Evidence map›Paper›PMID 24102579›Full record

ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2014

Ebola virus-like particles stimulate type I interferons and proinflammatory cytokine expression through the toll-like receptor and interferon signaling pathways.

Natarajan Ayithan, Steven B Bradfute, Scott M Anthony, Kelly S Stuthman, John M Dye, Sina Bavari, Mike Bray, Keiko Ozato

Open access · greenAbstract read
In one paragraph

Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. BATF2 enhances proinflammatory cytokine responses in macrophages and improves early host defense against pulmonaryAmerican journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  4. Regulation and functions of the NLRP3 inflammasome in RNA virus infection.Frontiers in cellular and infection microbiology · 2023
    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 1 institution in 1 country.

Natarajan Ayithan1 Program in Genomics of Differentiation, National Institute of Child Health and Human Development , National Institutes of Health, Bethesda, Maryland.
Steven B Bradfute
Scott M Anthony
Kelly S Stuthman
John M Dye
Sina Bavari
Mike Bray
Keiko Ozato
United States Army Medical Research Institute of Infectious Diseases · US

Funding

Gene Regulation In The Immune SystemZIAHD001310 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI OZATO, KEIKO · 2009 to 2025
$15.0M
Intramural NIH HHS
6 · The paper itself

Abstract

Ebola viruses (EBOV) can cause severe hemorrhagic disease with high case fatality rates. Currently, no vaccines or therapeutics are approved for use in humans. Ebola virus-like particles (eVLP) comprising of virus protein (VP40), glycoprotein, and nucleoprotein protect rodents and nonhuman primates from lethal EBOV infection, representing as a candidate vaccine for EBOV infection. Previous reports have shown that eVLP stimulate the expression of proinflammatory cytokines in dendritic cells (DCs) and macrophages (MΦs) in vitro. However, the molecular mechanisms and signaling pathways through which eVLP induce innate immune responses remain obscure. In this study, we show that eVLP stimulate not only the expression of proinflammatory cytokines but also the expression of type I interferons (IFNs) and IFN-stimulated genes (ISGs) in murine bone marrow-derived DCs (BMDCs) and MΦs. Our data indicate that eVLP trigger host responses through toll-like receptor (TLR) pathway utilizing 2 distinct adaptors, MyD88 and TRIF. More interestingly, eVLP activated the IFN signaling pathway by inducing a set of potent antiviral ISGs. Last, eVLP and synthetic adjuvants, Poly I:C and CpG DNA, cooperatively increased the expression of cytokines and ISGs. Further supporting this synergy, eVLP when administered together with Poly I:C conferred mice enhanced protection against EBOV infection. These results indicate that eVLP stimulate early innate immune responses through TLR and type I IFN signaling pathways to protect the host from EBOV infection.

Indexed as

Vaccines, Virus-Like ParticleAdaptor Proteins, Vesicular TransportAnimalsCells, CulturedCytokinesDendritic CellsEbolavirusHemorrhagic Fever, EbolaHumansImmunity, InnateInflammation MediatorsInterferon Type IMacrophagesMiceMice, Inbred BALB CMice, Inbred C57BLAdaptor Proteins, Vesicular TransportCytokinesIfnar1 protein, mouseInflammation MediatorsInterferon Type IMyeloid Differentiation Factor 88Poly I-CReceptor, Interferon alpha-betaTicam1 protein, mouseToll-Like ReceptorsVaccines, Virus-Like Particle

Identifiers

PMID24102579
PMCPMC3924795
OpenAlexW1998424117

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.