#syncytia — Public Fediverse posts

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

Multifaceted #activation of #STING axis upon #Nipah and #measles virus-induced #syncytia formation https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1012569

These results contribute to improve our understanding about NiV and MeV immunopathogenesis and provide potential paths for alternative therapeutic strategies.

#SARS-CoV-2 #Variants from Long-Term, Persistently Infected Immunocompromised Patients Have Altered #Syncytia Formation, Temperature-Dependent Replication, & Serum Neutralizing #Antibody #Escape, Viruses: https://www.mdpi.com/1999-4915/16/9/1436

Isolates from an individual who never mounted an antibody response despite administration of convalescent plasma showed slight reductions in plaque size & some showed temperature-dependent replication attenuation...