Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), the cause of COVID-19 disease, has the potential to elicit autoimmunity because mimicry of human molecular chaperones by viral proteins. We compared viral proteins with human molecular chaperones, many of which are heat shock proteins, to determine if they share amino acid-sequence segments with immunogenic-antigenic potential, which can elicit cross-reactive antibodies and effector immune cells with the capacity to damage-destroy human cells by a mechanism of autoimmunity. We identified the chaperones that can putatively participate in molecular mimicry phenomena after SARS-CoV-2 infection, focusing on those for which endothelial cell plasma-cell membrane localization has already been demonstrated. We also postulate that post-translational modifications, induced by physical (shear) and chemical (metabolic) stress caused respectively by the risk factors hypertension and diabetes, might have a role in determining plasma-cell membrane localization and, in turn, autoimmune-induced endothelial damage.

中文翻译：

---

人类分子伴侣与 SARS-CoV-2 抗原表位共享，可能能够引发针对内皮细胞的自身免疫：分子拟态在 COVID-19 中的可能作用。

严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 是 COVID-19 疾病的病因，由于病毒蛋白模仿人类分子伴侣，因此有可能引发自身免疫。我们将病毒蛋白与人类分子伴侣（其中许多是热休克蛋白）进行比较，以确定它们是否共享具有免疫原性抗原潜力的氨基酸序列片段，这可以引发交叉反应抗体和效应免疫细胞，从而能够破坏-通过自身免疫机制破坏人体细胞。我们鉴定了可能参与 SARS-CoV-2 感染后分子拟态现象的分子伴侣，重点关注那些已证实内皮细胞浆细胞膜定位的分子伴侣。我们还假设，分别由高血压和糖尿病危险因素引起的物理（剪切）和化学（代谢）应激诱导的翻译后修饰可能在确定浆细胞膜定位方面发挥作用，进而在确定自身免疫诱导的过程中发挥作用。内皮损伤。