Journal
MEDICAL SCIENCE MONITOR
Volume 27, Issue -, Pages -Publisher
INT SCIENTIFIC INFORMATION, INC
DOI: 10.12659/MSM.933015
Keywords
Editorial; Central Nervous System; Inflammation Mediators; Neuropsychiatry; Mitochondria; Microglia; Severe Acute Respiratory Syndrome Coronavirus 2; COVID-19; Cognitive Dysfunction
Categories
Ask authors/readers for more resources
Patients recovering from acute COVID-19 infection may experience persistent comorbidities related to the central nervous system, possibly involving mitochondria, microglia, and ongoing neuroinflammation. This hypothesis suggests long-term effects on cognitive functioning and immune processes within the CNS.
Persistent comorbidities occur in patients who initially recover from acute coronavirus disease 2019 (COVID-19) due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). 'Long COVID' involves the central nervous system (CNS), resulting in neuropsychiatric symptoms and signs, including cognitive impairment or `brain fog' and chronic fatigue syndrome. There are similarities in these persistent complications between SARS-CoV-2 and the Ebola, Zika, and influenza A viruses. Normal CNS neuronal mitochondrial function requires high oxygen levels for oxidative phosphorylation and ATP production. Recent studies have shown that the SARS-CoV-2 virus can hijack mitochondrial function. Persistent changes in cognitive functioning have also been reported with other viral infections. SARS-CoV-2 infection may result in long-term effects on immune processes within the CNS by causing microglial dysfunction. This short opinion aims to discuss the hypothesis that the pathogenesis of long-term neuropsychiatric COVID-19 involves microglia, mitochondria, and persistent neuroinflammation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available