Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Host cell gene expression in Influenza A virus (A/Singapore/478/2009 (pH1N1)) infected A549 cells at 2, 4, 6, 8 and 10 hours post infection

ABSTRACT: We used the microarray data to analyze host cells response on A549 cells infected with Influenza A virus (A/Singapore/478/2009 (pH1N1)) The Influenza A virus (A/Singapore/478/2009 (pH1N1)) infected A549 cells were harvested at 2, 4, 6, 8 and 10 hpi and RNA extraction was performed using standard protocol as described by Affymetrix. The aim of this experiment is to analyze host response to Influenza A virus (A/Singapore/478/2009 (pH1N1)) infection.

ORGANISM(S): Homo sapiens

SUBMITTER: Richard Sugrue

PROVIDER: E-GEOD-31518 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Activation of type I and III interferon signalling pathways occurs in lung epithelial cells infected with low pathogenic avian influenza viruses.

Sutejo Richard R Yeo Dawn S DS Myaing Myint Zu MZ Hui Chen C Xia Jiajia J Ko Debbie D Cheung Peter C F PC Tan Boon-Huan BH Sugrue Richard J RJ

PloS one 20120321 3

The host response to the low pathogenic avian influenza (LPAI) H5N2, H5N3 and H9N2 viruses were examined in A549, MDCK, and CEF cells using a systems-based approach. The H5N2 and H5N3 viruses replicated efficiently in A549 and MDCK cells, while the H9N2 virus replicated least efficiently in these cell types. However, all LPAI viruses exhibited similar and higher replication efficiencies in CEF cells. A comparison of the host responses of these viruses and the H1N1/WSN virus and low passage pH1N1 ...[more]

PMID: 22470468

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Project description:Background: The 2009 pandemic H1N1 influenza virus emerged in swine and quickly became a major global health threat. In mouse, non-human primate, and swine infection models, the pH1N1 virus efficiently replicates in the lung and induces pro-inflammatory host responses; however, whether similar or different cellular pathways were impacted by pH1N1 virus across independent infection models remains to be further defined. To address this, we have performed a comparative transcriptomic analysis of acute host responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine. Results: Despite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. The retinoid X receptor (RXR) signaling pathway controlling pro-inflammatory and metabolic processes was differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns differed in each species. Conclusions: By comparing transcriptional changes in the context of clinical and virological measures, we identified differences in the host transcriptional response to pH1N1 virus across independent models of acute infection. Antiviral resistance and the emergence of new influenza viruses have placed more focus on developing drugs that target the immune system. Underlying overt clinical disease are molecular events that suggest therapeutic targets identified in one host may not be appropriate in another. The goal of this experiment was to use global gene expression profiling to understand swine lung host responses to pandemic H1N1 influenza A/Californica/04/2009 (CA04) virus infection and compare acute host responses across independent species. Four-week-old crossbred pigs (Sus Scrofa) were inoculated intratracheally with either 10^6 TCID50/pig egg-derived 2009 pandemic influenza A/California/04/2009 virus (n = 5) or mock inoculated with non-infectious cell culture supernatant (control; n = 4). Animals were euthanized on day 7 post-infection and lung samples were used for microarray.

Dataset Information

Host cell gene expression in Influenza A virus (A/Singapore/478/2009 (pH1N1)) infected A549 cells at 2, 4, 6, 8 and 10 hours post infection

Publications

Activation of type I and III interferon signalling pathways occurs in lung epithelial cells infected with low pathogenic avian influenza viruses.

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