Evidence map›Paper›PMID 28240256›Full record

ArticleScientific reports2017

A comparison of host gene expression signatures associated with infection in vitro by the Makona and Ecran (Mayinga) variants of Ebola virus.

Andrew Bosworth, Stuart D Dowall, Isabel Garcia-Dorival, Natasha Y Rickett, Christine B Bruce, David A Matthews, Yongxiang Fang, Waleed Aljabr, John Kenny, Charlotte Nelson and 6 more

Abstract readComparative Study
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Ebola virus exploits host lncRNAbioRxiv : the preprint server for biology · 2026
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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

16 authors.

Andrew BosworthNational Infection Service, Public Health England, Porton Down, Salisbury, UK.
Stuart D DowallNational Infection Service, Public Health England, Porton Down, Salisbury, UK.
Isabel Garcia-DorivalInstitute of Infection and Global Health, University of Liverpool, UK.
Natasha Y RickettNational Institute of Health Research, Health Protection Research Unit in Emerging and Zoonotic Infections, Liverpool, UK.
Christine B BruceHigh Containment Microbiology, Public Health England, Porton Down, Salisbury, UK.
David A MatthewsSchool of Molecular and Cellular Medicine, University of Bristol, UK.
Yongxiang FangCentre for Genomics Research, University of Liverpool, UK.
Waleed AljabrInstitute of Infection and Global Health, University of Liverpool, UK.
John KennyCentre for Genomics Research, University of Liverpool, UK.
Charlotte NelsonCentre for Genomics Research, University of Liverpool, UK.
Thomas R LawsDefence Science and Technology Laboratory, Porton Down, UK.
E Diane WilliamsonDefence Science and Technology Laboratory, Porton Down, UK.
James P StewartInstitute of Infection and Global Health, University of Liverpool, UK.
Miles W CarrollNational Infection Service, Public Health England, Porton Down, Salisbury, UK.
Roger HewsonNational Infection Service, Public Health England, Porton Down, Salisbury, UK.
Julian A HiscoxNational Institute of Health Research, Health Protection Research Unit in Emerging and Zoonotic Infections, Liverpool, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Ebola virus (EBOV) variant Makona (which emerged in 2013) was the causative agent of the largest outbreak of Ebola Virus Disease recorded. Differences in virus-host interactions between viral variants have potential consequences for transmission, disease severity and mortality. A detailed profile of the cellular changes induced by the Makona variant compared with other Ebola virus variants was lacking. In this study, A549 cells, a human cell line with a robust innate response, were infected with the Makona variant or with the Ecran variant originating from the 1976 outbreak in Central Africa. The abundance of viral and cellular mRNA transcripts was profiled using RNASeq and differential gene expression analysis performed. Differences in effects of each virus on the expression of interferon-stimulated genes were also investigated in A549 NPro cells where the type 1 interferon response had been attenuated. Cellular transcriptomic changes were compared with those induced by human respiratory syncytial virus (HRSV), a virus with a similar genome organisation and replication strategy to EBOV. Pathway and gene ontology analysis revealed differential expression of functionally important genes; including genes involved in the inflammatory response, cell proliferation, leukocyte extravasation and cholesterol biosynthesis. Whilst there was overlap with HRSV, there was unique commonality to the EBOV variants.

Indexed as

Host-Pathogen InteractionsTranscriptomeA549 CellsEbolavirusGene Expression ProfilingHumansRespiratory Syncytial Virus, HumanSequence Analysis, RNA

Identifiers

PMID28240256
PMCPMC5327407

What OpenQuestion holds

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Registered trials

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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.