Evidence map›Paper›PMID 42421497›Full record

ReviewEuropean cytokine network2026

Emerging viral infections: role of flavivirus NS1-mediated rewiring of PRR signaling.

Matteo Ferraresi, Giulia Pezzi, Silvia Beltrami, Giorgia Cianci, Gloria Maini, Alessia Liboni, Marcello Baroni, Daria Bortolotti, Giovanna Schiuma, Sabrina Rizzo and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in European cytokine network, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Matteo FerraresiDepartment of Environmental and Prevention Sciences, University of Ferrara, Ferrara, Italy.
Giulia PezziDepartment of Environmental and Prevention Sciences, University of Ferrara, Ferrara, Italy.
Silvia BeltramiDepartment of Environmental and Prevention Sciences, University of Ferrara, Ferrara, Italy.
Giorgia CianciDepartment of Environmental and Prevention Sciences, University of Ferrara, Ferrara, Italy.
Gloria MainiDepartment of Environmental and Prevention Sciences, University of Ferrara, Ferrara, Italy.
Alessia LiboniDepartment of Chemical, Pharmaceutical and Agricultural Sciences, University of Ferrara, Ferrara, Italy.
Marcello BaroniDepartment of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy.
Daria BortolottiDepartment of Environmental and Prevention Sciences, University of Ferrara, Ferrara, Italy.
Giovanna SchiumaDepartment of Environmental and Prevention Sciences, University of Ferrara, Ferrara, Italy.
Sabrina Rizzo *Department of Environmental and Prevention Sciences, University of Ferrara, Ferrara, Italy.
Giovanni Strazzabosco *Department of Environmental and Prevention Sciences, University of Ferrara, Ferrara, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Flaviviruses, including Dengue, West Nile, Zika, and Japanese encephalitis viruses, are arthropod-borne RNA viruses that pose an increasing global health threat. This review summarizes the role of nonstructural protein 1 (NS1), a multifunctional glycoprotein found in intracellular and secreted forms, as a key regulator of innate immunity. NS1 modulates several pattern recognition receptor pathways, including TLRs, RLRs, SR-B1-related mechanisms, and inflammasome platforms, thereby altering cytokine and interferon responses. Its effects are virus- and context-dependent. WNV NS1 inhibits TLR3/TRIF signaling, reducing IRF3 activation, type I interferon production, and interferon-stimulated gene expression. In contrast, DENV NS1 is linked to inflammatory signaling, particularly through TLR4. At the cytosolic level, NS1 from DENV, WNV, and ZIKV disrupts RIG-I/MDA5-MAVS signaling and weakens IFN-β induction. NS1 also affects inflammasome pathways: DENV promotes IL-1β release through a CD14-dependent mechanism, ZIKV suppresses cGAS-mediated antiviral signaling, and JEV promotes NLRP3 inflammasome assembly. Overall, NS1 selectively dampens interferon-mediated antiviral defenses while sustaining or enhancing inflammation, contributing to endothelial dysfunction, neuroinflammation, and severe disease.

Indexed as

FlavivirusFlavivirus InfectionsReceptors, Pattern RecognitionSignal TransductionViral Nonstructural ProteinsAnimalsHumansImmunity, InnateInflammasomesInnate Immunity RecognitionInflammasomesNS1 protein, FlavivirusReceptors, Pattern RecognitionViral Nonstructural Proteinsantiviral immunityFlavivirusinflammationnonstructural protein 1 (NS1)pattern recognition receptor (PRR) signaling modulation

Identifiers

PMID42421497

What OpenQuestion holds

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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.