Evidence map›Paper›PMID 37365222›Full record

ArticleScientific reports2023

Longitudinal whole blood transcriptomic analysis characterizes neutrophil activation and interferon signaling in moderate and severe COVID-19.

Christian Prebensen, Yohan Lefol, Peder L Myhre, Torben Lüders, Christine Jonassen, Anita Blomfeldt, Torbjørn Omland, Hilde Nilsen, Jan-Erik Berdal

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  3. Early Fc-effector antibody signatures impact COVID-19 disease trajectory.medRxiv : the preprint server for health sciences · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Christian Prebensen *Department of Infectious Diseases, Oslo University Hospital, Kirkeveien 166, 0450, Oslo, Norway. christian.prebensen@medisin.uio.no.
Yohan Lefol *Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Peder L MyhreInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Torben LüdersInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Christine JonassenCenter for Laboratory Medicine, Østfold Hospital Trust, Grålum, Norway.
Anita BlomfeldtDepartment of Microbiology and Infection Control, Akershus University Hospital, Lørenskog, Norway.
Torbjørn OmlandInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Hilde NilsenInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Jan-Erik BerdalInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
University of Oslo · NOAkershus University Hospital · NOOslo University Hospital · NOØstfold Hospital Trust · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A maladaptive inflammatory response has been implicated in the pathogenesis of severe COVID-19. This study aimed to characterize the temporal dynamics of this response and investigate whether severe disease is associated with distinct gene expression patterns. We performed microarray analysis of serial whole blood RNA samples from 17 patients with severe COVID-19, 15 patients with moderate disease and 11 healthy controls. All study subjects were unvaccinated. We assessed whole blood gene expression patterns by differential gene expression analysis, gene set enrichment, two clustering methods and estimated relative leukocyte abundance using CIBERSORT. Neutrophils, platelets, cytokine signaling, and the coagulation system were activated in COVID-19, and this broad immune activation was more pronounced in severe vs. moderate disease. We observed two different trajectories of neutrophil-associated genes, indicating the emergence of a more immature neutrophil phenotype over time. Interferon-associated genes were strongly enriched in early COVID-19 before falling markedly, with modest severity-associated differences in trajectory. In conclusion, COVID-19 necessitating hospitalization is associated with a broad inflammatory response, which is more pronounced in severe disease. Our data suggest a progressively more immature circulating neutrophil phenotype over time. Interferon signaling is enriched in COVID-19 but does not seem to drive severe disease.

Indexed as

COVID-19Gene Expression ProfilingHumansInterferonsNeutrophil ActivationNeutrophilsTranscriptomeInterferons

Identifiers

PMID37365222
PMCPMC10293211
OpenAlexW4382139272

What OpenQuestion holds

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LicenceCC BY
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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.