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Cited by 45Influenza Virus Research Studiesinterferon and immune responsesRespiratory viral infections research

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

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Lee, Suki MY, Chan, Renee WY, Gardy, Jennifer L, Lo, Cheuk-kin, Sihoe, Alan DL, Kang, Sara SR, Cheung, Timothy KW, Guan, Yi +3 more·2010·Respiratory Research
DOI 10.1186/1465-9921-11-147PMC PMC2988725
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Abstract

BACKGROUND: 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.

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  • In severe infections affecting the deep tissues of the respiratory tract, it is probable that the immunological cascade that takes place directly in the deep tissues is crucial to immunopathology rather than what can be measured as a 'spillover' in the peripheral blood.

    “For instance, in severe infections affecting the deep tissues of the respiratory tract (as has been described in avian influenza or severe primary influenza virus infections), it is probable that it is the immunological cascade that takes place directly in the deep tissues that is crucial to immunopathology rather than what can be measured as a “spillover” in the peripheral blood (28,82,128).”

    From Into the Eye of the Cytokine Storm (2012) · cites this paper as [82]

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  1. NCBI: GEO Gene Expression Omnibus http://www.ncbi.nlm.nih.gov/geo/

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Authors
Lee, S. M., Chan, R. W., Gardy, J. L., Lo, C.-K., Sihoe, A. D., Kang, S. S., Cheung, T. K., Guan, Y., Chan, M. C., Hancock, R. E., & Peiris, M. J.
Affiliations
  • University of Hong Kong (HK)
  • BC Centre for Disease Control (CA)
  • Queen Elizabeth Hospital (CN)
  • Queen Mary Hospital (CN)
  • University of British Columbia (CA)
Corresponding author
  • Lee, Suki MY
  • Chan, Renee WY
  • Peiris, Malik JS
ORCID
Venue
Respiratory Research
Publisher
Springer Science and Business Media LLC
Published
2010-10-28
Volume
11
Issue
1
Pages
147-147
ISSN
  • 1465-9921 (ISSN-L)
  • 1465-993X
DOI
10.1186/1465-9921-11-147
PMC
PMC2988725
OpenAlex
W2110990442
Cited by
43
References
26
Citations by year
2022: 1 · 2021: 2 · 2020: 1 · 2019: 2 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 3 · 2014: 6 · 2013: 4 · 2012: 9
FWCI
4.89
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Respiratory Research (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • HAL (submittedVersion, other-oa)
  • cIRcle (University of British Columbia) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • The HKU Scholars Hub (University of Hong Kong) (submittedVersion, cc-by-nc-nd)
  • Open Collections
Funders
  • University Grants Committee (AoE/M‐12/06)
  • University of Hong Kong
  • National Institutes of Health (HHSN266200700005C)
  • U.S. Public Health Service (HHSN26620 0700005C)
  • Canadian Institutes of Health Research (90195_1)
  • National Institute of Allergy and Infectious Diseases (HHSN266200700005C)
Topics
  • Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
  • Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
Keywords
pandemic influenza A(H1N1), host response, alveolar epithelial cells, gene expression profiling, interferon response, interferon-beta, cytokine imbalance, zinc finger proteins, small nucleolar RNA, influenza pneumonia, translation initiation
MeSH terms
Cell Line, Epithelial Cells, Humans, Influenza, Human, Pulmonary Alveoli, Seasons, Cytokines, Immunocompromised Host, Influenza A Virus, H1N1 Subtype, Pandemics

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