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)
Hi Brian, Thanks for your comment, for publicising this article on GETTR: https://gettr.com/post/pmwzxxfb2a and for finding the typo.
Your https://unglossed.substack.com looks most interesting. Unfortunately I can only read a fraction of what I would like to. Have you seen Modern Discontent's https://moderndiscontent.substack.com? He/she writes thoughtful, well researched, analysis on highly pertinent health, biochemical and social matters.
There are surely going to be further variants, but I think they will face a tough time out-competing Omicron unless they strongly escape the infection-acquired immunity from Omicron, which I think most of us are likely to acquire by the middle of this year.
Zahradnik et al. (published in early 202o, see: https://vitamindstopscovid.info/#zahradnik) drove evolution of the spike protein's RBD (Receptor Binding Domain) in yeast and discovered mutations in actual SARS-CoV-2 variants and other combinations of mutations which apparently increased the physical binding attraction to ~~640 times that of the early 2020 variant's RBD.
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)
Hi Brian, Thanks for your comment, for publicising this article on GETTR: https://gettr.com/post/pmwzxxfb2a and for finding the typo.
Your https://unglossed.substack.com looks most interesting. Unfortunately I can only read a fraction of what I would like to. Have you seen Modern Discontent's https://moderndiscontent.substack.com? He/she writes thoughtful, well researched, analysis on highly pertinent health, biochemical and social matters.
There are surely going to be further variants, but I think they will face a tough time out-competing Omicron unless they strongly escape the infection-acquired immunity from Omicron, which I think most of us are likely to acquire by the middle of this year.
Zahradnik et al. (published in early 202o, see: https://vitamindstopscovid.info/#zahradnik) drove evolution of the spike protein's RBD (Receptor Binding Domain) in yeast and discovered mutations in actual SARS-CoV-2 variants and other combinations of mutations which apparently increased the physical binding attraction to ~~640 times that of the early 2020 variant's RBD.
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.