COVID-19 and Neurocognitive Disorders

Elizabeta B. Mukaetova-Ladinska; Golo Kronenberg; Ruma Raha-Chowdhury

Disclosures

Curr Opin Psychiatry. 2021;34(2):149-156. 

In This Article

Immune-mediated Injury and Role for Cytokines

Nervous system damage caused by viral infection may be mediated by the immune system.[22] The cytokine storm is due to the release of high levels of pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, tumour necrosis factor (TNF) and chemokines (CCL-2, CCL-3 and CCL-5) by respiratory epithelial and dendritic cells, and macrophages.[42] COVID-19 disease severity is characterized by increased IL-2, IL-7, granulocyte-colony stimulating factor, interferon-γ inducible protein 10, monocyte chemoattractant protein 1, macrophage inflammatory protein 1-α and hyperferritinimia. The release of IL-6 causes vascular leakage, activation of complement and coagulation cascade, suggesting that mortality in COVID-19 infection might be due to virally driven hyperinflammation.[43]

The persistence of COVID-19 infections and its ability to infect macrophages, microglia and astrocytes in the CNS are particularly important. A neurotropic virus can activate glial cells and induce a pro-inflammatory state.[44] IL-6, an important member of the cytokine storm, is positively correlated with the severity of COVID-19 symptoms.[43] In addition, experiments have confirmed that primary glial cells cultured in vitro secrete a large amount of inflammatory factors such as IL-6, IL-12, IL-15 and TNF-α after being infected with CoVs.[23] Furthermore, activation of immune cells in the brain will cause chronic inflammation and brain damage.

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