Time you took your own advice mate. No building stands on rotten foundations - period. Not running away, just facing a truth based in reality. PCR is a great lab research tool, not a clinical diagnosis whatever Drosten claimed 9and made a bundle of money from).
You have as many ways to say "I simply refuse to consider changing my mind on PCR, even though I lecture others to do the same" as the eskimos do for "snow."
Are you not the one doing the preaching. I am looking and listening and yet I see only claims built on claims with your arguments in favour of PCR based 'tests' for a poorly defined if not artificially created part of a claimed genetic code. Support your claim not with yet more claims - with evidence of the claim fails.
Go back to December 14. Look at your reply to my reply. Do you address a single point I make? No. You just retreat into Army training camp myths. You are not debating, you are tantruming.
If the foundation of the claim is false, ALL ARE FALSE that stand on that foundation. IT IS THAT simple. Basic engineering, basic logic, and good reasoning skills are needed, in fact maybe not - just a bit of simple thinking anyone can do. A subset stands on the primary which if false knocks the lot down.
The PCR is an amplification process which relies on knowing how it works, AND having a reliable reference to identify what is amplified against that reference. Poor reference or porr technique and the results are rubbish. Since February 2020 I have figured out how the PCR amplification works and then went looking for a virus the evidence for which appears to live in the minds of some Virologists because they say it exists. Not good enough for me to accept ANY PCR claimed evidence as solid.
You are simply running away from my point rather than addressing it. Note, as well, that my point concerns what was observed about PCR in practice after you made up your mind. So you aren't willing to accept any evidence contradicting what you predicted, that is all.
Sorry Brian, that just walked me around in a circle and I found i was looking at the beginning again. I di NOT say anything about 'unlikelihood' in sequential so called PCR tests. I am simply saying ALL PCR 'tests' are suspect results - ie random results. Anyone using a PCR must know from the design that at some point they will gat a positive depending upon the sample AND the Ct number chosen for that run. PCR amplifies EVERYTHING, thats all it ever can do. Then if you are looking for X it is only a matter of how high the Ct to show an X assuming there is a X in the sample to start with. how can anyone call that a Clinical Diagnosis tool beats me.
To say you did not say anything about a subset, only all, is a contradiction. All includes the subset. Therefore if the subset falsifies the statement, the statement is false for “all.” It just seems like you are so fixed in your conclusion you can’t accept basic logical statements.
I've been meaning to comment on this post, however similar to the previous ones leading up to this one I was still trying to parse the data (I do, however, understand Akira! Probably not something I should have watched while little...).
With that being said, I do appreciate your attempts to construct your hypothesis. As we've come to witness, there's a great deal of hubris in science that doesn't make room for corrections or negative results, so it's nice to see a hypothesis constructed but then reassessed due to looking at different information. I think we need more people willing to be wrong in this space. It's the only way we can add to the discourse.
"Wrong?" I have only acknowledged failure to prove being correct, not proof of being incorrect. In other words, I have shown that if there was a crime, the definitive evidence must have been obscured!
The latter comment was a broader remark about the discourse, and how there doesn't appear to be any correction made, and so we have a ton of hypotheses out there that muddy any assessment. And so, if one were to construct a hypothesis, find there to be issues, we would hope that someone offers corrections or caveats, rather than move on without addressing it.
That goes with the idea that many hypotheses put out are done more as theories, as if to say the evidence is robust enough to make an argument when in many cases that isn't quite the situation.
No, no Brian it's the internet and you have misinterpreted my words! I shall remember this forever and it shall be etched into my gravestone! No excuses!!
Perhaps - my angle here would still be, ok if there is this “chamber” where the virus can go evolve without collecting the same mutation signature that it collects in human transmission, why do none of the circulating versions after early 2020 go in that chamber? So for anything with microbiome, whether it’s strange selection pressure dynamics or direct bacterial infection by the virus, it still remains mysterious why markers for the virus after early 2020 are not present when the virus emerges as a VOC. Both silent and/or C>U mutations are not going to come with an undo button, there is less than a 1/30000 per mutation chance of losing each one after it becomes fixed. So we know it is only these really early versions coming back out as VOCs.
What if it is not a viral epidemic but something else again? The so called Spanish Flu epidemic (pandemic?) of 1918 has been said to have been a Bacterial one, that may also have been propagated by a Bacterial Vaccination project. Considering what many are claiming to have found and identified in the blood of sufferers, almost all of whom have received two or more shots, and the arguments suggesting shedding as a transmission medium for 'infection' (to those unvaccinated?), surely other possibilities than a viral impact should be considered. Seeing all through a lens of Virology may be a monumental error limiting investigation to a myopic one.
I am quite satisfied that 1918 was the flu virus. People alive after 1925 didn't have antibodies to Shope's swine flu which entered serial passage in 1928 but was still a "time capsule" of 1918, meaning that here was this virus that you could passage from Shope's pigs to a ferret, but if you mixed in blood of people alive before 1925 then the ferrets didn't get sick. And pigs on US farms never got flu symptoms before 1918. So the thing that made them sick is the thing that made people sick.
The role of bacteria in death "following flu" in 1918 is potentially apocryphal. I usually don't see it come up much in contemporary writing, and this is writing by people who at the time still thought flu itself might be a bacteria. https://quod.lib.umich.edu/f/flu/8580flu.0016.858 And you have cases like in tropical island tribes where 1/10 or more of the adults died in 1918 (because they had been too insulated in the last years of H1's previous spread before 1885); they should have been better off than the West one way or the other if bacteria were very important in flu deaths. But I say "potentially" because I haven't finished reviewing the evidence on this topic.
For SARS-CoV-2, the problem with any "the virus is just a passenger to something else" theory is that natural immunity wouldn't be apparent in that case. You wouldn't be able, in the pre-vaccine era, to follow around people with antibodies *to the virus* and see that they don't get sick as much, but that is exactly what you can do (as well as for people who were at some point PCR+ for, once again, the virus).
Additionally, McKernan does a better job than I could in summarizing the many ways by which this virus was spot-check "authenticated" as being active in infections - https://anandamide.substack.com/p/quasi-species-swarms-in-sars-cov (However I still would say the natural immunity point is more important here)
I was not suggesting that people died of a Bacterial illness post Flu. Two things bother me about the 1918 epidemic. 1. The origin was an army recruitment training camp exploded in activity to rapidly grow the army for war and the trail spread with the outbound mobilisation of the men leaving AND that is where the Rockefeller Institute sent their top scientist on a government mission to investigate what was viewed as the source of the original outbreak and who wrote the official report describing it as a effectively a viral Flu. 2. That same Rockefeller Institute has been reported as conducting a clinical trial of an experimental Bacterial Vaccine most likely using the army recruits as participants - a Vaccine it is suggested was rolled out around the world into the civilian population in near parallel timing to the epidemic. Coincidence does not prove causation and I have yet to find more sources to put more weight to this story.
What it does do is suggest we should not assume all Flu like symptoms indicate a viral infection and the complexity of Pneumonia, a not unrelated respiratory condition puts weight on my contention that we must look for non-viral possibilities with the Covid-19 condition.
In many activities, a target fixation can be deadly in that we blind ourselves to all else that will not fit, and especially if it conflict with, our one and only conception. BTW, I do NOT accept that the PCR process can reliably detect as a diagnostic tool any specific virus - it simply is not designed to function in that way. The Ct is critical to the process as is the specific reference chosen.
Bacteria and 1918 is just amyloid and alzheimer’s, I’ll put it that way. A lot of post-90s research jumping to wild conclusions. I work with what was written at the time. Shope, swine flu, done.
It doesn’t matter what one “accepts” about PCR or not. People who were PCR+ before the vax could be and were followed around to see if they were PCR+ again later, and they weren’t. So being PCR+ granted immunity to being PCR+ again later. If you want to form a theory for how that could happen if the test was not for a specific virus that people developed immunity to then go ahead, but to not “accept” the fact is just retreating into fantasy.
Brian, those more familiar with PCR than most always ask what was the Ct to achieve a PCR+? As Kari Mullis said clearly, wind up the Ct and you WILL ALWAYS get a PCR+ at some point and by a Ct of aboutn 60 you are guaranteed all results will be PCR+'s. Call that a reliable 'test'? Very few reported and I suspect recorded PCR+ results were ever given WITH a Ct number for that result. No objective use can be made of claimed results without the means to know how the result was obtained. And there is the question of 'What is being looked for' meaning the reference. A broad enough or vague identity for the target and you will be almost guaranteed to find it - depending upon the Ct. PCR is NOT an objective reliable tool for clinical diagnosis - and BTW nor is a rapid antigen process.
Was a busy weekend. I don't see how the possibility of de-specifying PCR is a counter to the fact that PCR+ was systematically used in multiple instances to correlate with unlikelihood of later PCR+. False positives *cannot* cause "unlikelihood of later false positive." Therefore, if multiple cases exist (the Cleveland Clinic study, Israel's dashboard) where people set some Ct threshold that resulted in unlikelihood of later PCR+, they used appropriate thresholds *by definition.* They didn't get false positives.
I think Peter makes an excellent point here. Scientists are baffled by the behavior of this elusive "virus" that is just bouncing to every corner of the world (even Antarctica multiple times!) but no one is asking if all of these are simply vaccination-driven waves of illness that possibly have environmental triggers.
Yes, and all viruses have always been baffling. If you want to see open minded debate on the mysteries of transmission and seasonality, etc., there is in fact no better place to look than the second leader of the “Rockefeller Virologists” himself https://www.ncbi.nlm.nih.gov/pmc/articles/PMC374955/
This was one year before Shope started passaging swine flu so you’ll note that grippe/influenza is still on the table as a bacteria despite the trouble with validating one on 1918.
Environmental triggers have always been implicated in viral diseases. These are simply facts about viruses that were true long before “maybe it’s X Files deep state chem trails” was available as an out for accepting that viruses are mysterious. That doesn’t mean XFDSCT isn’t what is happening, just that “germ theory dogma doesn’t predict infections accurately” is not the bar that has to be met to throw out the virus.
I'm of the mindset that we may just learn that our microbiome will include viruses of all sorts, and that being a viral reservoir is par for the course of being human. And so bacteria live in and on us, so likely are viruses, and we are now looking at possible ramifications for going "parasite-free" as that could possibly be related to the uptick in allergies being seen.
So to that extent it's possible that many viruses are pathobionts (pathoabionts?), in that they become infectious under certain circumstances. However, similar to bacteria and parasites there are likely to be some that are pathogenic irrespective of the circumstances.
(I need to change my screen name to "Not A Scientist"); however, I'm having trouble understanding how a virus that was "first seen in the west in January 2020" could have propelled AZ to develop a vaccine that was ready for Trials on April 23, 2020. Talk about the speed of science! /s
Also not to mention the overlap between Oxford and the Zoonati origins team.
Also not to mention the AZ shot potentially only having been developed in order to hype a suspiciously quickly-acknowledged harm signal and make RNA look better in comparison.
I greatly appreciate your willingness to entertain a hypothesis, investigate it thoroughly, and then change your perspective based on the results. This is obviously how the scientific method is supposed to work, but seldom how it actually works (which is sadly true now in both the mainstream and skeptic worlds).
I still find your lab-mouse origin story for the Omicrons quite convincing.
I wonder if the strange transmission dynamics of the pre-Omicrons might play into the strange evolutionary dynamics.
The earlier variants were not fit enough to infect most people (i.e. most people avoided infection despite no adaptive immunity) except in certain "super spreader" situations that appeared to be driven by particular hosts or particular environmental conditions. The BA variants, on the other hand, seem to be behaving more like a typical respiratory virus.
Perhaps. For example you could postulate that extreme rates of lineage or "transmission chain" death reduce Clonal Interference - it is so easy for entire clades to suddenly die out that all that needs to happen is for the current wave, which is from a not-most-fit clone, to die out and then clonal interference gets out of the way and the Cinderella mutant is poised to do better when innate antiviral immunity has settled down. So every wave is showing us the "past" in the present, and we have to wait to the next wave to see what the present most fit version of the virus really is, and this version won't have a lot of dS or C>U because it isn't replicating a lot yet and so it's not clocking up the background genetic signature. So that's the vault. Maybe it's a normal part of how viruses operate when they are "not quite a match" for the host. But again it's hard to see what "having transversion chains" really did for the VOCs besides Delta - the rest I don't find impressive in terms of fitness gains, and none outdo ancestral summer 2020 variants in terms of generating "immune escape mutations" on the RBD. All that they have different from the dominant summer clades is "purity" in of itself.
Lastly, it's not clear why this purity doesn't reach back behind B.1 to show any versions of the virus from before December-Italy entering "the vault." This implies that the B.1 mutations granted the virus fitness in a less crazy, stepwise manner, so no weird Being Akira Lights model of mutation was required except in a window between December 2019 to November 2021.
And so if the Omi's ended this hyper-rate of lineage death, by finally attaining homogeneous individual transmission, then they established clonal interference and so now we stop getting "pure" versions that displace the dominant clades.
Hello and many thanks for your article.
The variants of concern were all the minds of those who made it all up. All faked and imagined. I did some imagining myself. I am not PC.
https://alphaandomegacloud.wordpress.com/2021/12/02/various-variants-covid-19/
https://alphaandomegacloud.wordpress.com/2022/05/11/100-up-and-stupid-20-variants/
An early 2020 paper on Antibody-Dependent Enhancement. My brain hurts just reading the abstract, but it seems interesting:
Molecular Mechanism for Antibody-Dependent Enhancement of Coronavirus Entry.
https://europepmc.org/article/MED/31826992
Time you took your own advice mate. No building stands on rotten foundations - period. Not running away, just facing a truth based in reality. PCR is a great lab research tool, not a clinical diagnosis whatever Drosten claimed 9and made a bundle of money from).
You have as many ways to say "I simply refuse to consider changing my mind on PCR, even though I lecture others to do the same" as the eskimos do for "snow."
Are you not the one doing the preaching. I am looking and listening and yet I see only claims built on claims with your arguments in favour of PCR based 'tests' for a poorly defined if not artificially created part of a claimed genetic code. Support your claim not with yet more claims - with evidence of the claim fails.
Who is the one that refuses to open their mind?
You.
Hahahaha. Where is YOUR evidence. Its Put up or Shut up time me thinks.
Go back to December 14. Look at your reply to my reply. Do you address a single point I make? No. You just retreat into Army training camp myths. You are not debating, you are tantruming.
If the foundation of the claim is false, ALL ARE FALSE that stand on that foundation. IT IS THAT simple. Basic engineering, basic logic, and good reasoning skills are needed, in fact maybe not - just a bit of simple thinking anyone can do. A subset stands on the primary which if false knocks the lot down.
The PCR is an amplification process which relies on knowing how it works, AND having a reliable reference to identify what is amplified against that reference. Poor reference or porr technique and the results are rubbish. Since February 2020 I have figured out how the PCR amplification works and then went looking for a virus the evidence for which appears to live in the minds of some Virologists because they say it exists. Not good enough for me to accept ANY PCR claimed evidence as solid.
You are simply running away from my point rather than addressing it. Note, as well, that my point concerns what was observed about PCR in practice after you made up your mind. So you aren't willing to accept any evidence contradicting what you predicted, that is all.
Sorry Brian, that just walked me around in a circle and I found i was looking at the beginning again. I di NOT say anything about 'unlikelihood' in sequential so called PCR tests. I am simply saying ALL PCR 'tests' are suspect results - ie random results. Anyone using a PCR must know from the design that at some point they will gat a positive depending upon the sample AND the Ct number chosen for that run. PCR amplifies EVERYTHING, thats all it ever can do. Then if you are looking for X it is only a matter of how high the Ct to show an X assuming there is a X in the sample to start with. how can anyone call that a Clinical Diagnosis tool beats me.
To say you did not say anything about a subset, only all, is a contradiction. All includes the subset. Therefore if the subset falsifies the statement, the statement is false for “all.” It just seems like you are so fixed in your conclusion you can’t accept basic logical statements.
I've been meaning to comment on this post, however similar to the previous ones leading up to this one I was still trying to parse the data (I do, however, understand Akira! Probably not something I should have watched while little...).
With that being said, I do appreciate your attempts to construct your hypothesis. As we've come to witness, there's a great deal of hubris in science that doesn't make room for corrections or negative results, so it's nice to see a hypothesis constructed but then reassessed due to looking at different information. I think we need more people willing to be wrong in this space. It's the only way we can add to the discourse.
"Wrong?" I have only acknowledged failure to prove being correct, not proof of being incorrect. In other words, I have shown that if there was a crime, the definitive evidence must have been obscured!
The latter comment was a broader remark about the discourse, and how there doesn't appear to be any correction made, and so we have a ton of hypotheses out there that muddy any assessment. And so, if one were to construct a hypothesis, find there to be issues, we would hope that someone offers corrections or caveats, rather than move on without addressing it.
That goes with the idea that many hypotheses put out are done more as theories, as if to say the evidence is robust enough to make an argument when in many cases that isn't quite the situation.
Ah - yes, I see how your wording in the original comment is more general than my hurried reading. It was a very busy weekend, haha
No, no Brian it's the internet and you have misinterpreted my words! I shall remember this forever and it shall be etched into my gravestone! No excuses!!
I love how open you are with your scientific reasoning, including the blind alleys and red herrings you encounter. Two thumbs up!
Thanks!
https://hiddencomplexity.substack.com/p/covid-infection-causes-long-lasting?utm_medium=email
Just saw this and wonder if the effects on the microbiome could somehow be responsible for variants?
Perhaps - my angle here would still be, ok if there is this “chamber” where the virus can go evolve without collecting the same mutation signature that it collects in human transmission, why do none of the circulating versions after early 2020 go in that chamber? So for anything with microbiome, whether it’s strange selection pressure dynamics or direct bacterial infection by the virus, it still remains mysterious why markers for the virus after early 2020 are not present when the virus emerges as a VOC. Both silent and/or C>U mutations are not going to come with an undo button, there is less than a 1/30000 per mutation chance of losing each one after it becomes fixed. So we know it is only these really early versions coming back out as VOCs.
What if it is not a viral epidemic but something else again? The so called Spanish Flu epidemic (pandemic?) of 1918 has been said to have been a Bacterial one, that may also have been propagated by a Bacterial Vaccination project. Considering what many are claiming to have found and identified in the blood of sufferers, almost all of whom have received two or more shots, and the arguments suggesting shedding as a transmission medium for 'infection' (to those unvaccinated?), surely other possibilities than a viral impact should be considered. Seeing all through a lens of Virology may be a monumental error limiting investigation to a myopic one.
I am quite satisfied that 1918 was the flu virus. People alive after 1925 didn't have antibodies to Shope's swine flu which entered serial passage in 1928 but was still a "time capsule" of 1918, meaning that here was this virus that you could passage from Shope's pigs to a ferret, but if you mixed in blood of people alive before 1925 then the ferrets didn't get sick. And pigs on US farms never got flu symptoms before 1918. So the thing that made them sick is the thing that made people sick.
The role of bacteria in death "following flu" in 1918 is potentially apocryphal. I usually don't see it come up much in contemporary writing, and this is writing by people who at the time still thought flu itself might be a bacteria. https://quod.lib.umich.edu/f/flu/8580flu.0016.858 And you have cases like in tropical island tribes where 1/10 or more of the adults died in 1918 (because they had been too insulated in the last years of H1's previous spread before 1885); they should have been better off than the West one way or the other if bacteria were very important in flu deaths. But I say "potentially" because I haven't finished reviewing the evidence on this topic.
For SARS-CoV-2, the problem with any "the virus is just a passenger to something else" theory is that natural immunity wouldn't be apparent in that case. You wouldn't be able, in the pre-vaccine era, to follow around people with antibodies *to the virus* and see that they don't get sick as much, but that is exactly what you can do (as well as for people who were at some point PCR+ for, once again, the virus).
Additionally, McKernan does a better job than I could in summarizing the many ways by which this virus was spot-check "authenticated" as being active in infections - https://anandamide.substack.com/p/quasi-species-swarms-in-sars-cov (However I still would say the natural immunity point is more important here)
I was not suggesting that people died of a Bacterial illness post Flu. Two things bother me about the 1918 epidemic. 1. The origin was an army recruitment training camp exploded in activity to rapidly grow the army for war and the trail spread with the outbound mobilisation of the men leaving AND that is where the Rockefeller Institute sent their top scientist on a government mission to investigate what was viewed as the source of the original outbreak and who wrote the official report describing it as a effectively a viral Flu. 2. That same Rockefeller Institute has been reported as conducting a clinical trial of an experimental Bacterial Vaccine most likely using the army recruits as participants - a Vaccine it is suggested was rolled out around the world into the civilian population in near parallel timing to the epidemic. Coincidence does not prove causation and I have yet to find more sources to put more weight to this story.
What it does do is suggest we should not assume all Flu like symptoms indicate a viral infection and the complexity of Pneumonia, a not unrelated respiratory condition puts weight on my contention that we must look for non-viral possibilities with the Covid-19 condition.
In many activities, a target fixation can be deadly in that we blind ourselves to all else that will not fit, and especially if it conflict with, our one and only conception. BTW, I do NOT accept that the PCR process can reliably detect as a diagnostic tool any specific virus - it simply is not designed to function in that way. The Ct is critical to the process as is the specific reference chosen.
Bacteria and 1918 is just amyloid and alzheimer’s, I’ll put it that way. A lot of post-90s research jumping to wild conclusions. I work with what was written at the time. Shope, swine flu, done.
It doesn’t matter what one “accepts” about PCR or not. People who were PCR+ before the vax could be and were followed around to see if they were PCR+ again later, and they weren’t. So being PCR+ granted immunity to being PCR+ again later. If you want to form a theory for how that could happen if the test was not for a specific virus that people developed immunity to then go ahead, but to not “accept” the fact is just retreating into fantasy.
Brian, those more familiar with PCR than most always ask what was the Ct to achieve a PCR+? As Kari Mullis said clearly, wind up the Ct and you WILL ALWAYS get a PCR+ at some point and by a Ct of aboutn 60 you are guaranteed all results will be PCR+'s. Call that a reliable 'test'? Very few reported and I suspect recorded PCR+ results were ever given WITH a Ct number for that result. No objective use can be made of claimed results without the means to know how the result was obtained. And there is the question of 'What is being looked for' meaning the reference. A broad enough or vague identity for the target and you will be almost guaranteed to find it - depending upon the Ct. PCR is NOT an objective reliable tool for clinical diagnosis - and BTW nor is a rapid antigen process.
Was a busy weekend. I don't see how the possibility of de-specifying PCR is a counter to the fact that PCR+ was systematically used in multiple instances to correlate with unlikelihood of later PCR+. False positives *cannot* cause "unlikelihood of later false positive." Therefore, if multiple cases exist (the Cleveland Clinic study, Israel's dashboard) where people set some Ct threshold that resulted in unlikelihood of later PCR+, they used appropriate thresholds *by definition.* They didn't get false positives.
I think Peter makes an excellent point here. Scientists are baffled by the behavior of this elusive "virus" that is just bouncing to every corner of the world (even Antarctica multiple times!) but no one is asking if all of these are simply vaccination-driven waves of illness that possibly have environmental triggers.
Yes, and all viruses have always been baffling. If you want to see open minded debate on the mysteries of transmission and seasonality, etc., there is in fact no better place to look than the second leader of the “Rockefeller Virologists” himself https://www.ncbi.nlm.nih.gov/pmc/articles/PMC374955/
This was one year before Shope started passaging swine flu so you’ll note that grippe/influenza is still on the table as a bacteria despite the trouble with validating one on 1918.
Environmental triggers have always been implicated in viral diseases. These are simply facts about viruses that were true long before “maybe it’s X Files deep state chem trails” was available as an out for accepting that viruses are mysterious. That doesn’t mean XFDSCT isn’t what is happening, just that “germ theory dogma doesn’t predict infections accurately” is not the bar that has to be met to throw out the virus.
I'm of the mindset that we may just learn that our microbiome will include viruses of all sorts, and that being a viral reservoir is par for the course of being human. And so bacteria live in and on us, so likely are viruses, and we are now looking at possible ramifications for going "parasite-free" as that could possibly be related to the uptick in allergies being seen.
So to that extent it's possible that many viruses are pathobionts (pathoabionts?), in that they become infectious under certain circumstances. However, similar to bacteria and parasites there are likely to be some that are pathogenic irrespective of the circumstances.
Agree, agree
(I need to change my screen name to "Not A Scientist"); however, I'm having trouble understanding how a virus that was "first seen in the west in January 2020" could have propelled AZ to develop a vaccine that was ready for Trials on April 23, 2020. Talk about the speed of science! /s
Not to mention the "STORY" study launching from the Oxford Vaccine Group exactly in October, 2019 https://unglossed.substack.com/i/76838100/the-set-up-what-indeed-is-the-story
Also not to mention the overlap between Oxford and the Zoonati origins team.
Also not to mention the AZ shot potentially only having been developed in order to hype a suspiciously quickly-acknowledged harm signal and make RNA look better in comparison.
I greatly appreciate your willingness to entertain a hypothesis, investigate it thoroughly, and then change your perspective based on the results. This is obviously how the scientific method is supposed to work, but seldom how it actually works (which is sadly true now in both the mainstream and skeptic worlds).
I still find your lab-mouse origin story for the Omicrons quite convincing.
I wonder if the strange transmission dynamics of the pre-Omicrons might play into the strange evolutionary dynamics.
The earlier variants were not fit enough to infect most people (i.e. most people avoided infection despite no adaptive immunity) except in certain "super spreader" situations that appeared to be driven by particular hosts or particular environmental conditions. The BA variants, on the other hand, seem to be behaving more like a typical respiratory virus.
Perhaps. For example you could postulate that extreme rates of lineage or "transmission chain" death reduce Clonal Interference - it is so easy for entire clades to suddenly die out that all that needs to happen is for the current wave, which is from a not-most-fit clone, to die out and then clonal interference gets out of the way and the Cinderella mutant is poised to do better when innate antiviral immunity has settled down. So every wave is showing us the "past" in the present, and we have to wait to the next wave to see what the present most fit version of the virus really is, and this version won't have a lot of dS or C>U because it isn't replicating a lot yet and so it's not clocking up the background genetic signature. So that's the vault. Maybe it's a normal part of how viruses operate when they are "not quite a match" for the host. But again it's hard to see what "having transversion chains" really did for the VOCs besides Delta - the rest I don't find impressive in terms of fitness gains, and none outdo ancestral summer 2020 variants in terms of generating "immune escape mutations" on the RBD. All that they have different from the dominant summer clades is "purity" in of itself.
Lastly, it's not clear why this purity doesn't reach back behind B.1 to show any versions of the virus from before December-Italy entering "the vault." This implies that the B.1 mutations granted the virus fitness in a less crazy, stepwise manner, so no weird Being Akira Lights model of mutation was required except in a window between December 2019 to November 2021.
And so if the Omi's ended this hyper-rate of lineage death, by finally attaining homogeneous individual transmission, then they established clonal interference and so now we stop getting "pure" versions that displace the dominant clades.