Multi-omics identify falling LRRC15 as a COVID-19 severity marker and persistent pro-thrombotic signals in convalescence

Jack S. Gisby, Norzawani B. Buang, Artemis Papadaki, Candice L. Clarke, Talat H. Malik, Nicholas Medjeral-Thomas, Damiola Pinheiro, Paige M. Mortimer, Shanice Lewis, Eleanor Sandhu, Stephen P. McAdoo, Maria F. Prendecki, Michelle Willicombe, Matthew C. Pickering, Marina Botto, David C. Thomas () and James E. Peters ()
Additional contact information
Jack S. Gisby: Imperial College London
Norzawani B. Buang: Imperial College London
Artemis Papadaki: Imperial College London
Candice L. Clarke: Imperial College London
Talat H. Malik: Imperial College London
Nicholas Medjeral-Thomas: Imperial College London
Damiola Pinheiro: Imperial College London
Paige M. Mortimer: Imperial College London
Shanice Lewis: Imperial College London
Eleanor Sandhu: Imperial College London
Stephen P. McAdoo: Imperial College London
Maria F. Prendecki: Imperial College London
Michelle Willicombe: Imperial College London
Matthew C. Pickering: Imperial College London
Marina Botto: Imperial College London
David C. Thomas: Imperial College London
James E. Peters: Imperial College London

Nature Communications, 2022, vol. 13, issue 1, 1-21

Abstract: Abstract Patients with end-stage kidney disease (ESKD) are at high risk of severe COVID-19. Here, we perform longitudinal blood sampling of ESKD haemodialysis patients with COVID-19, collecting samples pre-infection, serially during infection, and after clinical recovery. Using plasma proteomics, and RNA-sequencing and flow cytometry of immune cells, we identify transcriptomic and proteomic signatures of COVID-19 severity, and find distinct temporal molecular profiles in patients with severe disease. Supervised learning reveals that the plasma proteome is a superior indicator of clinical severity than the PBMC transcriptome. We show that a decreasing trajectory of plasma LRRC15, a proposed co-receptor for SARS-CoV-2, is associated with a more severe clinical course. We observe that two months after the acute infection, patients still display dysregulated gene expression related to vascular, platelet and coagulation pathways, including PF4 (platelet factor 4), which may explain the prolonged thrombotic risk following COVID-19.

Date: 2022
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DOI: 10.1038/s41467-022-35454-4

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