Figure 1.

Schematic depiction of SARS-CoV-2 binding to the ACE-2 receptor in airway epithelium with the nose being the first portal of entry. This may be followed in more severe cases by subsequent involvement of the lung with development of pneumonitis and adult respiratory distress syndrome (ARDS), a need for invasive ventilation, and ultimately death. In tandem, there is a cytokine-mediated systemic hyperinflammatory and hypercoagulopathic state. It is postulated that intranasal corticosteroids might attenuate disease progression by preventing epithelial cell entry via ACE-2, suppressing local cytokine release, and inhibiting viral replication (mometasone furoate and ciclesonide). TNF-α, Tumor necrosis factor-alpha.