Figure 1.

The activation of inflammation during SARS-CoV-2 infection. The virus enters the host cell by interacting with the ACE2 receptor and the cellular serine protease TMPRSS2 through its spike protein. ACE2 internalization weakens the anti-inflammatory ACE2/Ang-(17)/MAS receptor axis maintained by ACE2. At low SARS-CoV-2 viral load, cells do not initiate the interferon response; however, upregulation of Ang II stimulates its receptor AT1R and promotes the transcription of several inflammatory cytokine-related genes through proinflammatory pathways such as the NF-κB and MAPK signaling pathways. Proinflammatory cytokines activate and recruit a variety of immune cells to migrate to the site of infection, and the activated immune cells will secrete more inflammatory cytokines. In this stage, the inflammation leads to an increase in capillary permeability and consequent liquid exudation. PRR, pattern recognition receptor; PAMPs, Pathogen-associated molecular patterns; DAMPs, damage-associated molecular patterns.