Fig. 5.

Pathophysiology of SARS-CoV-2 systemic infection. Infection initiates in the upper respiratory tract and progresses to lower regions of the lung in severe cases. Respiratory droplets carrying SARS-CoV-2 infect epithelial and endothelial cells, neurons, microglia, and lung macrophages containing angiotensin-converting enzyme 2 (ACE-2). Viral replication and release of damage-associated molecular patterns induce pyroptosis, causing a dysfunctional innate immune response. Release of pro-inflammatory agents can induce a cytokine storm, increasing vasodilation, capillary permeability, and hypoxemia that can often lead to multiple organ failure