Thank you for this excellent dissection of the new results. (BTW an "Omega" makes it into one of the paragraphs.)
SARS-CoV-2 is enigmatic in its response to apparent selection pressures. If removing the TMPRSS2 requirement could have "solved" the problem of how to spread in children all along, it's a wonder it didn't do so sooner. It's still unclear how much Omicron spreads in children but the age range certainly looks on the younger side. That it took two years to get around this barrier is a challenge for the theories that the vaccines are exerting much selection pressure.
Meanwhile, many of the mouse serial passage studies achieve huge gains in binding/infectivity after only a few passages. Evolution is mysterious. (I've reviewed the mouse origins study and compiled notes on the mouse serial passage experiments at https://unglossed.substack.com/p/mouse-party)
Thanks so much for this post! I should have looked this up while writing my post on Omicron. I really could have used that "endosomal pathway" paper to explain the change in viral transmission, as it really seems like that would be the best explanation for why Omicron doesn't seem to require both ACEII and the serine protease to the same extent as prior variants.
I do plan on writing about fluvoxamine in the future. I think you, as well as a few others, have provided plenty of information on Vitamin D3!
I'll make sure to reference this post when I create my "Omicron Anthology Series" to hammer down that fact on the endosomal pathway, including your remarks on syncytia formation.
Thank you for this excellent dissection of the new results. (BTW an "Omega" makes it into one of the paragraphs.)
SARS-CoV-2 is enigmatic in its response to apparent selection pressures. If removing the TMPRSS2 requirement could have "solved" the problem of how to spread in children all along, it's a wonder it didn't do so sooner. It's still unclear how much Omicron spreads in children but the age range certainly looks on the younger side. That it took two years to get around this barrier is a challenge for the theories that the vaccines are exerting much selection pressure.
Meanwhile, many of the mouse serial passage studies achieve huge gains in binding/infectivity after only a few passages. Evolution is mysterious. (I've reviewed the mouse origins study and compiled notes on the mouse serial passage experiments at https://unglossed.substack.com/p/mouse-party)
Thanks so much for this post! I should have looked this up while writing my post on Omicron. I really could have used that "endosomal pathway" paper to explain the change in viral transmission, as it really seems like that would be the best explanation for why Omicron doesn't seem to require both ACEII and the serine protease to the same extent as prior variants.
I do plan on writing about fluvoxamine in the future. I think you, as well as a few others, have provided plenty of information on Vitamin D3!
I'll make sure to reference this post when I create my "Omicron Anthology Series" to hammer down that fact on the endosomal pathway, including your remarks on syncytia formation.