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Review Article

SARS-CoV-2感染、炎症、免疫营养与COVID-19的发病机制

卷 30, 期 39, 2023

发表于: 16 May, 2023

页: [4390 - 4408] 页: 19

弟呕挨: 10.2174/0929867330666230330092725

价格: $65

摘要

由冠状病毒SARS-CoV-2引起的COVID-19大流行在过去两年中夺去了全球数百万人的生命。患有潜在心血管疾病、肺病和糖尿病的老年人死亡率尤其高。对作者的关键词进行文献计量学分析，搜索过去50年来各种冠状病毒研究之间可能存在的联系，并进行整合。我们发现免疫系统、免疫力、营养、营养不良、微量营养素、运动、炎症和过度炎症等关键词彼此高度相关。基于这些发现，我们假设人类免疫系统是一个多层次的超复杂系统，它采用多种策略来控制微生物感染和恢复体内平衡。研究还发现，免疫系统的行为不能用单一的免疫学理论来描述。然而，一种主要的策略是“自我毁灭和重建”，它由一系列炎症反应组成:1)受损/功能失调的体细胞主动自我毁灭;2)清除碎片和细胞;3)组织重建。因此，入侵微生物的清除可能只是对这一破坏-重建过程的被动旁观者反应。微生物感染可能是自我限制的，并作为微生物中存在的大量基因不可缺少的必需营养而促进。自毁细胞碎片降解导致的短暂性营养激增，再加上患者现有的营养状态，可能在COVID-19的发病机制中发挥重要作用。最后，讨论了几种可能缓解COVID-19的应对策略，包括疫苗接种。

关键词: COVID-19、细胞因子风暴、免疫、炎症反应、营养不良、吞噬、限制性饮食、自限性感染。

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