Deep sequencing of primary human lung epithelial cells challenged with H5N1 influenza virus reveals a proviral role for CEACAM1

Ye, Siying, Cowled, Christopher J., Yap, Cheng-Hon and Stambas, John 2018, Deep sequencing of primary human lung epithelial cells challenged with H5N1 influenza virus reveals a proviral role for CEACAM1, Scientific reports, vol. 8, no. 1, doi: 10.1038/s41598-018-33605-6.

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Title Deep sequencing of primary human lung epithelial cells challenged with H5N1 influenza virus reveals a proviral role for CEACAM1
Author(s) Ye, SiyingORCID iD for Ye, Siying orcid.org/0000-0002-0882-1642
Cowled, Christopher J.
Yap, Cheng-Hon
Stambas, JohnORCID iD for Stambas, John orcid.org/0000-0002-5690-2551
Journal name Scientific reports
Volume number 8
Issue number 1
Article ID 15468
Total pages 13
Publisher Springer Nature
Place of publication London, Eng.
Publication date 2018-10-19
ISSN 2045-2322
Keyword(s) Science & Technology
Multidisciplinary Sciences
Science & Technology - Other Topics
CARCINOEMBRYONIC ANTIGEN FAMILY
A H7N9 VIRUS
HUMAN ALVEOLAR
ADHESION MOLECULE-1
EXPRESSION ANALYSIS
DIFFERENTIAL GENE
NONHUMAN-PRIMATES
OXIDATIVE STRESS
NK CELLS
CD66A
Summary Current prophylactic and therapeutic strategies targeting human influenza viruses include vaccines and antivirals. Given variable rates of vaccine efficacy and antiviral resistance, alternative strategies are urgently required to improve disease outcomes. Here we describe the use of HiSeq deep sequencing to analyze host gene expression in primary human alveolar epithelial type II cells infected with highly pathogenic avian influenza H5N1 virus. At 24 hours post-infection, 623 host genes were significantly upregulated, including the cell adhesion molecule CEACAM1. H5N1 virus infection stimulated significantly higher CEACAM1 protein expression when compared to influenza A PR8 (H1N1) virus, suggesting a key role for CEACAM1 in influenza virus pathogenicity. Furthermore, silencing of endogenous CEACAM1 resulted in reduced levels of proinflammatory cytokine/chemokine production, as well as reduced levels of virus replication following H5N1 infection. Our study provides evidence for the involvement of CEACAM1 in a clinically relevant model of H5N1 infection and may assist in the development of host-oriented antiviral strategies.
Language eng
DOI 10.1038/s41598-018-33605-6
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2018, The Authors
Persistent URL http://hdl.handle.net/10536/DRO/DU:30114850

Document type: Journal Article
Collections: School of Medicine
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