I have been worrying about this for days but don't have the spoons to dig in:

BA.3.2 lost its ability to bind tightly to ACE-2 receptors on cells [1]

Remember that Long COVID rates were much higher during Delta? Remember that Delta was much more prone to syncytia (not needing ACE2 at all) in part because it had reduced ACE-2 affinity?

syncytia formation via the highly fusogenic Delta spike promotes cellular senescence and extracellular cytokine release [2]

and I know I read (skimmed) a paper suggesting that this method of direct contact cell-cell transmission was driving Long COVID - aha here:

We propose the hypothesis that SARS-CoV-2 transitions to persistent infection, facilitated by syncytia formation [3]

[1] https://archive.md/HWOHt#selection-3205.38-3205.105
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC10785701/
[3] https://pubmed.ncbi.nlm.nih.gov/40535019/

#COVID #COVID19 #SARSCoV2 #CovidIsNotOver #BA32 #syncytia #syncytial