Autoimmunity in long COVID
- PMID: 39956285
- DOI: 10.1016/j.jaci.2025.02.005
Autoimmunity in long COVID
Abstract
Long COVID (also termed postacute sequelae of SARS-CoV-2, or PASC) affects up to 10% of people recovering from infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Diagnosis is hampered by diffuse symptomatology, lack of biomarkers, incomplete understanding of pathogenesis, and lack of validated treatments. In terms of pathogenesis, hypothesized causes include virus persistence, the legacy of endotheliitis and thrombosis, low-grade tissue-based inflammation and/or scarring, perturbation of the host virome/microbiome, or triggering of autoimmunity. Several studies show preexisting and/or de novo production of autoantibodies after infection with SARS-CoV-2, but the persistence of these antibodies and their role in causing long COVID is debated. Here, we review the mechanisms through which autoimmune responses can arise during and after viral infection, focusing on the evidence for B-cell dysregulation and autoantibody production in acute and long COVID.
Keywords: B-cell dysregulation; Long COVID; autoantibodies; autoimmunity.
Copyright © 2025 The Authors. Published by Elsevier Inc. All rights reserved.
Conflict of interest statement
Disclosure statement This research was co-funded by the NIHR Imperial Biomedical Research Centre (BRC), an Imperial College Presidents Scholarship (to S.T.), the NIHR health protection research unit (HPRU) in respiratory infections at Imperial College and the UK Coronavirus Immunology Consortium (UK-CIC). Disclosure of potential conflict of interest: The authors declare that they have no relevant conflicts of interest.
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