Evidence map›Paper›PMID 29903832›Full record

ArticleRNA (New York, N.Y.)2018

Influenza A virus-derived siRNAs increase in the absence of NS1 yet fail to inhibit virus replication.

Kevin Tsai, David G Courtney, Edward M Kennedy, Bryan R Cullen

Open access · bronzeAbstract read
In one paragraph

Article in RNA (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Kevin TsaiDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
David G CourtneyDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Edward M KennedyDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Bryan R CullenDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Duke University · US

Funding

Viral Oncology Training GrantT32CA009111 · NCI · DUKE UNIVERSITY · PI LUFTIG, MICAH A. · 1985 to 2023
$8.9M
Effect of m6A editing of RNA on influenza A virus replicationR21AI130574 · NIAID · DUKE UNIVERSITY · PI CULLEN, BRYAN R. · 2017 to 2018
$437k
Reconstitution of a protective antiviral RNAi response in somatic human cellsR21AI113098 · NIAID · DUKE UNIVERSITY · PI CULLEN, BRYAN R. · 2014 to 2015
$434k
NCI NIH HHS T32 CA009111NIAID NIH HHS R21 AI113098NIAID NIH HHS R21 AI130574
6 · The paper itself

Abstract

While the issue of whether RNA interference (RNAi) ever forms part of the antiviral innate immune response in mammalian somatic cells remains controversial, there is considerable evidence demonstrating that few, if any, viral small interfering RNAs (siRNAs) are produced in infected cells. Moreover, inhibition of RNAi by mutational inactivation of key RNAi factors, such as Dicer or Argonaute 2, fails to enhance virus replication. One potential explanation for this lack of inhibitory effect is that mammalian viruses encode viral suppressors of RNAi (VSRs) that are so effective that viral siRNAs are not produced in infected cells. Indeed, a number of mammalian VSRs have been described, of which the most prominent is the influenza A virus (IAV) NS1 protein, which has not only been reported to inhibit RNAi in plants and insects but also to prevent the production of viral siRNAs in IAV-infected human cells. Here, we confirm that an IAV mutant lacking NS1 indeed differs from wild-type IAV in that it induces the production of readily detectable levels of Dicer-dependent viral siRNAs in infected human cells. However, we also demonstrate that these siRNAs have little if any inhibitory effect on IAV gene expression. This is likely due, at least in part, to their inefficient loading into RNA-induced silencing complexes.

Indexed as

RNA InterferenceDEAD-box RNA HelicasesHEK293 CellsHost-Pathogen InteractionsHumansInfluenza A virusMutationRibonuclease IIIRNA, ViralSequence Analysis, RNAViral Nonstructural ProteinsVirus ReplicationDEAD-box RNA HelicasesDICER1 protein, humanINS1 protein, influenza virusRibonuclease IIIRNA, ViralViral Nonstructural Proteinsantiviral responseinfluenza A virusNS1 proteinRNA interferencesiRNA

Identifiers

PMID29903832
PMCPMC6097656
OpenAlexW2808691051

What OpenQuestion holds

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LicenceCC BY-NC
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.