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

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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.