Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease.

Felicity Liew ; Claudia Efstathiou ORCID logo ; Sara Fontanella ; Matthew Richardson ; Ruth Saunders ; Dawid Swieboda ; Jasmin K Sidhu ; Stephanie Ascough ; Shona C Moore ORCID logo ; Noura Mohamed ; +41 more... Jose Nunag ORCID logo ; Clara King ; Olivia C Leavy ; Omer Elneima ; Hamish JC McAuley ; Aarti Shikotra ; Amisha Singapuri ORCID logo ; Marco Sereno ORCID logo ; Victoria C Harris ; Linzy Houchen-Wolloff ORCID logo ; Neil J Greening ORCID logo ; Nazir I Lone ORCID logo ; Matthew Thorpe ; AA Roger Thompson ORCID logo ; Sarah L Rowland-Jones ; Annemarie B Docherty ORCID logo ; James D Chalmers ; Ling-Pei Ho ORCID logo ; Alexander Horsley ORCID logo ; Betty Raman ; Krisnah Poinasamy ; Michael Marks ORCID logo ; Onn Min Kon ; Luke S Howard ORCID logo ; Daniel G Wootton ; Jennifer K Quint ; Thushan I de Silva ORCID logo ; Antonia Ho ; Christopher Chiu ORCID logo ; Ewen M Harrison ORCID logo ; William Greenhalf ; J Kenneth Baillie ORCID logo ; Malcolm G Semple ORCID logo ; Lance Turtle ; Rachael A Evans ORCID logo ; Louise V Wain ; Christopher Brightling ; Ryan S Thwaites ORCID logo ; Peter JM Openshaw ORCID logo ; PHOSP-COVID collaborative group ; ISARIC investigators ; (2024) Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease. Nature immunology, 25 (4). pp. 607-621. ISSN 1529-2908 DOI: 10.1038/s41590-024-01778-0
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One in ten severe acute respiratory syndrome coronavirus 2 infections result in prolonged symptoms termed long coronavirus disease (COVID), yet disease phenotypes and mechanisms are poorly understood1. Here we profiled 368 plasma proteins in 657 participants ≥3 months following hospitalization. Of these, 426 had at least one long COVID symptom and 233 had fully recovered. Elevated markers of myeloid inflammation and complement activation were associated with long COVID. IL-1R2, MATN2 and COLEC12 were associated with cardiorespiratory symptoms, fatigue and anxiety/depression; MATN2, CSF3 and C1QA were elevated in gastrointestinal symptoms and C1QA was elevated in cognitive impairment. Additional markers of alterations in nerve tissue repair (SPON-1 and NFASC) were elevated in those with cognitive impairment and SCG3, suggestive of brain-gut axis disturbance, was elevated in gastrointestinal symptoms. Severe acute respiratory syndrome coronavirus 2-specific immunoglobulin G (IgG) was persistently elevated in some individuals with long COVID, but virus was not detected in sputum. Analysis of inflammatory markers in nasal fluids showed no association with symptoms. Our study aimed to understand inflammatory processes that underlie long COVID and was not designed for biomarker discovery. Our findings suggest that specific inflammatory pathways related to tissue damage are implicated in subtypes of long COVID, which might be targeted in future therapeutic trials.


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