Arévalo-Cortés Andrea, Rodriguez-Pinto Daniel, Aguilar-Ayala Leonardo
Faculty of Human Health Universidad Nacional de Loja, Loja 110103, Ecuador.
Department of Health Sciences Faculty of Health Sciences Universidad Técnica Particular de Loja, Loja 110108, Ecuador.
Autoimmune Dis. 2024 Aug 31;2024:8359683. doi: 10.1155/2024/8359683. eCollection 2024.
As for other viral diseases, the mechanisms behind the apparent relationship between COVID-19 and autoimmunity are yet to be clearly defined. Molecular mimicry, the existence of sequence and/or conformational homology between viral and human antigens, could be an important contributing factor. Here, we review the accumulated evidence supporting the occurrence of mimicry between SARS-CoV-2 and human proteins. Both bioinformatic approaches and antibody cross-reactions have yielded a significant magnitude of mimicry events, far more common than expected to happen by chance. The clinical implication of this phenomenon is ample since many of the identified antigens may participate in COVID-19 pathophysiology or are targets of autoimmune diseases. Thus, autoimmunity related to COVID-19 may be partially explained by molecular mimicry and further research designed specifically to address this possibility is needed.
至于其他病毒性疾病,新冠病毒与自身免疫之间明显关联背后的机制尚未明确界定。分子模拟,即病毒抗原与人类抗原之间存在序列和/或构象同源性,可能是一个重要的促成因素。在此,我们回顾支持新型冠状病毒与人类蛋白质之间存在模拟现象的累积证据。生物信息学方法和抗体交叉反应均已产生大量的模拟事件,其频繁程度远超偶然发生的预期。由于许多已确定的抗原可能参与新冠病毒的病理生理过程或为自身免疫性疾病的靶点,这一现象的临床意义十分重大。因此,与新冠病毒相关的自身免疫可能部分由分子模拟来解释,需要专门针对这一可能性开展进一步研究。