Evidence map›Paper›PMID 36741372›Full record

ArticleFrontiers in immunology2022

Blood transcriptome responses in patients correlate with severity of COVID-19 disease.

Ya Wang, Klaus Schughart, Tiana Maria Pelaia, Tracy Chew, Karan Kim, Thomas Karvunidis, Ben Knippenberg, Sally Teoh, Amy L Phu, Kirsty R Short and 9 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.5field-weighted citation impact, top 5% 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, 23 citations in OpenAlex.

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  11. Targeting PRMT7-mediated monomethylation of MAVS enhances antiviral innate immune responses and inhibits RNA virus replication.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Upregulation of inflammatory genes and pathways links obesity to severe COVID-19.Biochimica et biophysica acta. Molecular basis of disease · 2024
    Article
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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

19 authors at 11 institutions in 4 countries.

Ya WangDepartment of Intensive Care Medicine, Nepean Hospital, Penrith, NSW, Australia.
Klaus SchughartDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
Tiana Maria PelaiaDepartment of Intensive Care Medicine, Nepean Hospital, Penrith, NSW, Australia.
Tracy ChewSydney Informatics Hub, Core Research Facilities, The University of Sydney, Sydney, NSW, Australia.
Karan KimCentre for Immunology and Allergy Research, The Westmead Institute for Medical Research, Westmead, NSW, Australia.
Thomas KarvunidisMedical ICU, 1st Department of Internal Medicine, Charles University and Teaching Hospital, Pilsen, Czechia.
Ben KnippenbergDepartment of Microbiology. St George Hospital, Kogarah, NSW, Australia.
Sally TeohDepartment of Intensive Care Medicine, Nepean Hospital, Penrith, NSW, Australia.
Amy L PhuResearch and Education Network, Western Sydney Local Health District, Westmead Hospital, NSW, Westmead, Australia.
Kirsty R ShortSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.
Jonathan IredellCentre for Infectious Diseases and Microbiology, The Westmead Institute for Medical Research, Westmead, NSW, Australia.
Irani ThevarajanVictorian Infectious Disease Service, The Royal Melbourne Hospital at the Peter Doherty Institute for Infection and Immunity, Melbourne, VIC, Australia.
Jennifer AudsleyVictorian Infectious Disease Service, The Royal Melbourne Hospital at the Peter Doherty Institute for Infection and Immunity, Melbourne, VIC, Australia.
Stephen MacdonaldCentre for Clinical Research in Emergency Medicine, Harry Perkins Institute of Medical Research, Royal Perth Hospital, Perth, WA, Australia.
Jonathon BurchamCentre for Clinical Research in Emergency Medicine, Royal Perth Bentley Group, Perth, WA, Australia.
Anthony McLeanDepartment of Intensive Care Medicine, Nepean Hospital, Penrith, NSW, Australia.
PREDICT-19 consortium
Benjamin TangDepartment of Intensive Care Medicine, Nepean Hospital, Penrith, NSW, Australia.
Maryam ShojaeiDepartment of Intensive Care Medicine, Nepean Hospital, Penrith, NSW, Australia.
Westmead Institute for Medical Research · AUNepean Hospital · AUWestmead Hospital · AUCharles University · CZHarry Perkins Institute of Medical Research · AUSt George Hospital · AUThe Royal Melbourne Hospital · AUThe University of Melbourne · AUThe University of Queensland · AUThe University of Sydney · AUUniversity of Münster · DE

Funding

Unlocking Zika Virus Immune Control and Pathogenesis with the Collaborative CrossU19AI100625 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MCWEENEY, SHANNON K. · 2012 to 2021
$36.6M
NIAID NIH HHS U19 AI100625
6 · The paper itself

Abstract

Background: Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Infected individuals display a wide spectrum of disease severity, as defined by the World Health Organization (WHO). One of the main factors underlying this heterogeneity is the host immune response, with severe COVID-19 often associated with a hyperinflammatory state. Aim: Our current study aimed to pinpoint the specific genes and pathways underlying differences in the disease spectrum and outcomes observed, through in-depth analyses of whole blood transcriptomics in a large cohort of COVID-19 participants. Results: All WHO severity levels were well represented and mild and severe disease displaying distinct gene expression profiles. WHO severity levels 1-4 were grouped as mild disease, and signatures from these participants were different from those with WHO severity levels 6-9 classified as severe disease. Severity level 5 (moderate cases) presented a unique transitional gene signature between severity levels 2-4 (mild/moderate) and 6-9 (severe) and hence might represent the turning point for better or worse disease outcome. Gene expression changes are very distinct when comparing mild/moderate or severe cases to healthy controls. In particular, we demonstrated the hallmark down-regulation of adaptive immune response pathways and activation of neutrophil pathways in severe compared to mild/moderate cases, as well as activation of blood coagulation pathways. Conclusions: Our data revealed discrete gene signatures associated with mild, moderate, and severe COVID-19 identifying valuable candidates for future biomarker discovery.

Indexed as

COVID-19Gene Expression ProfilingHumansNeutrophilsSARS-CoV-2Transcriptomedeconvolutionhost immune responseRNA sequencingSARS-CoV-2WGCNA

Identifiers

PMID36741372
PMCPMC9896980
OpenAlexW4317738256

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.