Abstract
Multiple studies have investigated the role of blood circulating proteins in COVID-19 disease using the Olink affinity proteomics platform. However, study inclusion criteria and sample collection conditions varied between studies, leading to sometimes incongruent associations. To identify the most robust protein markers of the disease and the underlying pathways that are relevant under all conditions, it is essential to identify proteins that replicate most widely. Here we combined the Olink proteomics profiles of two newly recruited COVID-19 studies (N=68 and N=98) with those of three previously published COVID-19 studies (N=383, N=83, N=57). For these studies, three Olink panels (Inflammation and Cardiovascular II & III) with 253 unique proteins were compared. Case/control analysis revealed thirteen proteins (CCL16, CCL7, CXCL10, CCL8, LGALS9, CXCL11, IL1RN, CCL2, CD274, IL6, IL18, MERTK, IFNγ, and IL18R1) that were differentially expressed in COVID-19 patients in all five studies. Except CCL16, which was higher in controls, all proteins were overexpressed in COVID-19 patients. Pathway analysis revealed concordant trends across all studies with pathways related to cytokine-cytokine interaction, IL18 signaling, fluid shear stress and rheumatoid arthritis. Our results reaffirm previous findings related to a COVID-19 cytokine storm syndrome. Cross-study robustness of COVID-19 specific protein expression profiles support the utility of affinity proteomics as a tool and for the identification of potential therapeutic targets.
Highlights
The recent COVID-19 pandemic has brought global socio-economic activity to a halt and devastated major health-care systems all over the world
The ICU cohort is composed of 43 patients who met criteria for acute respiratory distress syndrome (ARDS) as defined by the Berlin definition [18] and tested positive for SARS-CoV-2 by RT-PCR, while 25 nonsepsis ICU patients served as controls
The GIM cohort was comprised of 48 patients with confirmed SARS-CoV-2 RT-PCR, and 50 non-COVID-19 controls with negative RT-PCR results who were hospitalized at the New York-Presbyterian Hospital/Weill Cornell Medical Center between March and April 2020
Summary
The recent COVID-19 pandemic has brought global socio-economic activity to a halt and devastated major health-care systems all over the world. COVID-19 manifests as an asymptomatic or a mild respiratory tract infection [1]. The disease may exacerbate to severe pneumonia or acute respiratory distress syndrome (ARDS) in some individuals, COVID-19 Olink Replication Study especially in those with high age, obesity, diabetes, and other underlying comorbidities. A cytokine storm syndrome has been associated with a large portion of the mortality in patients hospitalized with COVID-19 [2]. WHO has recently announced a fourth wave of virus outbreaks, this time involving the delta version of the virus, which pushed some countries that had lifted and re-imposed restrictions. The virus shares a close genetic resemblance with SARS-CoV and Middle East Respiratory Syndrome (MERS), the infectious agent that caused the 2002 SARS and 2012 MERS epidemics, respectively [6]
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