Evidence map›Paper›PMID 33193389›Full record

ArticleFrontiers in immunology2020

Zika Virus Inhibits IFN-α Response by Human Plasmacytoid Dendritic Cells and Induces NS1-Dependent Triggering of CD303 (BDCA-2) Signaling.

Sandra Bos, Béatrice Poirier-Beaudouin, Valérie Seffer, Maria Manich, Cartini Mardi, Philippe Desprès, Gilles Gadea, Marie-Lise Gougeon

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Virulence · 2025
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  7. Drugs to limit Zika virus infection and implication for maternal-fetal health.Frontiers in virology (Lausanne, Switzerland) · 2022
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  9. Review
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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 4 institutions in 2 countries.

Sandra BosInstitut Pasteur, Innate Immunity and Viruses Unit, Global Health Department, Paris, France.
Béatrice Poirier-BeaudouinInstitut Pasteur, Innate Immunity and Viruses Unit, Global Health Department, Paris, France.
Valérie SefferInstitut Pasteur, Innate Immunity and Viruses Unit, Global Health Department, Paris, France.
Maria ManichInstitut Pasteur, Biological Image Analysis Unit, Cell Biology and Infection Department, Paris, France.
Cartini MardiInstitut Pasteur, Innate Immunity and Viruses Unit, Global Health Department, Paris, France.
Philippe DesprèsUniversité de la Réunion, INSERM U1187, CNRS UMR 9192, IRD UMR 249, Unité Mixte Processus Infectieux en Milieu Insulaire Tropical, Plateforme Technologique CYROI, La Réunion, France.
Gilles GadeaUniversité de la Réunion, INSERM U1187, CNRS UMR 9192, IRD UMR 249, Unité Mixte Processus Infectieux en Milieu Insulaire Tropical, Plateforme Technologique CYROI, La Réunion, France.
Marie-Lise GougeonInstitut Pasteur, Innate Immunity and Viruses Unit, Global Health Department, Paris, France.
Immunité et Cancer · FRCentre National de la Recherche Scientifique · FRInstitut Pasteur · FRInstitut de Recherche pour le Développement · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zika virus (ZIKV) dramatically emerged in French Polynesia and subsequently in the Americas where it has been associated with severe neurological complications in adults and newborns, respectively. Although plasmacytoid dendritic cells (pDCs) are a key sensor of viral infection and are critical for initiating an antiviral response, little is known about the impact of ZIKV infection on pDCs. Here, we investigated the susceptibility of human pDCs to infection with multiple strains of ZIKV and further investigated the impact of infection on pDCs functions. We observed that pDCs were refractory to cell-free ZIKV virions but were effectively infected when co-cultured with ZIKV-infected cells. However, exposure of pDCs to ZIKV-infected cells resulted in limited maturation/activation with significant down regulation of CD303 expression, a severe impairment of inflammatory cytokine production, and an inability to mount an IFN-α response. We show that ZIKV developed a strategy to inhibit the IFN-α response in primary human pDCs likely mediated through NS1-dependent CD303 signaling, thus suggesting a new mechanism of immune evasion.

Indexed as

AnimalsCell LineChlorocebus aethiopsCytokinesDendritic CellsDown-RegulationHumansInflammationInterferon-alphaLectins, C-TypeMembrane GlycoproteinsReceptors, ImmunologicSignal TransductionVero CellsZika VirusZika Virus InfectionCLEC4C protein, humanCytokinesInterferon-alphaLectins, C-TypeMembrane GlycoproteinsReceptors, ImmunologicCD303IFN—interferonnon-structural protein 1 (NS1)plasmacytoid dendritic cells (pDC)Zika virus (ZIKV)

Identifiers

PMID33193389
PMCPMC7655658
OpenAlexW3096653538

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.