Fig. 1.

Interaction between ACE2 and the viral spike protein leading to infection. Representation of the interaction of an inhibitory ligand on the interface between ACE2 and the viral spike protein. The epithelial cells at the infection site express the enzymes ACE2, ADAM-17 and TMPRSS2 on the outer surface. The SARS-CoV-2 virus spike protein binds to the ACE2 enzyme as the very first step of a potential invasion. If this occurs, then the proteases ADAM-17 or TMPRSS2 can cleave ACE2, and in the case of the latter, also cleave the spike protein leading to infection of the epithelial cells and beginning of the invasion [18]. A ligand that binds to the interface of the ACE2 protein and the viral spike protein can inhibit the interaction, reducing the chance of infection. Note that the ligands that bind to the interface are not necessarily inhibitors of ACE2 enzyme activity. ADAM-17, ADAM metallopeptidase domain 17; TMPRSS2, Transmembrane protease, serine 2.