Underlying mechanisms of multi-organ manifestations and exacerbated inflammation in COVID-19 are yet to be delineated. The hypothesis of SARS-CoV-2 triggering autoimmunity is gaining attention and, in the present study, we have identified 28 human proteins harbouring regions homologous to SARS-CoV-2 peptides that could possibly be acting as autoantigens in COVID-19 patients displaying autoimmune conditions. Interestingly, these conserved regions are amongst the experimentally validated B cell epitopes of SARS-CoV-2 proteins. The reported human proteins have demonstrated presence of autoantibodies against them in typical autoimmune conditions which may explain the frequent occurrence of autoimmune conditions following SARS-CoV-2 infection. Moreover, the proposed autoantigens’ widespread tissue distribution is suggestive of their involvement in multi-organ manifestations via molecular mimicry. We opine that our report may aid in directing subsequent necessary antigen-specific studies, results of which would be of long-term relevance in management of extrapulmonary symptoms of COVID-19.

COVID-19 多器官表现和炎症加剧的潜在机制尚待阐明。SARS-CoV-2 引发自身免疫的假说越来越受到关注，在本研究中，我们已经确定了 28 种人类蛋白质含有与 SARS-CoV-2 肽同源的区域，这些蛋白质可能在表现出自身免疫的 COVID-19 患者中充当自身抗原状况。有趣的是，这些保守区域属于 SARS-CoV-2 蛋白经实验验证的 B 细胞表位。报道的人类蛋白质已证明在典型的自身免疫性疾病中存在针对它们的自身抗体，这可以解释 SARS-CoV-2 感染后自身免疫性疾病的频繁发生。而且，所提出的自身抗原广泛的组织分布表明它们通过分子模拟参与了多器官表现。我们认为，我们的报告可能有助于指导后续必要的抗原特异性研究，其结果将与 COVID-19 肺外症状的管理具有长期相关性。