Evidence map›Paper›PMID 32839386›Full record

ReviewViruses2020

Structures and Functions of Viral 5' Non-Coding Genomic RNA Domain-I in Group-B Enterovirus Infections.

Marie Glenet, Laetitia Heng, Domitille Callon, Anne-Laure Lebreil, Paul-Antoine Gretteau, Yohan Nguyen, Fatma Berri, Laurent Andreoletti

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 15 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

8 authors at 2 institutions in 1 country.

Marie GlenetEA-4684 CardioVir, Faculty of Medicine, University of Reims Champagne-Ardenne (URCA), 51097 Reims, France.
Laetitia HengEA-4684 CardioVir, Faculty of Medicine, University of Reims Champagne-Ardenne (URCA), 51097 Reims, France.
Domitille CallonEA-4684 CardioVir, Faculty of Medicine, University of Reims Champagne-Ardenne (URCA), 51097 Reims, France.
Anne-Laure LebreilEA-4684 CardioVir, Faculty of Medicine, University of Reims Champagne-Ardenne (URCA), 51097 Reims, France.
Paul-Antoine GretteauEA-4684 CardioVir, Faculty of Medicine, University of Reims Champagne-Ardenne (URCA), 51097 Reims, France.ORCID 0000-0001-7250-9656
Yohan NguyenEA-4684 CardioVir, Faculty of Medicine, University of Reims Champagne-Ardenne (URCA), 51097 Reims, France.
Fatma BerriEA-4684 CardioVir, Faculty of Medicine, University of Reims Champagne-Ardenne (URCA), 51097 Reims, France.
Laurent AndreolettiEA-4684 CardioVir, Faculty of Medicine, University of Reims Champagne-Ardenne (URCA), 51097 Reims, France.
Infections Cardiovasculaires Virales et inflammation en pathologie humaineCentre Hospitalier Universitaire de Reims · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Group-B enteroviruses (EV-B) are ubiquitous naked single-stranded positive RNA viral pathogens that are responsible for common acute or persistent human infections. Their genome is composed in the 5' end by a non-coding region, which is crucial for the initiation of the viral replication and translation processes. RNA domain-I secondary structures can interact with viral or cellular proteins to form viral ribonucleoprotein (RNP) complexes regulating viral genomic replication, whereas RNA domains-II to -VII (internal ribosome entry site, IRES) are known to interact with cellular ribosomal subunits to initiate the viral translation process. Natural 5' terminally deleted viral forms lacking some genomic RNA domain-I secondary structures have been described in EV-B induced murine or human infections. Recent in vitro studies have evidenced that the loss of some viral RNP complexes in the RNA domain-I can modulate the viral replication and infectivity levels in EV-B infections. Moreover, the disruption of secondary structures of RNA domain-I could impair viral RNA sensing by RIG-I (Retinoic acid inducible gene I) or MDA5 (melanoma differentiation-associated protein 5) receptors, a way to overcome antiviral innate immune response. Overall, natural 5' terminally deleted viral genomes resulting in the loss of various structures in the RNA domain-I could be major key players of host-cell interactions driving the development of acute or persistent EV-B infections.

Indexed as

AnimalsEnterovirus B, HumanEnterovirus InfectionsGenome, ViralHost-Pathogen InteractionsHumansInterferonsNucleic Acid ConformationProtein BiosynthesisRNA, UntranslatedRNA, ViralSignal TransductionViral ProteinsVirus ReplicationInterferonsRNA, UntranslatedRNA, ViralViral Proteins5′ terminally deleted viral formsantiviral innate immune responseenterovirus replicationgroup-B enterovirusRNA domain-Itype I interferonviral ribonucleoprotein complexes

Identifiers

PMID32839386
PMCPMC7552046
OpenAlexW3046773540

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.