Evidence map›Paper›PMID 34338586›Full record

ArticleVirulence2021

Zika virus NS2A inhibits interferon signaling by degradation of STAT1 and STAT2.

Elisa Fanunza, Fabrizio Carletti, Marina Quartu, Nicole Grandi, Laura Ermellino, Jessica Milia, Angela Corona, Maria Rosaria Capobianchi, Giuseppe Ippolito, Enzo Tramontano

Open access · goldAbstract read
In one paragraph

Article in Virulence, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.7field-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

29 citing papers in PubMed, 38 citations in OpenAlex.

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  10. Functional Roles and Host Interactions ofPathogens (Basel, Switzerland) · 2025
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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 2 institutions in 1 country.

Elisa FanunzaDepartment of Life and Environmental Sciences, University of Cagliari, Monserrato, Italy.ORCID 0000-0002-2044-8473
Fabrizio CarlettiLaboratory of Virology, National Institute for Infectious Diseases, L.Spallanzani͟ IRCCS, Rome, Italy.
Marina QuartuDepartment of Biomedical Sciences, University of Cagliari, Monserrato, Italy.
Nicole GrandiDepartment of Life and Environmental Sciences, University of Cagliari, Monserrato, Italy.
Laura ErmellinoDepartment of Life and Environmental Sciences, University of Cagliari, Monserrato, Italy.
Jessica MiliaDepartment of Life and Environmental Sciences, University of Cagliari, Monserrato, Italy.
Angela CoronaDepartment of Life and Environmental Sciences, University of Cagliari, Monserrato, Italy.ORCID 0000-0002-6630-8636
Maria Rosaria CapobianchiLaboratory of Virology, National Institute for Infectious Diseases, L.Spallanzani͟ IRCCS, Rome, Italy.
Giuseppe IppolitoLaboratory of Virology, National Institute for Infectious Diseases, L.Spallanzani͟ IRCCS, Rome, Italy.
Enzo TramontanoDepartment of Life and Environmental Sciences, University of Cagliari, Monserrato, Italy.ORCID 0000-0002-4849-0980
University of Cagliari · ITIstituto Nazionale per le Malattie Infettive Lazzaro Spallanzani · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Interferon (IFN) response is crucial to restrain pathogenic infections. Investigations into flavivirus-host interactions reported that the high virulence is linked to innate immune evasion. Zika Virus (ZIKV) has developed diversified strategies to evade the innate immune system. We report that the viral protein NS2A counteracts the IFN response by strongly suppressing the IFN signaling. NS2A targets transcription factors STAT1 and STAT2, to impede their nuclear localization, thereby suppressing the transcription of ISRE promoter and IFN-stimulated genes. We found that NS2A promotes degradation of STAT1 and STAT2. Treatment of NS2A transfected cells with MG132 restores the levels of both transcription factors, suggesting the involvement of the proteasome system. Given the impact that the IFN antagonism has on flavivirus virulence, the knowledge gained by characterizing the mechanism through which ZIKV evades the IFN response paves the ground for new strategies to attenuate the pathogenesis and to develop countermeasures against effective pharmacological targets.

Indexed as

Immune EvasionSTAT1 Transcription FactorSTAT2 Transcription FactorViral Nonstructural ProteinsZika Virus InfectionHumansImmunity, InnateInterferonsZika VirusInterferonsSTAT1 protein, humanSTAT1 Transcription FactorSTAT2 protein, humanSTAT2 Transcription FactorViral Nonstructural ProteinsdegradationIfn evasionIfn signalinginterferonNs2aphosphorylationstat1stat2Zika virus

Identifiers

PMID34338586
PMCPMC8331042
OpenAlexW3191031280

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.