Evidence map›Paper›PMID 26209680›Full record

ArticleThe Journal of infectious diseases2015

Loss of Interleukin 1 Receptor Antagonist Enhances Susceptibility to Ebola Virus Infection.

Lindsay Hill-Batorski, Peter Halfmann, Andrea Marzi, Tiago J S Lopes, Gabriele Neumann, Heinz Feldmann, Yoshihiro Kawaoka

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Murine Models of Secondary Cytokine Storm Syndromes.Advances in experimental medicine and biology · 2024
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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.

Lindsay Hill-BatorskiDepartment of Pathobiological Sciences, School of Veterinary Medicine, Influenza Research Institute, University of Wisconsin-Madison.
Peter HalfmannDepartment of Pathobiological Sciences, School of Veterinary Medicine, Influenza Research Institute, University of Wisconsin-Madison.
Andrea MarziLaboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana.
Tiago J S LopesDepartment of Pathobiological Sciences, School of Veterinary Medicine, Influenza Research Institute, University of Wisconsin-Madison Division of Virology, Department of Microbiology and Immunology, International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo.
Gabriele NeumannDepartment of Pathobiological Sciences, School of Veterinary Medicine, Influenza Research Institute, University of Wisconsin-Madison.
Heinz FeldmannLaboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana.
Yoshihiro KawaokaDepartment of Pathobiological Sciences, School of Veterinary Medicine, Influenza Research Institute, University of Wisconsin-Madison Division of Virology, Department of Microbiology and Immunology, International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama, Japan.
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Viral Hemorrhagic Fevers: Disease Modeling and TransmissionZIAAI001089 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI FELDMANN, HEINRICH · 2009 to 2025
$50.7M
Systems Biology Identifies Restriction Factors for West Nile VirusU19AI106772 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI LIVNY, MIRON · 2013 to 2017
$26.1M
Intramural NIH HHSNIAID NIH HHS 5 U19 AI106772-02NIAID NIH HHS U19 AI106772
6 · The paper itself

Abstract

The current outbreak of Ebola virus (EBOV) infection in West Africa is unprecedented, with nearly 26 000 confirmed cases and >10 000 deaths. Comprehensive data on the pathogenesis of EBOV infection are lacking; however, recent studies suggested that fatal EBOV infections are characterized by dysregulation of the innate immune response and a subsequent cytokine storm. Specifically, several studies suggested that hypersecretion of interleukin 1 receptor antagonist (IL-1Ra) correlates with lethal EBOV infections. To examine the significance of IL-1Ra in EBOV infections, we infected mice that lack the gene encoding IL-1Ra, Il1rn (IL-1RN-KO), and mice with wild-type Il1rn (IL-1RN-WT) with a mouse-adapted EBOV (MA-EBOV). Infected IL-1RN-KO mice lost more weight and had a lower survival rate than IL-1RN-WT mice infected with MA-EBOV. In addition, IL-1RN-KO mice infected with wild-type EBOV, which does not cause lethal infection in adult immunocompetent mice, such as C57BL/6 mice, experienced greater weight loss than IL-1RN-WT mice infected with wild-type EBOV. Further studies revealed that the levels of 6 cytokines in spleens-IL-1α, IL-1β, interleukin 12p40, interleukin 17, granulocyte colony-stimulating factor, and regulated on activation, normal T-cell expressed and secreted-were significantly different between IL-1RN-KO mice and IL-1RN-WT mice infected with MA-EBOV. Collectively, our data suggest that IL-1Ra may have a protective effect upon EBOV infection, likely by damping an overactive proinflammatory immune response.

Indexed as

Africa, WesternAnimalsCytokinesDisease SusceptibilityEbolavirusFemaleGranulocyte Colony-Stimulating FactorHemorrhagic Fever, EbolaInterleukin 1 Receptor Antagonist ProteinMiceMice, Inbred C57BLMice, KnockoutT-LymphocytesCytokinesGranulocyte Colony-Stimulating FactorIl1rn protein, mouseInterleukin 1 Receptor Antagonist ProteinEbola virusIL-1RaIl1rninterleukin 1 receptor antagonist

Identifiers

PMID26209680
PMCPMC4564555
OpenAlexW2100171821

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.