COVID-19 as a Trigger of Brain Autoimmunity
Mayuri Gupta, Donald F. Weaver
Abstract
Entry of SARS-CoV-2 into the central nervous system (CNS) activates microglia, triggering chronic neuroinflammation and possibly neurodegeneration. The complex transcriptome of SARS-CoV-2 shares molecular similarities with diverse human CNS protein epitopes, leading to a cytokine storm and various autoantibodies, potentially culminating in an autoimmune state. A COVID-19 initiated CNS autoimmune cascade may occur via multiple pathways including molecular mimicry, bystander activation, epitope spreading, production of autoantibodies, and immortalization of effector B-cells.
Topics & Concepts
NeuroinflammationNeurodegenerationMolecular mimicryAutoantibodyAutoimmunityEpitopeBiologyBystander effectNeuroscienceImmunologyMicrogliaEffectorMultiple sclerosisNeuromyelitis opticaImmune systemInflammationMedicineAntibodyDiseasePathologyLong-Term Effects of COVID-19SARS-CoV-2 and COVID-19 ResearchCOVID-19 Clinical Research Studies