Evidence map›Paper›PMID 23153050›Full record

ArticleBMC genomics2012

2009 pandemic H1N1 influenza virus elicits similar clinical course but differential host transcriptional response in mouse, macaque, and swine infection models.

Jennifer T Go, Sarah E Belisle, Nicolas Tchitchek, Terrence M Tumpey, Wenjun Ma, Juergen A Richt, David Safronetz, Heinz Feldmann, Michael G Katze

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 45 citations in OpenAlex.

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  19. Boolean Modeling of Cellular and Molecular Pathways Involved in Influenza Infection.Computational and mathematical methods in medicine · 2016
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Jennifer T GoDepartment of Microbiology, University of Washington, Seattle, 98195, USA. tisoncik@u.washington.edu
Sarah E Belisle
Nicolas Tchitchek
Terrence M Tumpey
Wenjun Ma
Juergen A Richt
David Safronetz
Heinz Feldmann
Michael G Katze
University of Washington · USKansas State University · USCenters for Disease Control and Prevention · USNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Intramural NIH HHSPHS HHS HHSN266200700005CPHS HHS HHSN272200800060C
6 · The paper itself

Abstract

backgroundThe 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 phase responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine.

resultsDespite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. We found genes associated with the retinoid X receptor (RXR) signaling pathway known to control pro-inflammatory and metabolic processes that were differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns varied among the three species.

conclusionsBy 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.

Indexed as

TranscriptomeAnimalsFemaleGene Expression ProfilingHost-Pathogen InteractionsHost SpecificityInfluenza A Virus, H1N1 SubtypeLungMacacaMiceMice, Inbred BALB COrthomyxoviridae InfectionsPandemicsProtein MultimerizationRetinoid X ReceptorsSignal TransductionRetinoid X Receptors

Identifiers

PMID23153050
PMCPMC3532173
OpenAlexW2036583341

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.