Evidence map›Paper›PMID 28811340›Full record

ArticlemBio2017

Type III Interferon-Mediated Signaling Is Critical for Controlling Live Attenuated Yellow Fever Virus Infection

Florian Douam, Yentli E Soto Albrecht, Gabriela Hrebikova, Evita Sadimin, Christian Davidson, Sergei V Kotenko, Alexander Ploss

Open access · goldAbstract read
In one paragraph

Article in mBio, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
9.2field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 64 citations in OpenAlex.

  1. Powassan Virus NS5 Antagonizes TYK2-Mediated Immune Signaling Pathways.bioRxiv : the preprint server for biology · 2026
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  16. Synthetic Heterodimers of Type III Interferon Receptors Require TYK2 for STAT Activation.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023
    Article
  17. 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

7 authors at 2 institutions in 1 country.

Florian DouamDepartment of Molecular Biology, Princeton University, Princeton, New Jersey, USA.
Yentli E Soto AlbrechtDepartment of Molecular Biology, Princeton University, Princeton, New Jersey, USA.
Gabriela HrebikovaDepartment of Molecular Biology, Princeton University, Princeton, New Jersey, USA.
Evita SadiminDepartment of Pathology, Rutgers Cancer Institute of New Jersey, Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA.
Christian DavidsonDepartment of Pathology, Rutgers Cancer Institute of New Jersey, Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA.
Sergei V KotenkoDepartment of Microbiology, Biochemistry and Molecular Genetics, Center for Immunity and Inflammation, Cancer Institute of New Jersey, New Jersey Medical School, Rutgers Biomedical and Health Sciences, Newark, New Jersey, USA.
Alexander PlossDepartment of Molecular Biology, Princeton University, Princeton, New Jersey, USA aploss@princeton.edu.
Princeton University · USRutgers, The State University of New Jersey · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
Genetic Viral and Host Adaptations to Breach Species Barriers of HCVR01AI107301 · NIAID · PRINCETON UNIVERSITY · PI Thomas Pietschmann, Alexander Ploss · 2013 to 2026
$6.0M
Development of IFN-lambda3 for the Prevention and Treatment of Virus InfectionR01AI104669 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI DURBIN, JOAN E., KOTENKO, SERGEI V · 2013 to 2017
$5.9M
Impact of species-specific host responses on restriction of hepatotropic virusesR21AI117213 · NIAID · PRINCETON UNIVERSITY · PI PLOSS, ALEXANDER, SCHWARTZ, ROBERT E · 2015 to 2016
$471k
NCI NIH HHS P30 CA072720NIAID NIH HHS R01 AI104669NIAID NIH HHS R01 AI107301NIAID NIH HHS R21 AI117213
6 · The paper itself

Abstract

Yellow fever virus (YFV) is an arthropod-borne flavivirus, infecting ~200,000 people worldwide annually and causing about 30,000 deaths. The live attenuated vaccine strain, YFV-17D, has significantly contributed in controlling the global burden of yellow fever worldwide. However, the viral and host contributions to YFV-17D attenuation remain elusive. Type I interferon (IFN-α/β) signaling and type II interferon (IFN-γ) signaling have been shown to be mutually supportive in controlling YFV-17D infection despite distinct mechanisms of action in viral infection. However, it remains unclear how type III IFN (IFN-λ) integrates into this antiviral system. Here, we report that while wild-type (WT) and IFN-λ receptor knockout (λR

Indexed as

AnimalsBlood-Brain BarrierCytokinesDisease Models, AnimalImmunity, InnateInterferonsMiceReceptors, InterferonSignal TransductionVaccines, AttenuatedYellow FeverYellow Fever VaccineYellow fever virusCytokinesinterferon receptor, type IIInterferonsReceptors, InterferonVaccines, AttenuatedYellow Fever Vaccineflavivirusinnate immunityinterferonslive vector vaccinesyellow fever virus

Identifiers

PMID28811340
PMCPMC5559630
OpenAlexW2746402575

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.