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GEO help: Mouse over screen elements for information. |
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Status |
Public on May 27, 2014 |
Title |
Characterizing the transcriptomic response of mice infected with A/Anhui/01/2013 (H7N9), A/Netherlands/219/2003 (H7N7), and A/Vietnam/1203/2004 (H5N1), and a pandemic H1N1 human virus, A/Mexico/4482/2007 (H1N1) |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
Modulating the host response is a promising approach to treating influenza, a virus whose pathogenesis is determined in part by the host response it elicits. Though the pathogenicity of emerging H7N9 influenza virus has been reported in several animal models, these studies have not included a detailed characterization of the host response following infection. To this end, we characterized the transcriptomic response of BALB/c mice infected with H7N9 (A/Anhui/1/2013) virus and compared it to the responses induced by H5N1 (A/Vietnam/1203/2004), H7N7 (A/Netherlands/219/2003) or H1N1 (A/Mexico/4482/2009) viruses. We found that responses to the H7 subtype viruses were intermediate to those elicited by H5N1 and H1N1 early in infection, but that they evolved to resemble the H5N1 response as infection progressed. H5N1, H7N7 and H7N9 viruses were pathogenic in mice, and this pathogenicity correlated with increased cytokine response, decreased lipid metabolism and decreased coagulation signaling. This three-pronged signature has previously been observed in mice infected with pathogenic H1N1 strains such as the 1918 virus, indicating that it may be predictive of pathogenicity across multiple influenza strains.
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Overall design |
Groups of 6- to 8-week-old BALB/c mice were infected with either A/Anhui/01/2013 (H7N9), A/Netherlands/219/2003 (H7N7), A/Vietnam/1203/2004 (H5N1), or pandemic H1N1 human virus, A/Mexico/4482/2007 (H1N1). Infections were done at 10^5 PFU or time-matched mock infected. Time points were 1, 3 and 5 d.p.i. There were 4-5 infected and 3 mock infected animals/time point. Lung samples were collected for virus load and transcriptional analysis. Weight loss and animal survival were also monitored.
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Contributor(s) |
Katze M, Tumpey T, Josset L, Tchitchek N, Morrison J, Belser J, Chang J |
Citation(s) |
24991006 |
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Submission date |
Jan 13, 2014 |
Last update date |
Jan 12, 2017 |
Contact name |
Michael Katze |
E-mail(s) |
data@viromics.washington.edu
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Organization name |
University of Washington
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Department |
Microbiology
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Lab |
Michael G. Katze, Ph.D
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Street address |
Rosen Building 960 Republican St.
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City |
Seattle |
State/province |
WA |
ZIP/Postal code |
98109-4325 |
Country |
USA |
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Platforms (1) |
GPL7202 |
Agilent-014868 Whole Mouse Genome Microarray 4x44K G4122F (Probe Name version) |
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Samples (68)
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Relations |
BioProject |
PRJNA234450 |
Supplementary file |
Size |
Download |
File type/resource |
GSE54048_RAW.tar |
598.6 Mb |
(http)(custom) |
TAR (of TXT) |
Processed data included within Sample table |
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