/141719
ISSN
2010 Impact Factor: 2.859
2015 SCImago Journal Rankings: 1.601
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
National Institutes of Health (NIAID)HHSN266200700005C
Canadian Institutes of Health ResearchTPA-90195
Research Fund for Control of Infectious DiseaseLAB-15
06060552
University Grants Committee, Hong Kong SAR GovernmentAoE/M-12/06
Funding Information:

We thank WW Gai and Genome Research Centre, The University of Hong Kong for their technical support in this study. This work was supported by grants of National Institutes of Health (NIAID contract no. HHSN266200700005C), Canadian Institutes of Health Research (reference no: TPA-90195), Research Fund for Control of Infectious Disease (Ref: LAB-15, RFCID commissioned study on human swine influenza virus and RFCID grant, reference no. 06060552), and funding from the Area of Excellence Scheme of the University Grants Committee, Hong Kong SAR Government (AoE/M-12/06). We acknowledge support from the Canadian Institutes for Health Research to REWH. REWH held a Canada Research Chair.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorLee, SMYen_HK
dc.contributor.authorChan, RWYen_HK
dc.contributor.authorGardy, JLen_HK
dc.contributor.authorLo, Cen_HK
dc.contributor.authorSihoe, ADLen_HK
dc.contributor.authorKang, SSRen_HK
dc.contributor.authorCheung, TKWen_HK
dc.contributor.authorGuan, Yen_HK
dc.contributor.authorChan, MCWen_HK
dc.contributor.authorHancock, REWen_HK
dc.contributor.authorPeiris, MJSen_HK
dc.date.accessioned2011-09-27T02:59:08Z-
dc.date.available2011-09-27T02:59:08Z-
dc.date.issued2010en_HK
dc.identifier.citationRespiratory Research, 2010, v. 11en_HK
dc.identifier.issn1465-9921en_HK
dc.identifier.urihttp://hdl.handle.net/10722/141719-
dc.description.abstractBackground: Pandemic influenza H1N1 (pdmH1N1) virus causes mild disease in humans but occasionally leads to severe complications and even death, especially in those who are pregnant or have underlying disease. Cytokine responses induced by pdmH1N1 viruses in vitro are comparable to other seasonal influenza viruses suggesting the cytokine dysregulation as seen in H5N1 infection is not a feature of the pdmH1N1 virus. However a comprehensive gene expression profile of pdmH1N1 in relevant primary human cells in vitro has not been reported. Type I alveolar epithelial cells are a key target cell in pdmH1N1 pneumonia.Methods: We carried out a comprehensive gene expression profiling using the Affymetrix microarray platform to compare the transcriptomes of primary human alveolar type I-like alveolar epithelial cells infected with pdmH1N1 or seasonal H1N1 virus.Results: Overall, we found that most of the genes that induced by the pdmH1N1 were similarly regulated in response to seasonal H1N1 infection with respect to both trend and extent of gene expression. These commonly responsive genes were largely related to the interferon (IFN) response. Expression of the type III IFN IL29 was more prominent than the type I IFN IFNβ and a similar pattern of expression of both IFN genes was seen in pdmH1N1 and seasonal H1N1 infection. Genes that were significantly down-regulated in response to seasonal H1N1 but not in response to pdmH1N1 included the zinc finger proteins and small nucleolar RNAs. Gene Ontology (GO) and pathway over-representation analysis suggested that these genes were associated with DNA binding and transcription/translation related functions.Conclusions: Both seasonal H1N1 and pdmH1N1 trigger similar host responses including IFN-based antiviral responses and cytokine responses. Unlike the avian H5N1 virus, pdmH1N1 virus does not have an intrinsic capacity for cytokine dysregulation. The differences between pdmH1N1 and seasonal H1N1 viruses lay in the ability of seasonal H1N1 virus to down regulate zinc finger proteins and small nucleolar RNAs, which are possible viral transcriptional suppressors and eukaryotic translation initiation factors respectively. These differences may be biologically relevant and may represent better adaptation of seasonal H1N1 influenza virus to the host. © 2010 Lee et al; licensee BioMed Central Ltd.en_HK
dc.languageengen_US
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://respiratory-research.com/en_HK
dc.relation.ispartofRespiratory Researchen_HK
dc.rightsRespiratory Research. Copyright © BioMed Central Ltd.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCytokines - immunology-
dc.subject.meshImmunocompromised Host - immunology-
dc.subject.meshInfluenza A Virus, H1N1 Subtype - physiology-
dc.subject.meshInfluenza, Human - immunology-
dc.subject.meshPulmonary Alveoli - immunology - virology-
dc.titleSystems-level comparison of host responses induced by pandemic and seasonal influenza A H1N1 viruses in primary human type I-like alveolar epithelial cells in vitroen_HK
dc.typeArticleen_HK
dc.identifier.emailLee, SMY: suki@hku.hken_HK
dc.identifier.emailChan, RWY: reneewy@hku.hken_HK
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_HK
dc.identifier.emailChan, MCW: mchan@hku.hken_HK
dc.identifier.emailPeiris, MJS: malik@hkucc.hku.hken_HK
dc.identifier.authorityLee, SMY=rp01536en_HK
dc.identifier.authorityChan, RWY=rp01596en_HK
dc.identifier.authorityGuan, Y=rp00397en_HK
dc.identifier.authorityChan, MCW=rp00420en_HK
dc.identifier.authorityPeiris, MJS=rp00410en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1186/1465-9921-11-147en_HK
dc.identifier.pmid21029402-
dc.identifier.pmcidPMC2988725-
dc.identifier.scopuseid_2-s2.0-77958546404en_HK
dc.identifier.hkuros186634-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77958546404&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume11en_HK
dc.identifier.isiWOS:000284488700001-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.projectReplication and pathogenesis of avian influenza A (H5N1) viruses in polarized human bronchial and alveolar epithelium-
dc.relation.projectControl of Pandemic and Inter-pandemic Influenza-
dc.identifier.scopusauthoridLee, SMY=35435155600en_HK
dc.identifier.scopusauthoridChan, RWY=26661379100en_HK
dc.identifier.scopusauthoridGardy, JL=7801475389en_HK
dc.identifier.scopusauthoridLo, C=16162440300en_HK
dc.identifier.scopusauthoridSihoe, ADL=6603611976en_HK
dc.identifier.scopusauthoridKang, SSR=36925308900en_HK
dc.identifier.scopusauthoridCheung, TKW=16229531100en_HK
dc.identifier.scopusauthoridGuan, Y=7202924055en_HK
dc.identifier.scopusauthoridChan, MCW=26654715500en_HK
dc.identifier.scopusauthoridHancock, REW=7201916259en_HK
dc.identifier.scopusauthoridPeiris, MJS=7005486823en_HK
dc.identifier.citeulike8145262-

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