Collegium Medicum, Jan Kochanowski University, Kielce, Poland.
Department of Infectious Diseases and Allergology, Jan Kochanowski University, Kielce, Poland.
J Med Virol. 2023 Jun;95(6):e28864. doi: 10.1002/jmv.28864.
Accumulating evidence shows that SARS-CoV-2 can potentially trigger autoimmune processes, which can be responsible for the long-term consequences of COVID-19. Therefore, this paper aims to review the autoantibodies reported in COVID-19 convalescents. Six main groups were distinguished: (i) autoantibodies against components of the immune system, (ii) autoantibodies against components of the cardiovascular system, (iii) thyroid autoantibodies, (iv) autoantibodies specific for rheumatoid diseases, (v) antibodies against G-protein coupled receptors, and (vi) other autoantibodies. The evidence reviewed here clearly highlights that SARS-CoV-2 infection may induce humoral autoimmune responses. However, the available studies share number of limitations, such as: (1) the sole presence of autoantibodies does not necessarily implicate the clinically-relevant risks, (2) functional investigations were rarely performed and it is often unknown whether observed autoantibodies are pathogenic, (3) the control seroprevalence, in healthy, noninfected individuals was often not reported; thus it is sometimes unknown whether the detected autoantibodies are the result of SARS-CoV-2 infection or the accidental post-COVID-19 detection, (4) the presence of autoantibodies was rarely correlated with symptoms of the post-COVID-19 syndrome, (5) the size of the studied groups were often small, (6) the studies focused predominantly on adult populations, (7) age- and sex-related differences in seroprevalence of autoantibodies were rarely explored, (8) genetic predispositions that may be involved in generation of autoantibodies during SARS-CoV-2 infections were not investigated, and (9) the autoimmune reactions following infection with SARS-CoV-2 variants that vary in the clinical course of infection remain unexplored. Further longitudinal studies are advocated to assess the link between identified autoantibodies and particular clinical outcomes in COVID-19 convalescents.
越来越多的证据表明，SARS-CoV-2 可能会引发自身免疫过程，这可能是 COVID-19 的长期后果的原因。因此，本文旨在综述 COVID-19 恢复期患者中报道的自身抗体。区分出以下 6 个主要组：（i）针对免疫系统成分的自身抗体，（ii）针对心血管系统成分的自身抗体，（iii）甲状腺自身抗体，（iv）针对类风湿病的自身抗体，（v）针对 G 蛋白偶联受体的抗体，和（vi）其他自身抗体。本文回顾的证据清楚地强调，SARS-CoV-2 感染可能会引起体液自身免疫反应。然而，现有的研究存在一些局限性，例如：（1）仅存在自身抗体并不一定意味着存在临床相关的风险，（2）很少进行功能研究，而且通常不知道观察到的自身抗体是否具有致病性，（3）在健康、未感染的个体中，通常未报告对照血清阳性率；因此，有时不清楚检测到的自身抗体是 SARS-CoV-2 感染的结果还是 COVID-19 后偶然的检测结果，（4）自身抗体的存在很少与 COVID-19 后综合征的症状相关，（5）研究组的规模通常较小，（6）研究主要集中在成年人群，（7）年龄和性别相关的自身抗体血清阳性率差异很少被探索，（8）很少研究可能涉及 SARS-CoV-2 感染期间产生自身抗体的遗传倾向，（9）SARS-CoV-2 变异体感染后引起的自身免疫反应仍未被探索。建议进行进一步的纵向研究，以评估 COVID-19 恢复期患者中鉴定出的自身抗体与特定临床结果之间的联系。
