Evidence map›Paper›PMID 21900171›Full record

ArticleJournal of virology2011

2009 pandemic H1N1 influenza virus causes disease and upregulation of genes related to inflammatory and immune responses, cell death, and lipid metabolism in pigs.

Wenjun Ma, Sarah E Belisle, Derek Mosier, Xi Li, Evelyn Stigger-Rosser, Qinfang Liu, Chuanling Qiao, Jake Elder, Richard Webby, Michael G Katze and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Antiviral defenses are diminished at birth in cystic fibrosis pig airways.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026
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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

11 authors at 3 institutions in 1 country.

Wenjun MaDepartment of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, KS 66506, USA.
Sarah E Belisle
Derek Mosier
Xi Li
Evelyn Stigger-Rosser
Qinfang Liu
Chuanling Qiao
Jake Elder
Richard Webby
Michael G Katze
Juergen A Richt
Kansas State University · USSt. Jude Children's Research Hospital · USUniversity of Washington · US

Funding

YILMA SIV VACCINIA VACCINE TRIALP51RR000166 · NCRR · UNIVERSITY OF WASHINGTON · PI HU, SHIU-LOK · 1985 to 2011
$161.1M
Viral and Host cDNA Libraries from 1918 Influenza CasesP01AI058113 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GARCIA-SASTRE, ADOLFO · 2004 to 2010
$20.3M
NCRR NIH HHS P51 RR000166NCRR NIH HHS P51 RR00166-45NIAID NIH HHS HHSN266200700005CNIAID NIH HHS P01 AI058113NIAID NIH HHS P01 AI058113-06PHS HHS 266200700005C
6 · The paper itself

Abstract

There exists limited information about whether adaptation is needed for cross-species transmission of the 2009 pandemic H1N1 influenza virus (pH1N1). Here, we compare the pathogenesis of two pH1N1 viruses, one derived from a human patient (A/CA/04/09 [CA09]) and the other from swine (A/swine/Alberta/25/2009 [Alb09]), with that of the 1918-like classical swine influenza virus (A/swine/Iowa/1930 [IA30]) in the pig model. Both pH1N1 isolates induced clinical symptoms such as coughing, sneezing, decreased activity, fever, and labored breathing in challenged pigs, but IA30 virus did not cause any clinical symptoms except fever. Although both the pH1N1 viruses and the IA30 virus caused lung lesions, the pH1N1 viruses were shed from the nasal cavities of challenged pigs whereas the IA30 virus was not. Global gene expression analysis indicated that transcriptional responses of the viruses were distinct. pH1N1-infected pigs had an upregulation of genes related to inflammatory and immune responses at day 3 postinfection that was not seen in the IA30 infection, and expression levels of genes related to cell death and lipid metabolism at day 5 postinfection were markedly different from those of IA30 infection. These results indicate that both pH1N1 isolates are more virulent due in part to differences in the host transcriptional response during acute infection. Our study also indicates that pH1N1 does not need prior adaptation to infect pigs, has a high potential to be maintained in naïve swine populations, and might reassort with currently circulating swine influenza viruses.

Indexed as

Cell DeathGene Expression RegulationLipid MetabolismAnimalsDisease Models, AnimalGene Expression ProfilingHumansInflammationInfluenza A Virus, H1N1 SubtypeLungMetabolic Networks and PathwaysMolecular Sequence DataNasal MucosaOrthomyxoviridae InfectionsSequence Analysis, DNASwine

Identifiers

PMID21900171
PMCPMC3209293
OpenAlexW2101043191

What OpenQuestion holds

Textmetadata
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.