Evidence map›Paper›PMID 24953656›Full record

ArticleCell reports2014

The Mammalian response to virus infection is independent of small RNA silencing.

Simone Backes, Ryan A Langlois, Sonja Schmid, Andrew Varble, Jaehee V Shim, David Sachs, Benjamin R tenOever

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 72 citations in OpenAlex.

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  19. Review
  20. Small RNA-based antimicrobial immunity.Nature reviews. Immunology · 2019
    Review
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

7 authors at 1 institution in 1 country.

Simone BackesDepartment of Microbiology, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Ryan A LangloisDepartment of Microbiology, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Sonja SchmidDepartment of Microbiology, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Andrew VarbleDepartment of Microbiology, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Jaehee V ShimDepartment of Microbiology, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
David SachsDepartment of Genetics and Genomic Sciences, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Benjamin R tenOeverDepartment of Microbiology, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Global Health and Emerging Pathogens Institute, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: benjamin.tenoever@mssm.edu.
Icahn School of Medicine at Mount Sinai · US

Funding

Research Training Program in Molecular and Cellular HematologyT32HL094283 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BARON, MARGARET H · 2009 to 2013
$908k
NHLBI NIH HHS T32 HL094283NHLBI NIH HHS T32-HL094283
6 · The paper itself

Abstract

A successful cellular response to virus infection is essential for evolutionary survival. In plants, arthropods, and nematodes, cellular antiviral defenses rely on RNAi. Interestingly, the mammalian response to virus is predominantly orchestrated through interferon (IFN)-mediated induction of antiviral proteins. Despite the potency of the IFN system, it remains unclear whether mammals also have the capacity to employ antiviral RNAi. Here, we investigated this by disabling IFN function, small RNA function, or both activities in the context of virus infection. We find that loss of small RNAs in the context of an in vivo RNA virus infection lowers titers due to reduced transcriptional repression of the host antiviral response. In contrast, enabling a virus with the capacity to inhibit the IFN system results in increased titers. Taken together, these results indicate that small RNA silencing is not a physiological contributor to the IFN-mediated cellular response to virus infection.

Indexed as

RNA InterferenceAnimalsCells, CulturedChlorocebus aethiopsCricetinaeInterferonsMiceRhabdoviridae InfectionsRNA-Induced Silencing ComplexRNA, Small InterferingVero CellsVesiculovirusInterferonsRNA-Induced Silencing ComplexRNA, Small Interfering

Identifiers

PMID24953656
PMCPMC4096324
OpenAlexW2020406526

What OpenQuestion holds

Textmetadata
LicenceTDM
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.