Evidence map›Paper›PMID 19798431›Full record

ArticlePLoS pathogens2009

Induction of IFN-beta and the innate antiviral response in myeloid cells occurs through an IPS-1-dependent signal that does not require IRF-3 and IRF-7.

Stephane Daffis, Mehul S Suthar, Kristy J Szretter, Michael Gale, Michael S Diamond

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
4.1field-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

96 citing papers in PubMed, 131 citations in OpenAlex.

  1. Article
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  7. Cellular nucleic acid-binding protein is essential for type I interferon-mediated immunity to RNA virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  8. Article
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  12. Involvement of Interferon Regulatory Factor 7 in Nicotine's Suppression of Antiviral Immune Responses.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Article
  13. Review
  14. Article
  15. Article
  16. T cell fate followingCommunications biology · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. A Mouse Model of West Nile Virus Infection.Current protocols in mouse biology · 2017
    Article

36 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Stephane DaffisDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Mehul S Suthar
Kristy J Szretter
Michael Gale
Michael S Diamond
Washington University in St. Louis · USUniversity of Washington · US

Funding

The Burden of Chikungunya and Dengue Infection in KenyaU54AI081680 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI RYMAN, KATHERINE D · 2009 to 2013
$40.4M
West Nile Virus and host control of innate defensesU19AI083019 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL · 2009 to 2018
$22.5M
Cell-Specific Programs of Host Defense Against West Nile VirusR01AI074973 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL · 2009 to 2010
$774k
The host response to West Nile VirusR21AI057568 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL J · 2005 to 2006
$424k
NIAID NIH HHS AI057568NIAID NIH HHS AI074973NIAID NIH HHS R01 AI074973NIAID NIH HHS R21 AI057568NIAID NIH HHS U19 AI083019NIAID NIH HHS U54 AI081680
6 · The paper itself

Abstract

Interferon regulatory factors (IRF)-3 and IRF-7 are master transcriptional factors that regulate type I IFN gene (IFN-alpha/beta) induction and innate immune defenses after virus infection. Prior studies in mice with single deletions of the IRF-3 or IRF-7 genes showed increased vulnerability to West Nile virus (WNV) infection. Whereas mice and cells lacking IRF-7 showed reduced IFN-alpha levels after WNV infection, those lacking IRF-3 or IRF-7 had relatively normal IFN-b production. Here, we generated IRF-3(-/-)x IRF-7(-/-) double knockout (DKO) mice, analyzed WNV pathogenesis, IFN responses, and signaling of innate defenses. Compared to wild type mice, the DKO mice exhibited a blunted but not abrogated systemic IFN response and sustained uncontrolled WNV replication leading to rapid mortality. Ex vivo analysis showed complete ablation of the IFN-alpha response in DKO fibroblasts, macrophages, dendritic cells, and cortical neurons and a substantial decrease of the IFN-beta response in DKO fibroblasts and cortical neurons. In contrast, the IFN-beta response was minimally diminished in DKO macrophages and dendritic cells. However, pharmacological inhibition of NF-kappaB and ATF-2/c-Jun, the two other known components of the IFN-beta enhanceosome, strongly reduced IFN-beta gene transcription in the DKO dendritic cells. Finally, a genetic deficiency of IPS-1, an adaptor involved in RIG-I- and MDA5-mediated antiviral signaling, completely abolished the IFN-beta response after WNV infection. Overall, our experiments suggest that, unlike fibroblasts and cortical neurons, IFN-beta gene regulation after WNV infection in myeloid cells is IPS-1-dependent but does not require full occupancy of the IFN-beta enhanceosome by canonical constituent transcriptional factors.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBlotting, WesternBrainEnzyme-Linked Immunosorbent AssayGene ExpressionGene Expression RegulationImmunity, InnateInterferon-betaInterferon Regulatory Factor-3Interferon Regulatory Factor-7MiceMice, Inbred C57BLMice, KnockoutMyeloid CellsNeuronsAdaptor Proteins, Signal TransducingInterferon-betaInterferon Regulatory Factor-3Interferon Regulatory Factor-7MAVS protein, mouse

Identifiers

PMID19798431
PMCPMC2747008
OpenAlexW2155192432

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.