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To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1-11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely.

Original publication

DOI

10.1038/s41467-023-42320-4

Type

Journal article

Journal

Nature communications

Publication Date

12/2023

Volume

14

Addresses

Clinical Infection, Microbiology, and Immunology, Institute of Infection, Veterinary and Ecological Sciences, University of Liverpool, Liverpool, L69 7BE, UK. benmic@liverpool.ac.uk.

Keywords

ISARIC4C Investigators, COVID-CNS Consortium, Humans, Brain Injuries, Glial Fibrillary Acidic Protein, Inflammation Mediators, Autoantibodies, Cytokines, Follow-Up Studies, Biomarkers, COVID-19, COVID-19 Serotherapy