Rainy Saturday and SARS-CoV Binding.

It is raining on and off here this afternoon, so I have been delving a little into the SARS literature. Below is a model highlighting {I think} where the spike glycoprotein is changed in the various variants. The ACE2 is the human lung receptor{brown spirally thing}, the three variants on the top right-hand side change close to where the virus protein binds to the human lung at the receptor binding domain {RBD}.

Below is the near molecular detail of how SARS-CoV and SARS-CoV-2 bind to the receptor {the green spirally thing}. The mechanism between the two viruses looks quite different with what looks like hydrogen bonding in the more recent virus.

How strong these bonds are along with the ease of conformational change will affect the virus binding {and release} rate constants. It must bind to replicate and must release at some stage in order to spread via coughing etc..

I wondered has anybody tried making a compound that preferentially binds to the ACE2 site in competition to the virus. Seems like a strategy for treating the disease. Add a high concentration of the ACE2 site blocker and outcompete the virus. If only a few hydrogen bonds enable the virus to bind it might be possible to design an antagonist molecule that is not toxic.