Immune-mediated pathogenesis and development of autoimmunity in neurological manifestations of COVID-19

神经系统症状在COVID-19中很常见。基于我们之前的工作，我们假设部分COVID-19的急性、亚急性和感染后神经系统症状和并发症可以用SARS-CoV-2感染引发的过度病毒介导的炎症和自身免疫反应来解释。为了证实这一假设，需要对主诉神经症状的患者进行全面的临床描述。在脑脊液或血液中检测中枢和外周神经系统定向的自身抗体可能支持这一假设，并为进一步的免疫表型分析提供生物样本。HLA分型、细胞因子谱的评估以及血液和脑脊液中免疫细胞的细胞组成将提供更深入的见解，从而将病毒介导的炎症损伤与“真正的”自身免疫区分开来。与之前的外周评估相比，CSF分析将有助于更好地了解中枢神经系统炎症反应，并可能在COVID-19中产生新的生物标志物和临床相关治疗靶点。

Neurological symptoms are frequent in COVID-19. Based on our previous work, we hypothesize that a proportion of acute, subacute and post-infectious neurological symptoms and complications of COVID-19 can be explained by excessive viral-mediated inflammation and autoimmune reactions triggered by the infection with SARS-CoV-2. To confirm this hypothesis, thorough clinical characterization of patients complaining of neurological symptoms is needed. Detection of central and peripheral nervous system directed autoantibodies in CSF or blood may support this hypothesis and provide biosamples for further immune phenotyping. HLA typing, assessment of the cytokine profile, and the cellular composition of immune cells in blood and CSF will provide deeper insights, allowing to separate viral-mediated inflammatory damage from “true” autoimmunity. CSF analysis will contribute to a better understanding of CNS inflammatory reactions compared to previous assessments in the periphery, and could result in novel biomarkers and clinically relevant treatment targets in COVID-19.