[75dvtwin]

> while impairing ACE2 binding

It appears that COVID-19 can also enter cells (these would be immune cells that came to 'help') via so called Fc-pathway.

Therefore allow the virus to multiply even more

"... In addition to viral entry via ACE2, antibodies against coronavirus spike proteins (anti-spike-S-IgG) can induce antibody-dependent enhancement (ADE) of viral entry via type II Fcγ receptors. ..." [1]

[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406916/

[lamontcg]

That really has nothing to do with what I wrote, other than for you to write about ADE, which is not a practical issue for anyone to worry about with SARS-CoV-2:

https://www.science.org/content/blog-post/new-antibody-depen...

I can't flag you, but someone else really should since your followup is completely disingenuous.

[75dvtwin]

sorry, but your assessment of what is genuine vs disingenuous, is very disingenuous in itself.

Perhaps, it is time to relinquish the presumptions of moral superiority -- and just discuss technical details without the drama ...

I am saying that you wrote does not cover full spectrum of how the virus replicates, therefore your comment does illuminate the complexity that's present in interaction with our immune system. Which includes, according to the NIH paper I referenced, antibody-dependent-enhancement (ADE).