Elevated antiviral, myeloid and endothelial inflammatory markers in severe COVID-19

Thwaites, Ryan ORCID: 0000-0003-3052-2793, Sevilla Uruchurtu, Ashley Sanchez, Siggins, Matthew, Liew, Felicity ORCID: 0000-0002-8736-9198, Russell, Clark ORCID: 0000-0002-9873-8243, Moore, Shona ORCID: 0000-0001-8610-2806, Carter, Edwin, Abrams, Simon, Short, Charlotte-Eve ORCID: 0000-0002-4974-8824, Thaventhiran, Thilipan
et al (show 14 more authors) (2020) Elevated antiviral, myeloid and endothelial inflammatory markers in severe COVID-19. MedRxiv. 2020.10.08.20209411-.

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<h4>Introductory paragraph</h4> The mechanisms that underpin COVID-19 disease severity, and determine the outcome of infection, are only beginning to be unraveled. The host inflammatory response contributes to lung injury, but circulating mediators levels fall below those in classical ‘cytokine storms’. We analyzed serial plasma samples from 619 patients hospitalized with COVID-19 recruited through the prospective multicenter ISARIC clinical characterization protocol U.K. study and 39 milder community cases not requiring hospitalization. Elevated levels of numerous mediators including angiopoietin-2, CXCL10, and GM-CSF were seen at recruitment in patients who later died. Markers of endothelial injury (angiopoietin-2 and von-Willebrand factor A2) were detected early in some patients, while inflammatory cytokines and markers of lung injury persisted for several weeks in fatal COVID-19 despite decreasing antiviral cytokine levels. Overall, markers of myeloid or endothelial cell activation were associated with severe, progressive, and fatal disease indicating a central role for innate immune activation and vascular inflammation in COVID-19.

Item Type: Article
Uncontrolled Keywords: Rare Diseases, Lung, 2.1 Biological and endogenous factors, 2 Aetiology, Inflammatory and immune system, 3 Good Health and Well Being
Depositing User: Symplectic Admin
Date Deposited: 08 Jan 2021 15:09
Last Modified: 09 May 2024 18:59
DOI: 10.1101/2020.10.08.20209411
Open Access URL:
Related URLs:
URI: https://livrepository.liverpool.ac.uk/id/eprint/3112060