Evidence map›Paper›PMID 31578292›Full record

ArticleJournal of virology2019

Vesicular Stomatitis Virus Transcription Is Inhibited by TRIM69 in the Interferon-Induced Antiviral State.

Tonya Kueck, Louis-Marie Bloyet, Elena Cassella, Trinity Zang, Fabian Schmidt, Vesna Brusic, Gergely Tekes, Owen Pornillos, Sean P J Whelan, Paul D Bieniasz

Open access · hybridAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

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  14. Trim69 is a microtubule regulator that acts as a pantropic viral inhibitor.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

10 authors at 4 institutions in 1 country.

Tonya Kueck *Laboratory of Retrovirology, The Rockefeller University, New York, New York, USA.
Louis-Marie Bloyet *Department of Microbiology, Harvard Medical School, Boston, Massachusetts, USA.
Elena CassellaLaboratory of Retrovirology, The Rockefeller University, New York, New York, USA.
Trinity ZangLaboratory of Retrovirology, The Rockefeller University, New York, New York, USA.
Fabian SchmidtLaboratory of Retrovirology, The Rockefeller University, New York, New York, USA.
Vesna BrusicDepartment of Microbiology, Harvard Medical School, Boston, Massachusetts, USA.
Gergely TekesDepartment of Microbiology, Harvard Medical School, Boston, Massachusetts, USA.
Owen PornillosDepartment of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, Virginia, USA.
Sean P J WhelanDepartment of Microbiology, Harvard Medical School, Boston, Massachusetts, USA sean_whelan@hms.harvard.edu pbieniasz@rockefeller.edu.
Paul D BieniaszLaboratory of Retrovirology, The Rockefeller University, New York, New York, USA sean_whelan@hms.harvard.edu pbieniasz@rockefeller.edu.ORCID 0000-0002-2368-3719
Harvard University · USRockefeller University · USHoward Hughes Medical Institute · USUniversity of Virginia · US

Funding

RNA Processing in Non-Segmented Minus-Strand RNA VirusesR37AI059371 · NIAID · WASHINGTON UNIVERSITY · PI WHELAN, SEAN PJ · 2015 to 2024
$5.4M
Discovery and Mechanism of Antiretroviral FactorsR37AI064003 · NIAID · ROCKEFELLER UNIVERSITY · PI BIENIASZ, PAUL D. · 2011 to 2020
$4.9M
Structural Virology of Tripartite Motif ProteinsR37AI150479 · NIAID · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Owen Pornillos · 2022 to 2026
$3.0M
Structural Virology of Tripartite Motif ProteinsR01GM112508 · NIGMS · UNIVERSITY OF VIRGINIA · PI PORNILLOS, OWEN · 2014 to 2018
$1.6M
Structural Virology of Tripartite Motif ProteinsR01AI150479 · NIAID · UNIVERSITY OF VIRGINIA · PI PORNILLOS, OWEN · 2019 to 2021
$982k
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI150479NIAID NIH HHS R37 AI059371NIAID NIH HHS R37 AI064003NIAID NIH HHS R37 AI150479NIGMS NIH HHS R01 GM112508
6 · The paper itself

Abstract

Interferons (IFNs) induce the expression of interferon-stimulated genes (ISGs), many of which are responsible for the cellular antiviral state in which the replication of numerous viruses is blocked. How the majority of individual ISGs inhibit the replication of particular viruses is unknown. We conducted a loss-of-function screen to identify genes required for the activity of alpha interferon (IFN-α) against vesicular stomatitis virus, Indiana serotype (VSV

Indexed as

Antiviral AgentsCell LineCytokinesHumansInterferon-alphaModels, MolecularPhosphoproteinsProtein ConformationProtein DomainsRNA, MessengerRNA, ViralTripartite Motif ProteinsUbiquitin-Protein LigasesVesicular StomatitisVesicular stomatitis Indiana virusVesiculovirusAntiviral AgentsCytokinesInterferon-alphaPhosphoproteinsRNA, MessengerRNA, ViralTRIM69 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasesViral ProteinsinterferonTRIM69VSV

Identifiers

PMID31578292
PMCPMC6880163
OpenAlexW2978489913

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.