Fig. 3.

Infection mechanism of COVID-19. When alveolar epithelium cells are invaded by SARS-CoV-2, the cells express the surface receptors ACE 2 and TMPRSS2, and the virus is recognized by innate immune receptors such as the endosomal RNA sensors TLR7/8, RIG-I, and MDA5. This TLR7/8 can detect viral RNA species created during viral replication, such as viral genomic RNA and dsRNA. While RIG-I and MDA5 are responsible for sensing cytoplasmic viral RNAs such as 5′-3’ RNA or dsRNA. This causes NF-κB and IRF3/7 to become activated, resulting in the generation of proinflammatory cytokines and type I interferons, respectively. Type I interferons are important in restricting viral multiplication, and their effect is exacerbated by the production of ISGs like RNAse L. IL-6, IP-10, MIP-1α, MIPIE and MCP1 are the major pro-inflammatory cytokines and chemokines. These proteins draw monocytes, macrophages, and T cells to the infection site, causing further inflammation and triggering a pro-inflammatory feedback loop. In the case of a faulty immune response (left side), this can lead to increase inflammatory immune cell trafficking in the lungs, generating an overproduction of pro-inflammatory cytokines, and eventually causing lung damage. The cytokine storm that results spreads to other organs, causing multi-organ damage