SARS-CoV-2 与人类抗原之间的分子模拟证据:对 COVID-19 自身免疫的影响。

IF 1.7 Q4 IMMUNOLOGY
Autoimmune Diseases Pub Date : 2024-08-31 eCollection Date: 2024-01-01 DOI:10.1155/2024/8359683
Andrea Arévalo-Cortés, Daniel Rodriguez-Pinto, Leonardo Aguilar-Ayala
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引用次数: 0

摘要

至于其他病毒性疾病,COVID-19 与自身免疫之间的明显关系背后的机制尚待明确界定。分子拟态,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,我们回顾了支持 SARS-CoV-2 与人类蛋白质之间存在拟态的累积证据。通过生物信息学方法和抗体交叉反应,我们发现了大量的拟态事件,其普遍性远远超出了偶然发生的预期。这一现象的临床意义十分重大,因为许多已鉴定的抗原可能参与了 COVID-19 的病理生理学,或者是自身免疫性疾病的靶标。因此,与 COVID-19 相关的自身免疫性疾病可能可以部分地通过分子模拟来解释,因此需要进一步开展专门针对这种可能性的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Evidence for Molecular Mimicry between SARS-CoV-2 and Human Antigens: Implications for Autoimmunity in COVID-19.

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.

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来源期刊
Autoimmune Diseases
Autoimmune Diseases IMMUNOLOGY-
CiteScore
6.10
自引率
0.00%
发文量
9
审稿时长
17 weeks
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