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]
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.
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).
> However, using monkey and mouse models of SARS-CoV-2 infection, none of the in vitro infection-enhancing Abs enhanced SARS-CoV-2 virus replication or infectious virus in the lung in vivo. Three of 46 monkeys had lung pathology or bronchoalveolar lavage (BAL) cytokine levels greater than controls. However, repeat studies with dose ranges of in vitro enhancing Abs did not increase lung pathology. Thus, in vitro infection-enhancing RBD and NTD Abs controlled virus in vivo and was rarely associated with enhanced lung pathology. [1]
You're interjecting it because you want to talk about it because you're an antivaxxer.
It has no relevance outside of some narrow understanding of what happens during severe COVID itself and the mechanism behind why some people get very sick and most people do not.
And you're practicing sealioning acting like you're just innoccently interjecting.