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Blood transcriptome responses in patients correlate with severity of COVID-19 disease
Y. Wang, K. Schughart, TM. Pelaia, T. Chew, K. Kim, T. Karvunidis, B. Knippenberg, S. Teoh, AL. Phu, KR. Short, J. Iredell, I. Thevarajan, J. Audsley, S. Macdonald, J. Burcham, A. McLean, PREDICT-19 consortium, B. Tang, M. Shojaei
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
U19 AI100625
NIAID NIH HHS - United States
NLK
Directory of Open Access Journals
od 2010
Free Medical Journals
od 2010
PubMed Central
od 2010
Europe PubMed Central
od 2010
Open Access Digital Library
od 2010-01-01
Open Access Digital Library
od 2010-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2010
- MeSH
- COVID-19 * genetika MeSH
- lidé MeSH
- neutrofily MeSH
- SARS-CoV-2 MeSH
- stanovení celkové genové exprese MeSH
- transkriptom MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
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.
Centre for Clinical Research in Emergency Medicine Royal Perth Bentley Group Perth WA Australia
Department of Intensive Care Medicine Nepean Hospital Penrith NSW Australia
Department of Microbiology St George Hospital Kogarah NSW Australia
Emergency Department Royal Perth Hospital Perth WA Australia
Institute of Molecular Virology University of Münster Münster Germany
Medical School University of Western Australia Perth WA Australia
School of Chemistry and Molecular Biosciences The University of Queensland Brisbane QLD Australia
Sydney Informatics Hub Core Research Facilities The University of Sydney Sydney NSW Australia
Sydney Institute for Infectious Disease The University of Sydney Sydney NSW Australia
Westmead Hospital Western Sydney Local Health District Westmead NSW Australia
Citace poskytuje Crossref.org
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