ACE2 and Furin--2 human proteins that are candidate targets for COVID-19 drug development

This is rather exciting.  We may finally have an answer why SARS-CoV2 was able to infect humans so effectively (due to evolution), and why we might have another target to prevent/mitigate infection.

First of all, SARS-CoV2 sticks to human cells because it binds ACE2 very well (10 times as well as SARS) and human lung and GI tract cells express a lot of ACE2.  

Second, this article explains that the closest precursor to SARS-CoV2, CoV ZXC21 was discovered in bats but did not have human pathogenicity, because the spike protein did not have a site that allowed furin (a common human enzyme) to cleave it.  Lots of viruses use furin to cleave their proteins which lead to pathogenicity: HIV, H5N1 influenza, Ebola, Zika, Yellow Fever, among others.

www.sciencedirect.com/…

For a great layman’s summary:

www.smh.com.au/…

So drugs that potentially block the ACE2 binding site of SARS-CoV2, and inhibit furin cleavage of the spike protein (either by binding to the cleavage site, or inhibit furin directly) will be developed and tested hopefully in the near future.   There are already chemical compounds that inhibit furin that are used for experiments—maybe one of them is suitable for human use.