Fig. 5.

Pathophysiology orchestrated by SARS-CoV-2.

Type II pneumocytes infected with SARS-CoV 2 trigger the release of cytokines, chemokines and interferons. The secreted inflammatory mediators recruit macrophages, neutrophils and activated T cells. The stimulated macrophages secrete IL-1, IL-6 and TNF-α. This increases capillary permeability, causing plasma to leak into the interstitial space and the alveolus. The stimulated neutrophils release reactive oxygen species and proteinases, which destroy infected cells. The cell debris and the plasma combine to form a protein-rich fluid. The increasing fluid leads to dyspnoea and pneumonia. It also dilutes the surfactant lining of the alveolus causing alveolar collapse, which leads to hypoxaemia and acute respiratory distress syndrome. The sustained inflammation leads to systemic inflammatory response syndrome, which develops into septic shock causing multi-organ failure and death.