This is Dr Been’s simpler take on this issue. I guess you are dissecting it further. I can detect your sarcasm at some points, but because this is all new learning for me I can’t appreciate what you’re implying fully and most of these diagrams need a longer explanation!
From other reading I gather the T cell responses and NK/ dendritic cells are more important for our surviving the virus, so does the extent to which antibodies vary really matter on a practical level, other than to produce pretty papers?
I’ve also just watched Dr Been’s video about the Wuhan body/Omicron spike manufactured virus and that implies that something in the Wuhan body is what causes severe disease. It’s a while since I read about the origins of Omicron, but (apart from it having suspiciously lots of non synonymous mutations ) I thought most of its mutations were in the spike relative to the rest of the virus?
Well, Drbeen seems to have merely done a "reporting the abstract" in this case. I watched his video while writing this post just to see if it pointed out any findings I had overlooked but it isn't really showing any of the findings at all. So, my main argument is that the assertions in the title and abstract about imprinting affecting evolution don't have any backing in the actual paper.
Agree, that antibody escape might not translate to reinfection or especially not to infection survival. T Cells will still recognize infected cells. The only argument for antibody escape mattering is that the virus seems to want to do it, implying a fitness benefit - but the rest is just assumptions as far as whether antibodies actually correlate to "immunity."
Thank you for the feedback about the visuals - I usually put a bit more annotations on than I did this time, for whatever reason.
RE Omicron, yes - there was a ton of activity outside of spike. In fact what's really amazing, and for some reason no one else has looked at it this way, is that comparing BA.1 and BA.2 shows that evolutionary pressure starts in the receptor binding domain but then changed to other areas after BA.1 and BA.2 split - https://unglossed.substack.com/p/omicron-origins-summary-spoiler . BA.2 especially has a lot of action in Orf1 (the polyprotein that basically makes the "virus factories" inside cells) including for synonymous mutations; whereas BA.1 went on to make a lot of mutations to the NTD "elbow" of the spike protein. So it might be the case that BA.2 already "repairs" whatever problems BA.1 introduced with the non-spike part of the genes. There never really was a final answer on whether BA.2 was more pathogenic than BA.1 in actual human infection...
No wonder they laugh at us. While we're looking at charts and tables, they're spraying us with something all over the world. Probably setting us up for weather catastrophe while everyone plays tiddlywinks.
https://youtu.be/MAnvEO4Ixjk
This is Dr Been’s simpler take on this issue. I guess you are dissecting it further. I can detect your sarcasm at some points, but because this is all new learning for me I can’t appreciate what you’re implying fully and most of these diagrams need a longer explanation!
From other reading I gather the T cell responses and NK/ dendritic cells are more important for our surviving the virus, so does the extent to which antibodies vary really matter on a practical level, other than to produce pretty papers?
I’ve also just watched Dr Been’s video about the Wuhan body/Omicron spike manufactured virus and that implies that something in the Wuhan body is what causes severe disease. It’s a while since I read about the origins of Omicron, but (apart from it having suspiciously lots of non synonymous mutations ) I thought most of its mutations were in the spike relative to the rest of the virus?
Well, Drbeen seems to have merely done a "reporting the abstract" in this case. I watched his video while writing this post just to see if it pointed out any findings I had overlooked but it isn't really showing any of the findings at all. So, my main argument is that the assertions in the title and abstract about imprinting affecting evolution don't have any backing in the actual paper.
Agree, that antibody escape might not translate to reinfection or especially not to infection survival. T Cells will still recognize infected cells. The only argument for antibody escape mattering is that the virus seems to want to do it, implying a fitness benefit - but the rest is just assumptions as far as whether antibodies actually correlate to "immunity."
Thank you for the feedback about the visuals - I usually put a bit more annotations on than I did this time, for whatever reason.
RE Omicron, yes - there was a ton of activity outside of spike. In fact what's really amazing, and for some reason no one else has looked at it this way, is that comparing BA.1 and BA.2 shows that evolutionary pressure starts in the receptor binding domain but then changed to other areas after BA.1 and BA.2 split - https://unglossed.substack.com/p/omicron-origins-summary-spoiler . BA.2 especially has a lot of action in Orf1 (the polyprotein that basically makes the "virus factories" inside cells) including for synonymous mutations; whereas BA.1 went on to make a lot of mutations to the NTD "elbow" of the spike protein. So it might be the case that BA.2 already "repairs" whatever problems BA.1 introduced with the non-spike part of the genes. There never really was a final answer on whether BA.2 was more pathogenic than BA.1 in actual human infection...
No wonder they laugh at us. While we're looking at charts and tables, they're spraying us with something all over the world. Probably setting us up for weather catastrophe while everyone plays tiddlywinks.