Replies to post #145610 on NanoViricides Inc. (NNVC)

[KMBJN]

From that biospace article:

The strong effectiveness of nanoviricide drug candidates in this model is consistent with the effectiveness observed in cell culture studies against infection of both hCoV-NL63, which was used in this study, and hCoV-229E, another circulating coronavirus that uses a distinctly different receptor, namely APN.

CoVs NL63 SARS1 and SARS2 use primarily ACE2 for cellular entry.

CoV 229E uses APN.

CoV MERS uses DPP4.

How can a virus (229E) that has S1 spike protein peptides that bind to APN for cellular entry be blocked by a nanoviricide NV-CoV-2 that mimics ACE2?

I guess some of the 229E S1 has some conserved elements that still bind to ACE2 even though that is not how it enters cells.

I find that odd. If 229E S1 binds to NV-CoV-2 ACE2 mimic ligand to be destroyed by it, why doesn't it still bind to ACE2 to enter cells?

From your excellent paper:

Second, subtle structural changes in viral RBDs can lead to a complete receptor switch.

A virus can mutate away from a certain receptor to switch to a different receptor - but I think that would take quite a while (evolution / natural selection).