Brain immune response to SARS-CoV-2 infection Brain ImmuneResponse SARSCoV2 Coronavirus Disease COVID Neurology WUSTLmed ElsevierNews
Neuroinflammation and COVID-19. Image Credit: DOERS / Shutterstock
Evidence suggests that SARS-CoV-2 infection triggers cytokine release in the cerebrospinal fluid, which subsequently can impair normal brain activities. Cytokines can also directly target different neural cells to alter brain activities. By targeting neural stem cells, cytokines can reduce neurogenesis and cause learning and memory deficits. Similarly, cytokines can target neurons and astrocytes to trigger glutamate excitotoxicity.
Blood-brain barrier It is well-established that neurological symptoms in COVID-19 are associated with cerebral vascular dysfunction. The most common features are brain hemorrhage and ischemia. In addition, abnormal cerebral blood flow and frontoparietal hypometabolism have been observed in COVID-19 patients. All these changes are suggestive of disrupted BBB. Studies conducted on COVID-19 animal models have indicated that SARS-CoV-2 infection increases BBB permeability.
Post-mortem analysis of COVID-19 brain tissue has shown the increased formation of string vessels and vascular endothelial cell death. Specific viral proteins, including the main protease and spike protein, have been identified as potent inducers of string vessel formation. SARS-CoV-2 spike protein that enters the brain through disrupted BBB is recognized by the microglia, leading to activation of the brain's innate immune system and sustained induction of inflammatory response.
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