@article{Liew_F-2024_171687,
title = {Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease},
author = {Liew, F. and Efstathiou, C. and Fontanella, S. and Richardson, M. and Saunders, R. and Swieboda, D. and Sidhu, J. and Ascough, S. and Moore, S. and Mohamed, N. and Nunag, J. and King, C. and Leavy, O. and Elneima, O. and McAuley, H. and Shikotra, A. and Singapuri, A. and Sereno, M. and Harris, V. and Houchen-Wollof, L. and Greening, N. and Lone, N. and Thorpe, M. and Thompson, A. and Rowland-Jones, S. and Docherty, A. and Chalmers, J. and Ho, L. and Horsley, A. and Raman, B. and Poinasamy, K. and Marks, M. and Kon, O. and Howard, L. and Wootton, D. and Quint, J. and de Silva, T. and Ho, A. and Chiu, C. and Harrison, E. and Greenhalf, W. and Baillie, J. and Semple, M. and Turtle, L. and Evans, R. and Wain, L. and Brightling, C. and Thwaites, R. and Openshaw, P. and The PHOSP-COVID Collaborative Group and ISARIC Investigators},
month = {apr},
year = {2024},
abstract = {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.},
pages = {607-621},
volume = {25},
journal = {Nature Immunology},
publisher = {Springer Nature},
url = {https://doi.org/10.1038/s41590-024-01778-0},
}
