在COVID-19的神经疾病期间,免疫格局和氧化还原失衡在COVID-19的神经疾病期间
Abhimanyu Thakur1, Vartika Sharma2, Sera Averbek3,4
1Centre for Regenerative Medicine and Health, Hong Kong Institute of Science and Innovation-CAS Limited, Hong Kong SAR, Hong Kong. abithakur1211@gmail.com.
Cell death & disease
|September 6, 2023
概括
严重急性呼吸道综合征冠状病毒2 (SARS-CoV-2) 可以通过各种机制影响中枢神经系统 (CNS),包括受体结合,免疫反应和氧化还原失衡,导致COVID-19患者的神经复杂症.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
背景情况:
- 冠状病毒疾病2019 (COVID-19),由严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2) 引起,主要是一种呼吸系统疾病.
- 在COVID-19患者中,神经系统并发症越来越多地被报告,这表明潜在的中枢神经系统 (CNS) 参与.
研究的目的:
- 审查SARS-CoV-2可能进入中枢神经系统的机制.
- 探索免疫反应和氧化还原失衡在COVID-19病原和神经表现中的作用.
- 突出生物信息学在理解COVID-19的神经影响方面的应用.
主要方法:
- 对调查SARS-CoV-2进入中枢神经系统的研究进行文献综述.
- 对COVID-19中免疫事件和氧化还原失衡研究的分析.
- 检查生物信息学方法应用于COVID-19的神经并发症.
主要成果:
- 在大脑细胞中确定了潜在的SARS-CoV-2进入受体 (ACE2,CD147,TMPRSS2,NRP1).
- 突出了免疫系统调节失调 (细胞因子风暴) 和氧化还原失衡 (线粒体功能障碍) 对神经炎症和组织损伤的贡献.
- 强调生物信息学在分析复杂相互作用和确定治疗点方面的实用性.
结论:
- SARS-CoV-2 可能通过各种细胞受体进入中枢神经系统.
- 神经炎症,免疫系统激活和氧化还原失衡是COVID-19神经复杂症的关键因素.
- 生物信息学为剖析SARS-CoV-2的神经影响提供了强大的工具.
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