Evidence map›Paper›PMID 25127040›Full record

ArticlePloS one2014

Toll-like receptor-3 is dispensable for the innate microRNA response to West Nile virus (WNV).

Pauline E Chugh, Blossom A Damania, Dirk P Dittmer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  9. Review
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  11. Role of Immune Aging in Susceptibility to West Nile Virus.Methods in molecular biology (Clifton, N.J.) · 2016
    Review
  12. 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

3 authors at 1 institution in 1 country.

Pauline E ChughDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Blossom A DamaniaDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Dirk P DittmerDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
University of North Carolina at Chapel Hill · US

Funding

Virology, Immunology, and Microbiology CoreP30AI050410 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAVID M. MARGOLIS · 2001 to 2026
$76.9M
ART Modulation of Viral Pathogenesis in Oral EpitheliaR01DE018304 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DITTMER, DIRK P · 2007 to 2025
$6.9M
Innate Immunity and KSHVR01DE018281 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAMANIA, BLOSSOM A · 2007 to 2016
$3.5M
Regulation of the KSHV Latent PromoterR01CA109232 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DITTMER, DIRK P · 2004 to 2014
$2.5M
NCI NIH HHS R01 CA109232NCI NIH HHS R01 CA109232-08S1NIDCR NIH HHS DE018281NIDCR NIH HHS DE018304NIDCR NIH HHS R01 DE018281NIDCR NIH HHS R01 DE018304
6 · The paper itself

Abstract

The innate immune response to West Nile virus (WNV) infection involves recognition through toll-like receptors (TLRs) and RIG-I-like receptors (RLRs), leading to establishment of an antiviral state. MiRNAs (miRNAs) have been shown to be reliable biomarkers of TLR activation. Here, we sought to evaluate the contribution of TLR3 and miRNAs to the host response to WNV infection. We first analyzed HEK293-NULL and HEK293-TLR3 cells for changes in the innate immune response to infection. The presence of TLR3 did not seem to affect WNV load, infectivity or phosphorylation of IRF3. Analysis of experimentally validated NFκB-responsive genes revealed a WNV-induced signature largely independent of TLR3. Since miRNAs are involved in viral pathogenesis and the innate response to infection, we sought to identify changes in miRNA expression upon infection in the presence or absence of TLR3. MiRNA profiling revealed 70 miRNAs induced following WNV infection in a TLR3-independent manner. Further analysis of predicted gene targets of WNV signature miRNAs revealed genes highly associated with pathways regulating cell death, viral pathogenesis and immune cell trafficking.

Indexed as

Cell LineDEAD Box Protein 58DEAD-box RNA HelicasesGene Expression ProfilingHEK293 CellsHumansImmunity, InnateInterferon-Induced Helicase, IFIH1Interferon Regulatory Factor-3MicroRNAsNF-kappa BReceptors, ImmunologicRNA, MessengerSignal TransductionToll-Like Receptor 3Viral LoadDEAD Box Protein 58DEAD-box RNA HelicasesIFIH1 protein, humanInterferon-Induced Helicase, IFIH1Interferon Regulatory Factor-3IRF3 protein, humanMicroRNAsNF-kappa BReceptors, ImmunologicRIGI protein, humanRNA, MessengerTLR3 protein, humanToll-Like Receptor 3

Identifiers

PMID25127040
PMCPMC4134228
OpenAlexW2009693214

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.