Autoimmunity, SARS-CoV-2 Infections, and Neurological Disorders

August 5, 2022

Patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) present with a wide range of symptoms, from none at all to new neurological and neuropsychiatric syndromes. New evidence suggests that an autoimmune response to the SARS-CoV-2 virus is responsible for neurological disorders in some COVID-19 patients. A 2022 review by Dr. Daniela Latorre from the Institute of Microbiology in Zurich, Switzerland, explains the “current knowledge of immune responses occurring in Neuro-COVID patients” and the potential mechanisms for developing neurological complications alongside SARS-CoV-2 infection. 

Neuro-COVID refers to the range of neurological conditions in COVID-19 patients from loss of taste, headache, and fatigue to encephalitis, stroke, and polyneuropathies. In order to understand the causes of Neuro-COVID development, the cerebrospinal fluid (CSF) of patients was tested. CSF is the fluid surrounding the brain and spinal cord, the central nervous system (CNS). It was found that the cerebrospinal fluid had higher levels of specific biomarkers in Neuro-COVID patients with CNS diseases, suggesting the SARS-CoV-2 virus infected the CNS. It is still unknown whether this occurs due to a direct viral invasion of the neurons or an indirect effect of “immune-related mechanisms”.

COVID-19 infection has often been linked to a “cytokine storm,” where the patient’s immune system becomes hyperactivated, causing greater disease severity. The immune system releases large amounts of proinflammatory cytokines, which have been associated with neurological complications in other diseases. The CSF of Neuro-COVID patients in various studies was found to have high levels of these cytokines, supporting the argument that neurological manifestations of COVID-19 are immune-related. 

Some COVID-19 patients developed autoantibodies, often targeting white blood cell, or lymphocyte, function. Further, some patients developed many autoantibodies targeting antigens in the CNS. The paper hypothesizes that among a subclass of COVID-19 patients, autoantibodies develop as part of a humoral immune response, interfering with normal neurological function, which causes complications in Neuro-COVID disorders. On the other hand, it is emphasized that little research has been done on T lymphocyte behavior in Neuro-COVID patients, which makes up 80% of the CFS. 

This review states that the mechanisms behind the immune response in Neuro-COVID patients are likely a combination of molecular mimicry, bystander activation, and epitope spreading. These mechanisms cause the immune response to a foreign antigen to become elevated and to attack the body’s antigens. Still, the author underscores the need for further immunological studies of Neuro-COVID patients and those with Long COVID syndrome in order to fully understand how neurological conditions arise from the SARS-CoV-2 virus and to develop therapeutic treatment options.  





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