Evidence map›Paper›PMID 32555213›Full record

ArticleScientific reports2020

Epstein-Barr virus reactivation in sepsis due to community-acquired pneumonia is associated with increased morbidity and an immunosuppressed host transcriptomic endotype.

Cyndi Goh, Katie L Burnham, M Azim Ansari, Mariateresa de Cesare, Tanya Golubchik, Paula Hutton, Lauren E Overend, Emma E Davenport, Charles J Hinds, Rory Bowden and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

24 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. The Current Status ofPathogens (Basel, Switzerland) · 2026
    Article
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  10. Observational
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  15. Observational
  16. Review
  17. Open forum infectious diseases · 2023
    Article
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  19. Article
  20. Review
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

11 authors at 6 institutions in 1 country.

Cyndi GohWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Katie L BurnhamWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, UK.
M Azim AnsariWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Mariateresa de CesareWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Tanya GolubchikWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Paula HuttonAdult Intensive Care Unit, Oxford University Hospitals NHS Foundation Trust, Oxford, UK.
Lauren E OverendWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Emma E DavenportWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, UK.
Charles J HindsWilliam Harvey Research Institute, Barts and The London School of Medicine, Queen Mary University, London, UK.
Rory BowdenWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Julian C KnightWellcome Centre for Human Genetics, University of Oxford, Oxford, UK. julian@well.ox.ac.uk.
University of Oxford · GBCentre for Human Genetics · GBOpen Data Institute · GBWellcome Sanger Institute · GBOxford University Hospitals NHS Trust · GBWilliam Harvey Research Institute · GB

Funding

Medical Research Council MR/M018725/1Wellcome TrustWellcome Trust 090532/Z/09/ZWellcome Trust 204969/Z/16/Z
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) reactivation is common in sepsis patients but the extent and nature of this remains unresolved. We sought to determine the incidence and correlates of EBV-positivity in a large sepsis cohort. We also hypothesised that EBV reactivation would be increased in patients in whom relative immunosuppression was the major feature of their sepsis response. To identify such patients we aimed to use knowledge of sepsis response subphenotypes based on transcriptomic studies of circulating leukocytes, specifically patients with a Sepsis Response Signature endotype (SRS1) that we have previously shown to be associated with increased mortality and features of immunosuppression. We assayed EBV from the plasma of intensive care unit (ICU) patients with sepsis due to community-acquired pneumonia. In total 730 patients were evaluated by targeted metagenomics (n = 573 patients), digital droplet PCR (n = 565), or both (n = 408). We had previously analysed gene expression in peripheral blood leukocytes for a subset of individuals (n = 390). We observed a 37% incidence of EBV-positivity. EBV reactivation was associated with longer ICU stay (12.9 vs 9.2 days; p = 0.004) and increased organ failure (day 1 SOFA score 6.9 vs 5.9; p = 0.00011). EBV reactivation was associated with the relatively immunosuppressed SRS1 endotype (p = 0.014) and differential expression of a small number of biologically relevant genes. These findings are consistent with the hypothesis that viral reactivation in sepsis is a consequence of immune compromise and is associated with increasing severity of illness although further mechanistic studies are required to definitively illustrate cause and effect.

Indexed as

Immunocompromised HostTranscriptomeVirus ActivationAdolescentAdultAgedCommunity-Acquired InfectionsFemaleHerpesvirus 4, HumanHumansIntensive Care UnitsLength of StayMaleMetagenomicsMiddle AgedPneumonia

Identifiers

PMID32555213
PMCPMC7299986
OpenAlexW3035801559

What OpenQuestion holds

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LicenceCC BY
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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.