It's interesting how quickly people rushed onto this study given some of the contextual problems.
As Brian pointed out, the fact that they may tinker with this gene means that if they wanted to release a more deadly variant they may do so without needing to go through this S gene switcheroo.
I generally don't dwell on whether they are continuously construction more deadly pathogens for my own mental psyche, but when it comes to Omicron I tend to lean slightly more in the way of Brian Mowrey in thinking that Omicron was of lab origin. It's weird how many people have forgotten that Omicron itself just came out of nowhere and the current assumptions of its origins don't work with me personally.
Someone please correct me if I'm wrong, but the mRNA sequencing is an approximation of synthesizing that which approximates the target spike protein. Based on the demanding storage requirements, instability of mRNA, each cell's ability to process the mRNA, the possibility of mutation and reading wrong, all could create misfolds.
Secondly, this approximated possibly misfolded, unnatural protein may then change shape as it moves through the body due to temperature or pH changes and the havoc it could cause is quite unknown because it hasn't been studied in detail or through adverse events because they don't seem to be researched much, are ignored in clinical trials or in the real world, people are told "we don't know" or "you can go home".
Moreover, with the use of LNPs the mRNA can also cross the blood brain barrier creating the approximated, unnatural and possibly misfolded proteins among brain cells as well. With the frosting on the cake, being we don't know how long before this all stops due to the possibility of saRNA and reverse transcriptase.
Lastly, the cherry on top, mice are mice and humans are humans.
(I won't even touch on the possibility of graphene oxide for now.)
If I'm wrong about this please let me know. These things worry me much more than the infectiousness ness of the strain involved. My apologies, if my comments are out of place.
So there's a lot to cover here Lee, and note that a lot of what I state may either be ramblings or things I haven't fully developed through a post so it's really me just putting some of my thoughts out there (hopefully other people add onto your questions).
Graphene Oxide:
I suppose I can start with the graphene oxide since it was mentioned slightly (sorry!) but I sort of find the concerns over graphene oxide to sometimes serve almost like a red herring, or a distraction away from things to which we have strong evidence for. That is not to say that graphene oxide is not a concern or anything like that because, quite frankly, I haven't spent time looking at graphene oxide or anything related to that. We have a lot of evidence about the concerns over the spike being cytotoxic and the concerns over myocarditis across all vaccine platforms points to this possibly being the thing to look at. Overall, it doesn't mean that people shouldn't spend time looking at graphene oxide but by all accounts we have strong evidence pointing to the spike.
mRNA misfolding:
So this is something I've been thinking about for a while. It depends on what we mean by "approximation". By all accounts, the amino acid sequence should be the same, but the mRNA sequence has some funny business on account of the codon optimization and the pseudouridine.
The codon optimization is interesting. It's assumed that certain codons serve as "slow down" portions of translation possibly because the number of different tRNA molecules may be different. Some researchers have argued that these slow down portions of codons are important because it gives the already translated amino acid sequence time to be folded or undergo post-translational modification including glycosylation. This is sort of like making sausage and having the casing fill with some parts slowing down to tie the links or other things.
Now, one concern is that codon optimization, which may favor the end result of protein production, may override the slow down steps necessary to either fold the already translated protein or to make modifications to the protein. Now, you've taken a slower, methodical process and ramped up the production meaning that you may have sacrificed the proper folding. It's almost like sacrificing quantity over quality to say the least.
I think this I Love Lucy skit also puts it well (you probably know which one it is):
The problem is that no proper studies have been done to actually check how much properly folded spike protein is actually being produced.
Pseudouridine is something I haven't looked at extensively. Since it serves as a nucleoside analogue one may wonder if there may be some improper recognition and an insertion of the wrong amino acid in the sequence, but this would be a pretty blatant issue in that you would be able tell serious issues. But again, I'm not sure if such studies have been conducted.
Free-Roaming Spike
So there is likely an issue in which pH will alter the fold of the protein (salinity is critical as well), however this argument would mean that we may have to wonder what happens to the spike of the virus. It could be that being attached to the virion may alter the behavior or pathogenicity, or other mechanisms may limit the extent that different pH or salinity may influence the spike. However, the same can be said for nearly any protein in our body which themselves are dependent on pH, salinity, temperature, and other factors.
So this is one think that would really be up in the air and would at least implicate many proteins aside from spike protein, including many of our owns. There's really no way of telling, and this also doesn't take into account how well our body deals with these issues.
LNP and BBB:
This is something that may be shared with viruses in general, in that viruses are able to invade the CNS including influenza and HIV. It's assumed that some neurological issues may be associated with viral infection. Part of the work I was researching was Parkinson's because I was interested in that recent paper on the vaccine injuries and eventual death in the man with Parkinson's.
To the extent this may happen with the LNP is something that is, again, up in the air. What's important is making sure that the proper LNP is being assessed. There's an issue in which LNP is being lumped in as a broad category but many of the behaviors of LNPs depend on structural modifications. So pretty much one study that looks at using LNPs to carry drugs into the CNS may not use the same LNPs as the vaccines and these minor details are important.
So these are a few of my informal thoughts on some of these topics. I have a few more but like I said most of these haven't been researched yet so I can't form some opinions yet.
If there's any questions please let me know. And apologies if it didn't quite answer some of your questions as I'm trying to figure out many of these things as well.
There's a lot to say here Lee, so when I get the chance I'll try to provide my perspective as I have it right now, but that may take a while so I will leave this comment and try to come back and address your questions.
In the real world is the WT more infectious than Omicron? No, correct? Isn't that true both for vaccinated and unvaccinated? What is the explanation for why an older version of the virus is more infectious than Omicron? That doesn't fit with observed reality.
Let's all put on our "Geert Vanden Bossche hats" and then ask whether there would be differences in "intrinsic" infectiousness vs. vaccine antibody enhanced infectiousness. In other words, what about comparing vaccinated vs. unvaccinated mice? After all that's representative of the current human population.
In the real world it is true that Omicron was more infectious, but when we introduce those variables then we run into other extraneous factors that muddy the assessment of this study even more. We pretty much don't know what Omi-S would do in people because all of these experiments from the current study may not translate well into the general public.
The reason why I mentioned WT here is just on the basis of consistency, in that both the researchers and many writers have focused on the fact that this study would argue that this made a better Omicron when I could argue that this study also shows that a worse WT was made, if we were to be consistent here.
The fact is that it's really hard to extrapolate much from this study aside from the fact that more than spike serves as the determining factor for viral infection.
I've raised a few criticisms of GvB and OAS in general mostly for the fact I think there's a lot of issues in how OAS has been adopted on Substack. Brian Mowrey has written extensively on OAS and has raised a lot of criticisms of it.
One thing that doesn't appear to be addressed is the fact that Omicron appeared out of nowhere. Such a phenomenon isn't something that can properly worked into the OAS framework, and yet it feels as if many people have used Omicron to argue that this variant was an escape variant caused by the vaccines when in reality Omicron could have just escaped from a lab. The entire origins of Omicron are just as questionable as the original strain of SARS-COV2.
I will say Karl's argument of the Nucleocapsid protein doesn't quite hold up given other circumstances. The issue is that this anti-N argument seems to have stemmed from Alex Berenson who improperly looked at the UK Surveillance data and made assumptions that somehow we can look to the anti-N antibodies to argue what may happen in regards to the spike. Brian has written about this issue as well, so on that I would say that those who argue OAS shouldn't be looking at the Nucleocapsid protein to infer something with the spike.
So what reason would you give for the negative efficacy that apparently happens over time post the shots? Do you see no evidence of OAS? Karl specifically said in the comments section that he does not know, and does not think anyone knows, but it is the kind of issue that can occur, and a strong argument of why this "research" is insane, especially given that such research is likely the cause of Covid in the first place. (Karl is of course not one to understate)
The fact that infection appears more rapid, and more intense in the W tests, may not be all good news when it comes to potential spread, should this somehow escape.
It is an interesting study; of course it should have been assumed as unlikely from the start that the heavy mutations outside of spike had zero influence on virulence, and this non-zero influence was likely an attenuating one given that it's a milder variant. Pity it's been a year and no one's done a gene-by-gene teardown. But a one-gene teardown is better than nothing.
The response has been funny. As I've said before Omicron is an obvious lab creation and so if someone out there wants to release something less friendly, they're going to do it anyway.
Besides that, there are extreme differences in the non-spike region of BA.2 and as my origin analysis hints there could have been some pressure to resolve a secondary structure conflict* (Orf 1 ns and s selection pressure as noted in my timeline https://unglossed.substack.com/p/omicron-origins-part-1). If this was hammered out in BA.2 then it could already be matching "Omi-S" in terms of virulence in these same assays. Who knows. All we can do is speculate for now.
*For example, a single-point defect in the 5'UTR secondary structure is the main driver of attenuation in two of the polio strains in OPV.
It is interesting, if not still ambiguous. You never quite know exactly what will happen until you swap things around or remove them and see what changes, almost like tonsils or an appendix.
We may certainly argue that it should be obvious more than spike is critical for how the virus functions but it's nice to at least have some evidence out there.
However, like you stated, the fact that we aren't having up-to-date research on mutations in non-spike proteins means we're missing out on a ton of critical information. Such circumstances may lead to the assumption that absence of evidence is evidence of absence, as if to say that no research on the effects of these non-spike mutations may infer that these mutations (and these proteins) are not critical to how the virus operates.
It is the sum of a virus' mutations that we should look at when determining how it behaves. That Ba.2 inference is interesting. Maybe this will lead people to look back into Omicron sublineages and do more research on more than just the spike.
Brian says, The response has been funny. As I've said before Omicron is an obvious lab creation and so if someone out there wants to release something less friendly, they're going to do it anyway."
Sorry Brian, I see zero that is funny about it. Because it can be done certainly does not mean it should be. I consider Covid to very likely be the exact result of such GOF research. (Millions dead and, as a result of Government action, the global economy severely threatened, and economic collapse often also leads to war.) If Kay sarah, is the official and unofficial reaction, then humanity is likely to face unending pandemic destruction. There is no end to the harms that can be imagined, which to the Fauci like proponents of GOF research means there is no end to deadly pathogens that MUST be created so that we can then create antidotes for them. So while the fear reaction MAY, or may not (Karl may be correct, and if said GOF research continues it is only a matter of time until he is right) be overblown, the acceptance of such research will end in catastrophe.
Sure, but your sentiment doesn't actually characterize the response and so isn't really what I find funny. It's more the utter surprise - "Someone would actually TRY to make a version of SARS-CoV-2 worse than Omicron?!" Even just typing that, I have to laugh.
Look. I don't want them doing any of this viral genetic testing/altering/research. Have we not discovered over the last 2 years that these "experiments" have the potential to destroy society? This kind of research is like living next door to a polluting factory. I get none of the benefits from it, nor have I consented to have my environment destroyed. Where are the benefits of this viral research?
Me thinks you are missing the forest for the trees. GOF on Sars-Cov-2 should not be funded by the government. Period.
Also, we know in the real world Omicron is far more infectious and transmits more extensively than WT, otherwise Chinas population would have been decimated in the first wave and in the US it would have affected more states.
We also know the reason Omicron has a lower CFR is it does not replicate well in the lungs. Super Omicron replicates well in the lungs. Thats a problem.
Now other labs having this capability could seek to duplicate the experiment for nefarious purposes, or not, and may do so in labs less secure (BSL-2)
Thanks this is useful context but it is time the scientific world took a stand against all gain of function research. This paper must be retracted and must not be allowed to be published. We have done this before with unethical studies and only once we start imposing these ethical standards will trust ever start to come back.
Another good point is that cells in test tube are simply cells n a test tube - once exposed to the virus there is literally nothing to prevent them from being infected. Humans have an innate immune system which can prevent you from being infected in the first place. We are exposed to potential pathogens all the time, yet we are not always sick!
I had WT and lived. Basically everyone I know who has had Covid has been fine (except for my dad who was in very poor health). I have been exposed several times to people with Omicron and have not been reinfected (I even spent 2 days in very close proximity to a trainee who ended up testing positive). I never did despite being subjected to several PCR tests.
12-20 weeks isn't really the age used for an "aged" mouse model but it still seems to make a difference here. Or nothing explains the difference. Another day, another replication crisis.
Wonderful post, thank you for calmly pointing all these things out.
"And that brings us to the real question here: what the heck was the point of this study?" Perhaps simply to continue the fear narrative, "there will be a killer virus in the future that we will need more vaccine injections for".
I am just a layperson, but the graphs discussed all show omicron to be inferior to Wuhan by every metric, yet we know that omicron is a lot more contagious in humans today than the Wuhan variant a couple of years ago. Is it possible that this chimera would be as contagious as omicron and almost as deadly as Wuhan? Sorry if this is a dumb question.
Also, what sort of laboratory did the scientists use for this work? Wuhan's laboratory was not secure enough to keep their virus contained, and I wonder about Boston University's laboratory.
I do not know how deadly the first Covid was, although I think ALL versions had a CFR well below one percent. So, yes, the 80 percent mortality, despite the ambiguity, is highly concerning. A CFR of five to 10 percent would be horrible. Also the six days to real infection is concerning as far as infective spread, should this escape. Hi RO combined with high infectivity combined with slow onset, is a very bad scenario, that justifies overblown fear.
I consider this "S" variant a false flag.
The real concern is a genuine more lethal variant on the way, totally engineered of course.
Almost like this "S" variant gives them and others some deniability, "See we told you, Geert was right!"
It's interesting how quickly people rushed onto this study given some of the contextual problems.
As Brian pointed out, the fact that they may tinker with this gene means that if they wanted to release a more deadly variant they may do so without needing to go through this S gene switcheroo.
I generally don't dwell on whether they are continuously construction more deadly pathogens for my own mental psyche, but when it comes to Omicron I tend to lean slightly more in the way of Brian Mowrey in thinking that Omicron was of lab origin. It's weird how many people have forgotten that Omicron itself just came out of nowhere and the current assumptions of its origins don't work with me personally.
Someone please correct me if I'm wrong, but the mRNA sequencing is an approximation of synthesizing that which approximates the target spike protein. Based on the demanding storage requirements, instability of mRNA, each cell's ability to process the mRNA, the possibility of mutation and reading wrong, all could create misfolds.
Secondly, this approximated possibly misfolded, unnatural protein may then change shape as it moves through the body due to temperature or pH changes and the havoc it could cause is quite unknown because it hasn't been studied in detail or through adverse events because they don't seem to be researched much, are ignored in clinical trials or in the real world, people are told "we don't know" or "you can go home".
Moreover, with the use of LNPs the mRNA can also cross the blood brain barrier creating the approximated, unnatural and possibly misfolded proteins among brain cells as well. With the frosting on the cake, being we don't know how long before this all stops due to the possibility of saRNA and reverse transcriptase.
Lastly, the cherry on top, mice are mice and humans are humans.
(I won't even touch on the possibility of graphene oxide for now.)
If I'm wrong about this please let me know. These things worry me much more than the infectiousness ness of the strain involved. My apologies, if my comments are out of place.
Related articles:
https://www.forbes.com/sites/robtoews/2021/10/03/alphafold-is-the-most-important-achievement-in-ai-ever/
https://www.nature.com/articles/d41586-021-02483-w
So there's a lot to cover here Lee, and note that a lot of what I state may either be ramblings or things I haven't fully developed through a post so it's really me just putting some of my thoughts out there (hopefully other people add onto your questions).
Graphene Oxide:
I suppose I can start with the graphene oxide since it was mentioned slightly (sorry!) but I sort of find the concerns over graphene oxide to sometimes serve almost like a red herring, or a distraction away from things to which we have strong evidence for. That is not to say that graphene oxide is not a concern or anything like that because, quite frankly, I haven't spent time looking at graphene oxide or anything related to that. We have a lot of evidence about the concerns over the spike being cytotoxic and the concerns over myocarditis across all vaccine platforms points to this possibly being the thing to look at. Overall, it doesn't mean that people shouldn't spend time looking at graphene oxide but by all accounts we have strong evidence pointing to the spike.
mRNA misfolding:
So this is something I've been thinking about for a while. It depends on what we mean by "approximation". By all accounts, the amino acid sequence should be the same, but the mRNA sequence has some funny business on account of the codon optimization and the pseudouridine.
The codon optimization is interesting. It's assumed that certain codons serve as "slow down" portions of translation possibly because the number of different tRNA molecules may be different. Some researchers have argued that these slow down portions of codons are important because it gives the already translated amino acid sequence time to be folded or undergo post-translational modification including glycosylation. This is sort of like making sausage and having the casing fill with some parts slowing down to tie the links or other things.
Now, one concern is that codon optimization, which may favor the end result of protein production, may override the slow down steps necessary to either fold the already translated protein or to make modifications to the protein. Now, you've taken a slower, methodical process and ramped up the production meaning that you may have sacrificed the proper folding. It's almost like sacrificing quantity over quality to say the least.
I think this I Love Lucy skit also puts it well (you probably know which one it is):
https://www.youtube.com/watch?v=AnHiAWlrYQc
The problem is that no proper studies have been done to actually check how much properly folded spike protein is actually being produced.
Pseudouridine is something I haven't looked at extensively. Since it serves as a nucleoside analogue one may wonder if there may be some improper recognition and an insertion of the wrong amino acid in the sequence, but this would be a pretty blatant issue in that you would be able tell serious issues. But again, I'm not sure if such studies have been conducted.
Free-Roaming Spike
So there is likely an issue in which pH will alter the fold of the protein (salinity is critical as well), however this argument would mean that we may have to wonder what happens to the spike of the virus. It could be that being attached to the virion may alter the behavior or pathogenicity, or other mechanisms may limit the extent that different pH or salinity may influence the spike. However, the same can be said for nearly any protein in our body which themselves are dependent on pH, salinity, temperature, and other factors.
So this is one think that would really be up in the air and would at least implicate many proteins aside from spike protein, including many of our owns. There's really no way of telling, and this also doesn't take into account how well our body deals with these issues.
LNP and BBB:
This is something that may be shared with viruses in general, in that viruses are able to invade the CNS including influenza and HIV. It's assumed that some neurological issues may be associated with viral infection. Part of the work I was researching was Parkinson's because I was interested in that recent paper on the vaccine injuries and eventual death in the man with Parkinson's.
To the extent this may happen with the LNP is something that is, again, up in the air. What's important is making sure that the proper LNP is being assessed. There's an issue in which LNP is being lumped in as a broad category but many of the behaviors of LNPs depend on structural modifications. So pretty much one study that looks at using LNPs to carry drugs into the CNS may not use the same LNPs as the vaccines and these minor details are important.
So these are a few of my informal thoughts on some of these topics. I have a few more but like I said most of these haven't been researched yet so I can't form some opinions yet.
If there's any questions please let me know. And apologies if it didn't quite answer some of your questions as I'm trying to figure out many of these things as well.
Thank you for your response. Again I will need to review a few times.
Preoccupied and very concerned now about the ACIP vote taking place soon: https://leemuller.substack.com/p/the-names-and-faces-of-those-who
There's a lot to say here Lee, so when I get the chance I'll try to provide my perspective as I have it right now, but that may take a while so I will leave this comment and try to come back and address your questions.
In the real world is the WT more infectious than Omicron? No, correct? Isn't that true both for vaccinated and unvaccinated? What is the explanation for why an older version of the virus is more infectious than Omicron? That doesn't fit with observed reality.
Let's all put on our "Geert Vanden Bossche hats" and then ask whether there would be differences in "intrinsic" infectiousness vs. vaccine antibody enhanced infectiousness. In other words, what about comparing vaccinated vs. unvaccinated mice? After all that's representative of the current human population.
That's the real question that no researcher dare examine. And frankly I think the arguments against this research are very strong. Karl Denninger puts it bluntly here: https://market-ticker.org/akcs-www?blog=Market-Ticker-Nad
In the real world it is true that Omicron was more infectious, but when we introduce those variables then we run into other extraneous factors that muddy the assessment of this study even more. We pretty much don't know what Omi-S would do in people because all of these experiments from the current study may not translate well into the general public.
The reason why I mentioned WT here is just on the basis of consistency, in that both the researchers and many writers have focused on the fact that this study would argue that this made a better Omicron when I could argue that this study also shows that a worse WT was made, if we were to be consistent here.
The fact is that it's really hard to extrapolate much from this study aside from the fact that more than spike serves as the determining factor for viral infection.
I've raised a few criticisms of GvB and OAS in general mostly for the fact I think there's a lot of issues in how OAS has been adopted on Substack. Brian Mowrey has written extensively on OAS and has raised a lot of criticisms of it.
One thing that doesn't appear to be addressed is the fact that Omicron appeared out of nowhere. Such a phenomenon isn't something that can properly worked into the OAS framework, and yet it feels as if many people have used Omicron to argue that this variant was an escape variant caused by the vaccines when in reality Omicron could have just escaped from a lab. The entire origins of Omicron are just as questionable as the original strain of SARS-COV2.
I will say Karl's argument of the Nucleocapsid protein doesn't quite hold up given other circumstances. The issue is that this anti-N argument seems to have stemmed from Alex Berenson who improperly looked at the UK Surveillance data and made assumptions that somehow we can look to the anti-N antibodies to argue what may happen in regards to the spike. Brian has written about this issue as well, so on that I would say that those who argue OAS shouldn't be looking at the Nucleocapsid protein to infer something with the spike.
So what reason would you give for the negative efficacy that apparently happens over time post the shots? Do you see no evidence of OAS? Karl specifically said in the comments section that he does not know, and does not think anyone knows, but it is the kind of issue that can occur, and a strong argument of why this "research" is insane, especially given that such research is likely the cause of Covid in the first place. (Karl is of course not one to understate)
The fact that infection appears more rapid, and more intense in the W tests, may not be all good news when it comes to potential spread, should this somehow escape.
It is an interesting study; of course it should have been assumed as unlikely from the start that the heavy mutations outside of spike had zero influence on virulence, and this non-zero influence was likely an attenuating one given that it's a milder variant. Pity it's been a year and no one's done a gene-by-gene teardown. But a one-gene teardown is better than nothing.
The response has been funny. As I've said before Omicron is an obvious lab creation and so if someone out there wants to release something less friendly, they're going to do it anyway.
Besides that, there are extreme differences in the non-spike region of BA.2 and as my origin analysis hints there could have been some pressure to resolve a secondary structure conflict* (Orf 1 ns and s selection pressure as noted in my timeline https://unglossed.substack.com/p/omicron-origins-part-1). If this was hammered out in BA.2 then it could already be matching "Omi-S" in terms of virulence in these same assays. Who knows. All we can do is speculate for now.
*For example, a single-point defect in the 5'UTR secondary structure is the main driver of attenuation in two of the polio strains in OPV.
It is interesting, if not still ambiguous. You never quite know exactly what will happen until you swap things around or remove them and see what changes, almost like tonsils or an appendix.
We may certainly argue that it should be obvious more than spike is critical for how the virus functions but it's nice to at least have some evidence out there.
However, like you stated, the fact that we aren't having up-to-date research on mutations in non-spike proteins means we're missing out on a ton of critical information. Such circumstances may lead to the assumption that absence of evidence is evidence of absence, as if to say that no research on the effects of these non-spike mutations may infer that these mutations (and these proteins) are not critical to how the virus operates.
It is the sum of a virus' mutations that we should look at when determining how it behaves. That Ba.2 inference is interesting. Maybe this will lead people to look back into Omicron sublineages and do more research on more than just the spike.
I totally agree with you both.
It is almost like they are trying to divert resources toward the spike.
If I were them, depending on what they are doing or have done, it certainly may be what I would have done. Always an interesting way to look at it.
Brian says, The response has been funny. As I've said before Omicron is an obvious lab creation and so if someone out there wants to release something less friendly, they're going to do it anyway."
Sorry Brian, I see zero that is funny about it. Because it can be done certainly does not mean it should be. I consider Covid to very likely be the exact result of such GOF research. (Millions dead and, as a result of Government action, the global economy severely threatened, and economic collapse often also leads to war.) If Kay sarah, is the official and unofficial reaction, then humanity is likely to face unending pandemic destruction. There is no end to the harms that can be imagined, which to the Fauci like proponents of GOF research means there is no end to deadly pathogens that MUST be created so that we can then create antidotes for them. So while the fear reaction MAY, or may not (Karl may be correct, and if said GOF research continues it is only a matter of time until he is right) be overblown, the acceptance of such research will end in catastrophe.
Sure, but your sentiment doesn't actually characterize the response and so isn't really what I find funny. It's more the utter surprise - "Someone would actually TRY to make a version of SARS-CoV-2 worse than Omicron?!" Even just typing that, I have to laugh.
Ok Brian, you have kept your humor better than I through this.
All the Best...
“what the heck was the point of this study?”
That question was just rolling around my brain
Look. I don't want them doing any of this viral genetic testing/altering/research. Have we not discovered over the last 2 years that these "experiments" have the potential to destroy society? This kind of research is like living next door to a polluting factory. I get none of the benefits from it, nor have I consented to have my environment destroyed. Where are the benefits of this viral research?
Me thinks you are missing the forest for the trees. GOF on Sars-Cov-2 should not be funded by the government. Period.
Also, we know in the real world Omicron is far more infectious and transmits more extensively than WT, otherwise Chinas population would have been decimated in the first wave and in the US it would have affected more states.
We also know the reason Omicron has a lower CFR is it does not replicate well in the lungs. Super Omicron replicates well in the lungs. Thats a problem.
Now other labs having this capability could seek to duplicate the experiment for nefarious purposes, or not, and may do so in labs less secure (BSL-2)
Thanks this is useful context but it is time the scientific world took a stand against all gain of function research. This paper must be retracted and must not be allowed to be published. We have done this before with unethical studies and only once we start imposing these ethical standards will trust ever start to come back.
Another good point is that cells in test tube are simply cells n a test tube - once exposed to the virus there is literally nothing to prevent them from being infected. Humans have an innate immune system which can prevent you from being infected in the first place. We are exposed to potential pathogens all the time, yet we are not always sick!
I had WT and lived. Basically everyone I know who has had Covid has been fine (except for my dad who was in very poor health). I have been exposed several times to people with Omicron and have not been reinfected (I even spent 2 days in very close proximity to a trainee who ended up testing positive). I never did despite being subjected to several PCR tests.
A bit of a funny follow-up - another spike recomb study but with no weight loss for any of the Omi spike mutants. Mice were 8-10 week female only instead of 12-20 weeks m+f https://www.biorxiv.org/content/10.1101/2022.11.08.515725v1
12-20 weeks isn't really the age used for an "aged" mouse model but it still seems to make a difference here. Or nothing explains the difference. Another day, another replication crisis.
Wonderful post, thank you for calmly pointing all these things out.
"And that brings us to the real question here: what the heck was the point of this study?" Perhaps simply to continue the fear narrative, "there will be a killer virus in the future that we will need more vaccine injections for".
I am just a layperson, but the graphs discussed all show omicron to be inferior to Wuhan by every metric, yet we know that omicron is a lot more contagious in humans today than the Wuhan variant a couple of years ago. Is it possible that this chimera would be as contagious as omicron and almost as deadly as Wuhan? Sorry if this is a dumb question.
Also, what sort of laboratory did the scientists use for this work? Wuhan's laboratory was not secure enough to keep their virus contained, and I wonder about Boston University's laboratory.
I do not know how deadly the first Covid was, although I think ALL versions had a CFR well below one percent. So, yes, the 80 percent mortality, despite the ambiguity, is highly concerning. A CFR of five to 10 percent would be horrible. Also the six days to real infection is concerning as far as infective spread, should this escape. Hi RO combined with high infectivity combined with slow onset, is a very bad scenario, that justifies overblown fear.