In this section
@article{Talwar:2025:10.1016/j.jaci.2025.02.005,
author = {Talwar, S and Harker, J and Openshaw, P and Thwaites, R},
doi = {10.1016/j.jaci.2025.02.005},
journal = {Journal of Allergy and Clinical Immunology},
pages = {1082--1094},
title = {Autoimmunity in long COVID},
url = {http://dx.doi.org/10.1016/j.jaci.2025.02.005},
volume = {155},
year = {2025}
}
TY - JOUR
AB - 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.
AU - Talwar,S
AU - Harker,J
AU - Openshaw,P
AU - Thwaites,R
DO - 10.1016/j.jaci.2025.02.005
EP - 1094
PY - 2025///
SN - 0091-6749
SP - 1082
TI - Autoimmunity in long COVID
T2 - Journal of Allergy and Clinical Immunology
UR - http://dx.doi.org/10.1016/j.jaci.2025.02.005
VL - 155
ER -
