Evidence map›Paper›PMID 33087469›Full record

ArticleJournal of virology2020

The NSs Protein Encoded by the Virulent Strain of Rift Valley Fever Virus Targets the Expression of Abl2 and the Actin Cytoskeleton of the Host, Affecting Cell Mobility, Cell Shape, and Cell-Cell Adhesion.

Aline Bamia, Vasco Marcato, Magali Boissière, Zeyni Mansuroglu, Carole Tamietti, Mattea Romani, Dominique Simon, Guanfang Tian, Florence Niedergang, Jean-Jacques Panthier and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.3field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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  15. A Look intoViruses · 2021
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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

13 authors at 3 institutions in 1 country.

Aline Bamia *Université Paris Descartes, INSERM UMRS-1007 CICB-Paris, Paris, France.
Vasco Marcato *Université Paris Descartes, INSERM UMRS-1007 CICB-Paris, Paris, France.
Magali BoissièreInstitut Pasteur, Unité de Recherche de Virologie Structurale, Paris, France.
Zeyni MansurogluUniversité Paris Descartes, INSERM UMRS-1007 CICB-Paris, Paris, France.
Carole TamiettiInstitut Pasteur, Unité de Recherche de Virologie Structurale, Paris, France.
Mattea RomaniUniversité Paris Descartes, INSERM UMRS-1007 CICB-Paris, Paris, France.
Dominique SimonInstitut Pasteur, Unité de Génétique Fonctionnelle de la Souris, Paris, France.
Guanfang TianUniversité Paris Descartes, INSERM UMRS-1007 CICB-Paris, Paris, France.
Florence NiedergangUniversité de Paris, Institut Cochin, INSERM, U1016, CNRS, UMR 8104, Paris, France.
Jean-Jacques PanthierInstitut Pasteur, Unité de Génétique Fonctionnelle de la Souris, Paris, France.
Marie FlamandInstitut Pasteur, Unité de Recherche de Virologie Structurale, Paris, France.
Sylvie SouèsUniversité Paris Descartes, INSERM UMRS-1007 CICB-Paris, Paris, France.
Eliette BonnefoyUniversité Paris Descartes, INSERM UMRS-1007 CICB-Paris, Paris, France eliette.bonnefoy@inserm.fr.ORCID 0000-0002-9534-2104
Délégation Paris 5 · FRInstitut Pasteur · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rift Valley fever virus (RVFV) is a highly pathogenic zoonotic arbovirus endemic in many African countries and the Arabian Peninsula. Animal infections cause high rates of mortality and abortion among sheep, goats, and cattle. In humans, an estimated 1 to 2% of RVFV infections result in severe disease (encephalitis, hepatitis, or retinitis) with a high rate of lethality when associated with hemorrhagic fever. The RVFV NSs protein, which is the main virulence factor, counteracts the host innate antiviral response to favor viral replication and spread. However, the mechanisms underlying RVFV-induced cytopathic effects and the role of NSs in these alterations remain for the most part unknown. In this work, we have analyzed the effects of NSs expression on the actin cytoskeleton while conducting infections with the NSs-expressing virulent (ZH548) and attenuated (MP12) strains of RVFV and the non-NSs-expressing avirulent (ZH548ΔNSs) strain, as well as after the ectopic expression of NSs. In macrophages, fibroblasts, and hepatocytes, NSs expression prevented the upregulation of Abl2 (a major regulator of the actin cytoskeleton) expression otherwise induced by avirulent infections and identified here as part of the antiviral response. The presence of NSs was also linked to an increased mobility of ZH548-infected cells compared to ZH548ΔNSs-infected fibroblasts and to strong changes in cell morphology in nonmigrating hepatocytes, with reduction of lamellipodia, cell spreading, and dissolution of adherens junctions reminiscent of the ZH548-induced cytopathic effects observed

Indexed as

Actin CytoskeletonAnimalsCell AdhesionCell LineCell MovementCell ShapeHost-Pathogen InteractionsImmunity, InnateMiceMutationProtein-Tyrosine KinasesRift Valley FeverRift Valley fever virusViral Nonstructural ProteinsVirulence FactorsVirus ReplicationARG tyrosine kinaseProtein-Tyrosine KinasesViral Nonstructural ProteinsVirulence FactorsAbl2actin cytoskeletoninnate antiviral responseRift Valley fever virus

Identifiers

PMID33087469
PMCPMC7737741
OpenAlexW3094171163

What OpenQuestion holds

Textmetadata
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.