Fig. 2.

Possible mechanism of action of SARS-COV-2. Depiction of the binding of SARS-COV-2 to its receptor ACE-2. The S1 and S2 subunits are subsequently cleaved followed by the shedding of ACE-2 by ADAM 17. This resulting in an increased amount of Angiotensin II leading to respiratory distress. Upon binding, the virus fuses with the membrane and enters the cell, followed by translation, and replication of the proteins. ORF3a, ORF8b,E proteins and the NF-KB pathway activates the inflammasome pathway through various means, leading to the activation of cytokine. This results in a cytokine storm, further resulting in respiratory distress.