Autoimmunity in long COVID
File(s)
Published version
Author(s)
Talwar, Shubha
Harker, James
Openshaw, Peter
Thwaites, Ryan
Type
Journal Article
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.
Date Issued
2025-04-03
Date Acceptance
2025-02-07
Citation
Journal of Allergy and Clinical Immunology, 2025, 155 (4), pp.1082-1094
ISSN
0091-6749
Publisher
Elsevier
Start Page
1082
End Page
1094
Journal / Book Title
Journal of Allergy and Clinical Immunology
Volume
155
Issue
4
Copyright Statement
© 2025 The Authors. Published by Elsevier Inc. on behalf of the American Academy of Allergy, Asthma & Immunology. This is an open access article under the CC BY li- cense (http://creativecommons.org/licenses/by/4.0/)
License URL
Identifier
10.1016/j.jaci.2025.02.005
Subjects
Long COVID
autoimmunity
B-cell dysregulation
autoantibodies
Publication Status
Published
Date Publish Online
2025-02-14