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. 2022 Aug 18;320:198897. doi: 10.1016/j.virusres.2022.198897

Fig. 2.

Fig 2

Schematic representation of clinical features associated with cytokine response in SARS-CoV-2 infections. 1. Coronavirus infects the cells of the lung. 2. Immune cells such as macrophages produce cytokines in response to the virus. 3. Cytokines attract more immune cells such as monocytes, neutrophils, eosinophils, and other white blood cells which produce more inflammatory cytokines, resulting in hyperinflammation that damages lung cells. 4. Damage can occur through fibrin formation. 5. Weakened blood vessels allow fluid to seep in to the lung cavities, leading to respiratory failure. The activated cytokines result in clinical features involving fever (IFN-γ, TNF-α, IL-1β, IL-6), disseminated intravascular coagulation (IFN-γ, TNF-α), decreased serum protein (IFN-γ), hyperlipidemia (TNF-α), acute phase protein (IL-1β, IL-6), liver damage (TNF-α, IL-18), hemodynamic instability (IFN-γ, TNF-α), acute kidney injury (IL-6), and anemia (IL-6). Thapsigargin, Paroxetine, Parthenolide, Sertraline, and Spiperone are ERS pathway inhibitors that reduce the production of multiple proinflammatory cytokines (Step 2).