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

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 thi...

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Detalles Bibliográficos
Autores principales: Wang, Ya, Schughart, Klaus, Pelaia, Tiana Maria, Chew, Tracy, Kim, Karan, Karvunidis, Thomas, Knippenberg, Ben, Teoh, Sally, Phu, Amy L., Short, Kirsty R., Iredell, Jonathan, Thevarajan, Irani, Audsley, Jennifer, Macdonald, Stephen, Burcham, Jonathon, McLean, Anthony, Tang, Benjamin, Shojaei, Maryam
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9896980/
https://www.ncbi.nlm.nih.gov/pubmed/36741372
http://dx.doi.org/10.3389/fimmu.2022.1043219
Descripción
Sumario: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.