Evidence map›Paper›PMID 20926563›Full record

ArticleJournal of virology2010

Genomic profiling of tumor necrosis factor alpha (TNF-alpha) receptor and interleukin-1 receptor knockout mice reveals a link between TNF-alpha signaling and increased severity of 1918 pandemic influenza virus infection.

Sarah E Belisle, Jennifer R Tisoncik, Marcus J Korth, Victoria S Carter, Sean C Proll, David E Swayne, Mary Pantin-Jackwood, Terrence M Tumpey, Michael G Katze

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Nutrients · 2024
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Innate Immunity and Influenza A Virus Pathogenesis: Lessons for COVID-19.Frontiers in cellular and infection microbiology · 2020
    Review
  16. Dynamic Natural Killer Cell and T Cell Responses to Influenza Infection.Frontiers in cellular and infection microbiology · 2020
    Review
  17. Article
  18. Article
  19. Genetics of Sjögren's syndrome.Clinical immunology (Orlando, Fla.) · 2017
    Review
  20. Article
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 3 institutions in 1 country.

Sarah E BelisleDepartment of Microbiology, University of Washington, Box 358070, Seattle, WA 98195-8070, USA.
Jennifer R Tisoncik
Marcus J Korth
Victoria S Carter
Sean C Proll
David E Swayne
Mary Pantin-Jackwood
Terrence M Tumpey
Michael G Katze
University of Washington · USU.S. National Poultry Research Center · USCenters for Disease Control and Prevention · US

Funding

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
NIAID NIH HHS P01 AI058113NIAID NIH HHS P01AI058113
6 · The paper itself

Abstract

The influenza pandemic of 1918 to 1919 was one of the worst global pandemics in recent history. The highly pathogenic nature of the 1918 virus is thought to be mediated in part by a dysregulation of the host response, including an exacerbated proinflammatory cytokine response. In the present study, we compared the host transcriptional response to infection with the reconstructed 1918 virus in wild-type, tumor necrosis factor (TNF) receptor-1 knockout (TNFRKO), and interleukin-1 (IL-1) receptor-1 knockout (IL1RKO) mice as a means of further understanding the role of proinflammatory cytokine signaling during the acute response to infection. Despite reported redundancy in the functions of IL-1β and TNF-α, we observed that reducing the signaling capacity of each of these molecules by genetic disruption of their key receptor genes had very different effects on the host response to infection. In TNFRKO mice, we found delayed or decreased expression of genes associated with antiviral and innate immune signaling, complement, coagulation, and negative acute-phase response. In contrast, in IL1RKO mice numerous genes were differentially expressed at 1 day postinoculation, including an increase in the expression of genes that contribute to dendritic and natural killer cell processes and cellular movement, and gene expression profiles remained relatively constant at later time points. We also observed a compensatory increase in TNF-α expression in virus-infected IL1RKO mice. Our data suggest that signaling through the IL-1 receptor is protective, whereas signaling through the TNF-α receptor increases the severity of 1918 virus infection. These findings suggest that manipulation of these pathways may have therapeutic benefit.

Indexed as

Gene Expression ProfilingAnimalsBiomarkersBlotting, WesternCell CommunicationCell MovementDendritic CellsInfluenza A virusMiceMice, Inbred C57BLMice, KnockoutOligonucleotide Array Sequence AnalysisOrthomyxoviridae InfectionsPandemicsReceptors, Interleukin-1 Type IReceptors, Tumor Necrosis Factor, Type IBiomarkersDG 191Receptors, Interleukin-1 Type IReceptors, Tumor Necrosis Factor, Type IRNA, MessengerTriazolesTumor Necrosis Factor-alpha

Identifiers

PMID20926563
PMCPMC3004331
OpenAlexW2172025483

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.