SARS-CoV-2、疫苗尖峰蛋白、肾素-血管紧张素系统与癫痫之间的关系。

Ziad Fajloun, Layla Tajer, Hervé Kovacic, Jean-Marc Sabatier
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摘要

在 COVID-19 大流行和引入基于略微改良的 SARS-CoV-2 尖峰蛋白的疫苗接种后,出现了多种并发症和疾病。其中一种疾病是癫痫,功能失调的 RAS 在这种疾病的传播中起着至关重要的作用。SARS-CoV-2 利用血管紧张素转换酶 2 型(ACE2)受体感染宿主细胞,从而使病毒感染各种类型的细胞,包括肺、鼻咽、肾、淋巴结、小肠、胃、脾和大脑中的细胞,导致广泛的器官损伤。一旦 SARS-CoV-2 与 ACE2 受体结合,就会导致 ACE/Ang II/AT1R 轴过度激活。因此,较高水平的 Ang II 会激活促进炎症的几种有害途径,导致体内的炎症反应,并加重癫痫发作等病症。此外,SARS-CoV-2 或疫苗斯派克蛋白抑制 ACE2 导致的 Ang II 过量对 AT1R 的兴奋作用,也可能在癫痫发病机制中发挥进一步的作用。
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The Relationship among SARS-CoV-2, Vaccine Spike Protein, Renin- Angiotensin System, and Epilepsy.

Several comorbidities and illnesses have emerged after the COVID-19 pandemic and the introduction of vaccination based on a slightly modified SARS-CoV-2 spike protein. One of these diseases is epilepsy, where the dysfunctional RAS plays a crucial role in the propagation of the disorder. SARS-CoV-2 infects host cells by utilizing the angiotensin-converting enzyme Type 2 (ACE2) receptor, which allows the virus to infect various cell types, including those in the lungs, nasopharynx, kidneys, lymph nodes, small intestine, stomach, spleen, and brain, leading to widespread organ damage. Once SARS-CoV-2 binds to the ACE2 receptor, it can lead to the overactivation of the ACE/Ang II/AT1R axis. Consequently, higher levels of Ang II activate several deleterious pathways that promote inflammation, contributing to inflammatory responses in the body and exacerbating conditions such as seizures. Additionally, the excitatory effect of AT1R by Ang II excess due to ACE2 inhibition by SARS-CoV-2 or by the vaccine Spike protein may play a further role in the mechanism contributing to epilepsy.

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