Figure 1.

Proposed maladaptive hyperinflammatory response to SARS-CoV-2 infection

SARS-CoV-2 enters target host cells by interacting through its spike subunit with ACE2, after being primed by TMPRSS2. The virus induces cell damage through direct cytotoxic effects and after newly formed virions are released by exocytosis into the extracellular compartment. In addition, a dysregulated immune response eventually leads to the recruitment and activation of macrophages and neutrophils, with the release of cytokines, chemokines, and other inflammatory mediators determining hyperinflammation. At the same time, activation of the complement system and excessive cytokine production activate endothelial cells and disrupt vascular integrity leading to microthrombi deposition and microvascular dysfunction.