SARS-CoV-2及其细菌共同或超级感染协同触发COVID-19自身免疫性心脏病变
Robert Root-Bernstein1, Jack Huber1, Alison Ziehl1
1Department of Physiology, Michigan State University, East Lansing, MI 48824, USA.
International journal of molecular sciences
|August 12, 2023
概括
在COVID-19或疫苗接种后的自身免疫性心脏病可能源于SARS-CoV-2,细菌和心脏蛋白之间的分子模仿. 细菌疫苗接种和抗生素使用可以降低这种风险.
科学领域:
- 免疫学 免疫学 免疫学
- 心脏病学 心脏病学
- 传染性疾病 传染性疾病
背景情况:
- 在COVID-19和SARS-CoV-2疫苗接种后,自身免疫性心脏病 (AC) 越来越多地被认可,但其病因仍然不清楚.
- 研究病毒模仿,细菌模仿和共同感染的相互作用对于理解AC发育至关重要.
研究的目的:
- 探索病毒和细菌模仿在诱导COVID-19和SARS-CoV-2疫苗接种后自身免疫性心脏病的潜在作用.
- 阐明免疫反应的基础机制,针对心脏蛋白质.
主要方法:
- 包括BLAST和LALIGN在内的蛋白质组分析,以确定SARS-CoV-2,细菌蛋白和人类心脏蛋白之间的相似性.
- 与酶相关的免疫吸收试验 (ELISA) 用于验证抗体与心脏蛋白质的结合,使用针对SARS-CoV-2和相关细菌的多克隆抗体.
主要成果:
- SARS-CoV-2 呈现出与心脏蛋白质具有显著的蛋白质相似之处,与细菌如 *Streptococci*, *Staphylococci* 和 *Enterococci* 共有的蛋白质不同.
- ELISA证实了抗体与心脏蛋白质的高亲和结合,验证了对病毒和细菌触发物的模仿假设.
- 互补的心脏抗原 (例如,actin/myosin,collagen/laminin) 被不同的病毒和细菌抗体准,这表明一种双触发机制.
结论:
- 自免疫性心脏病可能是由SARS-CoV-2感染/接种疫苗和并发性细菌感染的组合引起的.
- 通过病毒和细菌抗体向分子互补的抗原,可能通过异型-抗异型相互作用,有助于AC病原体.
- 预防策略可能包括细菌疫苗接种 (* Streptococci * * Haemophilus *),在COVID-19患者中明智地使用抗生素,以及在接种疫苗之前对感染进行查.
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