Great, so we're going from a not-so-safe vaccine to a not-so-safe drug. Meanwhile, other countries like Thailand and India have already done some legwork on herbal remedies that are safe and possibly effective in mitigating covid...the Western world is so strangely backwards with its excessive focus on new technologies.
Human clinical trials are rendered into theatre so that the market can be transformed into the lab. The goal is to decipher the software of life; we're just the guinea pigs.
Thanks for this analysis. Nucleoside analogs sound like a terrible idea except perhaps as a last ditch treatment for the seriously ill.
As for the infection trends, I think it is important to consider that this virus, like influenza, rises and falls on its own rhythm regionally and that very little of this pattern is attributable to any human action or lack thereof. In almost all cases waves of infection have crested and declined despite failing to reach the level of population immunity that the models required in order to see a decline.
Even before vaccination some countries like Brazil have seen long plateaus while others like India have seen brief, intense waves.
My sense is that we don't create the waves, but we can modulate them. It also seems to me that vaccination has modulated the wave upward, with more infections in high-vax than in low-vax countries in recent months despite demonstrated short term efficacy. I still think spike tolerance may be playing a role, but not in a forever spike sort of way, more along the lines of affecting overdispersion of transmission and perhaps creating superspreaders among the vaccinated.
The modelers seem to believe we are in the last wave. I think that we could well see our worst wave yet this winter as the modulating effects of seasonal stimulus and waning (and quite possibly negative) vaccine efficacy combine.
And yes, the point about burning out before reaching everyone is extremely important. I don't think SARS-CoV-2 has *any* novelty in terms of infection susceptibility to coronavirus. The "novelty" seems to be related to superfluous epitopes that lead to pre-primed ADE among a select few, not to inherent contagiousness. Susceptibility to infection is based on already-in-progress coronavirus rhythms and susceptibility to severe outcomes is a totally different dynamic. It's like a pop song that 9-10ths of the population is bored of in a given year; for any individual, only one infection should be expected every ten years outside of bad luck. That's before the shots mess up innate immunity by whatever means they are doing so.
Somewhat unrelated, but I would be interested in your thoughts on the emerging story of direct spike binding to fibrinogen leading to polymerization, with diffuse fibrin clotting then triggering a reactive and largely dysfunctional immune response. (I should note that there is an alternative hypothesis of spike-ACE2 binding in blood/vascular cells leading to clotting, but to me the fibrinogen-binding route would appear to be higher impact.)
Along these lines it's worth noting that Dr. Charles Hoffe in BC has found elevated D-dimer levels, indicative of clotting, in 62% of his mRNA-injected patients.
The thing about clots is that they lead to very common causes of death: heart attack and stroke. Which means the signal needs to be very large in order to be detectable. And indeed it appears to be detectable:
Thanks for that, though it's going to take an entire day to process it! It does look convincing as far as the mechanism, but it doesn't attempt to interrogate the bigger question - how common are glycoproteins that can create the same effect? They used a "BALD" HIV control? Why not a coronavirus control? This is my personal bugbear with "pathologizing" the spike protein - no one checks against regular coronavirus, to sort which features of the SC2 spike "lead" to viremia and which result in post-viremia harms, and whether only the former category contains meaningful physical distinctions. Still seems like their mAB for the "cryptic" site could be *very* useful for preventing both severe infection and general vaccination clotting outcomes.
My one concern with that paper is that the authors are seeking to commercialize that mAB so they may be inclined to make the data look "cleaner" than it otherwise would. As for whether other coronavirus spikes might cause the same problem if they got into the bloodstream, that's an interesting question. It may not be that important of a question though if SARS-CoV-2 spikes *do* get into the bloodstream via infection or vaccination and other coranavirus spikes do not, in the course of typical infection.
Right, but "etiologies" should always be tagged for being unique to clinical illness or not. For those that aren't, that implies a pathway for spontaneous healing that should be pursued instead of medicine; the pathway of course always ends up being exercise.
This also runs into the same fear that JJ Couey often expresses - that we are on the verge of the successful creation of an immortal "immunomythology" where society is untaught the fact that humans could get sick a few times but still live through childhood without medicine, go on to be 70, etc.
Also, D-dimer is elevated during/following SARS-CoV-2 infection, but typically only in severe or fatal cases (see https://www.tandfonline.com/doi/pdf/10.1080/17474086.2020.1831383) - which would indicate viremia or free spike in the blood. With the current vaccinations it is much easier for the spike protein to access the vascular system.
Exactly - the stupidity of saying that inducing cells all over the body to produce spike is ok because in an infection (leading to measurable memory immune response, as opposed to subclinical innate suppression that doesn't even lead to viral shedding) it **might** get past the respiratory epithelium speaks for itself. I do wonder, however, if clotting is actually pretty common while running the gauntlet of childhood infections, and kids are actually subclinically walking around with vascular hazards that would kill the rest of us. But I wonder a lot of crazy things.
It does appear that there is some increase in clotting risk even in non-severe infections. That was widely reported last year as part of the initial covid hysteria. But quite possibly the clotting risk is also not universal across every infection, but requires some degree of viremia/systemic infection.
Hm, but superspreaders should just help things wrap up faster - the same way that NPIs just flatten the same number of cases out through time. You got me on Brazil, though. It is extremely hard to imagine that 10k people are testing positive day after day for a year straight in /Sao Paolo alone/ without resorting to wild epistemic leaps. For one thing - why bother to keep measuring daily cases if they don't change for an entire year! Now the rates are lower - "proof of vax success," clearly. I can only throw up my hands in bafflement.
I was more thinking song the lines of an increase in superspreaders - people releasing high viral loads into the environment - might overcome the innate immunity of more people and thereby cause a wave to be larger than it would otherwise have been.
Interesting that there is a plateau in Nucleocapsid antibodies given that we'd expect S to rise as more Brits have gotten their gmo-shot(s). Is no one else developing N antibodies, even after recovering from all of the breakthrough infections? Or, is it too soon to tell???
Remember that St. Jude study where the N T-cells seemed to drop off on 6 of 10 patients post jab and we didn't have enough samples to really know what was going on?
That's true, there's a possibility that "breakthrough" infections won't lead to immune response to the N protein to begin with. But, even assuming it does (which would be a good sign for improved memory immune response), comparing N protein seroprevalence by age group (instead of vaccination status per age group) has a big flaw - it discounts for the older morality rate in the elderly! So the N protein antibody positivity will always be higher in the young compared to the old, even if the vaccinated are being infected more.
Yes, but what I think is most interesting is that on figure 3 the N category seems to be flat lining. Hard to say what this means right now. Maybe it’ll go up, but if it doesn’t that doesn’t sound so great. I guess all we can do right now is stay tuned.
I agree that it seems like a more "sedated" pattern. But not completely robotic, yet. It must be remembered that the threshold for "seropositive" is usually based on very small sample sizes - 100 - 1000 - evaluated by the test manufacturers, which can flatten and obscure a lot of action in plasma antibodies.
One thing odd about Israel is that the IFR, after all these jabs and boosters, seems (eyeballing the cases and deaths data in the same frame) almost the same as in the first wave.
Which is that? The autumn 2020 wave is a bit hazardous to extrapolate IFR from because positivity rates were higher than in summer 2021, indicating a discount on the denominator. That only adds to your observation, of course. Still, IFR is a very fluid metric. Things look more positive for Covid vaccine "deaths efficacy" in the cumulative graphs at worldometers https://www.worldometers.info/coronavirus/country/israel/
Great, so we're going from a not-so-safe vaccine to a not-so-safe drug. Meanwhile, other countries like Thailand and India have already done some legwork on herbal remedies that are safe and possibly effective in mitigating covid...the Western world is so strangely backwards with its excessive focus on new technologies.
Human clinical trials are rendered into theatre so that the market can be transformed into the lab. The goal is to decipher the software of life; we're just the guinea pigs.
Thanks for this analysis. Nucleoside analogs sound like a terrible idea except perhaps as a last ditch treatment for the seriously ill.
As for the infection trends, I think it is important to consider that this virus, like influenza, rises and falls on its own rhythm regionally and that very little of this pattern is attributable to any human action or lack thereof. In almost all cases waves of infection have crested and declined despite failing to reach the level of population immunity that the models required in order to see a decline.
Even before vaccination some countries like Brazil have seen long plateaus while others like India have seen brief, intense waves.
My sense is that we don't create the waves, but we can modulate them. It also seems to me that vaccination has modulated the wave upward, with more infections in high-vax than in low-vax countries in recent months despite demonstrated short term efficacy. I still think spike tolerance may be playing a role, but not in a forever spike sort of way, more along the lines of affecting overdispersion of transmission and perhaps creating superspreaders among the vaccinated.
The modelers seem to believe we are in the last wave. I think that we could well see our worst wave yet this winter as the modulating effects of seasonal stimulus and waning (and quite possibly negative) vaccine efficacy combine.
And yes, the point about burning out before reaching everyone is extremely important. I don't think SARS-CoV-2 has *any* novelty in terms of infection susceptibility to coronavirus. The "novelty" seems to be related to superfluous epitopes that lead to pre-primed ADE among a select few, not to inherent contagiousness. Susceptibility to infection is based on already-in-progress coronavirus rhythms and susceptibility to severe outcomes is a totally different dynamic. It's like a pop song that 9-10ths of the population is bored of in a given year; for any individual, only one infection should be expected every ten years outside of bad luck. That's before the shots mess up innate immunity by whatever means they are doing so.
Somewhat unrelated, but I would be interested in your thoughts on the emerging story of direct spike binding to fibrinogen leading to polymerization, with diffuse fibrin clotting then triggering a reactive and largely dysfunctional immune response. (I should note that there is an alternative hypothesis of spike-ACE2 binding in blood/vascular cells leading to clotting, but to me the fibrinogen-binding route would appear to be higher impact.)
This could be a bombshell paper:
https://www.biorxiv.org/content/10.1101/2021.10.12.464152v1
An earlier investigation found the same thing:
https://www.medrxiv.org/content/10.1101/2021.03.05.21252960v1
Along these lines it's worth noting that Dr. Charles Hoffe in BC has found elevated D-dimer levels, indicative of clotting, in 62% of his mRNA-injected patients.
https://westernstandardonline.com/2021/07/bc-doc-says-hes-found-blood-clots-in-62-of-post-jab-patients/
The thing about clots is that they lead to very common causes of death: heart attack and stroke. Which means the signal needs to be very large in order to be detectable. And indeed it appears to be detectable:
https://www.thetimes.co.uk/article/mystery-rise-in-heart-attacks-from-blocked-arteries-m253drrnf
Thanks for that, though it's going to take an entire day to process it! It does look convincing as far as the mechanism, but it doesn't attempt to interrogate the bigger question - how common are glycoproteins that can create the same effect? They used a "BALD" HIV control? Why not a coronavirus control? This is my personal bugbear with "pathologizing" the spike protein - no one checks against regular coronavirus, to sort which features of the SC2 spike "lead" to viremia and which result in post-viremia harms, and whether only the former category contains meaningful physical distinctions. Still seems like their mAB for the "cryptic" site could be *very* useful for preventing both severe infection and general vaccination clotting outcomes.
My one concern with that paper is that the authors are seeking to commercialize that mAB so they may be inclined to make the data look "cleaner" than it otherwise would. As for whether other coronavirus spikes might cause the same problem if they got into the bloodstream, that's an interesting question. It may not be that important of a question though if SARS-CoV-2 spikes *do* get into the bloodstream via infection or vaccination and other coranavirus spikes do not, in the course of typical infection.
Right, but "etiologies" should always be tagged for being unique to clinical illness or not. For those that aren't, that implies a pathway for spontaneous healing that should be pursued instead of medicine; the pathway of course always ends up being exercise.
This also runs into the same fear that JJ Couey often expresses - that we are on the verge of the successful creation of an immortal "immunomythology" where society is untaught the fact that humans could get sick a few times but still live through childhood without medicine, go on to be 70, etc.
Also, D-dimer is elevated during/following SARS-CoV-2 infection, but typically only in severe or fatal cases (see https://www.tandfonline.com/doi/pdf/10.1080/17474086.2020.1831383) - which would indicate viremia or free spike in the blood. With the current vaccinations it is much easier for the spike protein to access the vascular system.
Exactly - the stupidity of saying that inducing cells all over the body to produce spike is ok because in an infection (leading to measurable memory immune response, as opposed to subclinical innate suppression that doesn't even lead to viral shedding) it **might** get past the respiratory epithelium speaks for itself. I do wonder, however, if clotting is actually pretty common while running the gauntlet of childhood infections, and kids are actually subclinically walking around with vascular hazards that would kill the rest of us. But I wonder a lot of crazy things.
It does appear that there is some increase in clotting risk even in non-severe infections. That was widely reported last year as part of the initial covid hysteria. But quite possibly the clotting risk is also not universal across every infection, but requires some degree of viremia/systemic infection.
Hm, but superspreaders should just help things wrap up faster - the same way that NPIs just flatten the same number of cases out through time. You got me on Brazil, though. It is extremely hard to imagine that 10k people are testing positive day after day for a year straight in /Sao Paolo alone/ without resorting to wild epistemic leaps. For one thing - why bother to keep measuring daily cases if they don't change for an entire year! Now the rates are lower - "proof of vax success," clearly. I can only throw up my hands in bafflement.
I was more thinking song the lines of an increase in superspreaders - people releasing high viral loads into the environment - might overcome the innate immunity of more people and thereby cause a wave to be larger than it would otherwise have been.
Hey Brian,
Did you see what's going with the UK S and N antibody testing?
https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/1025358/Vaccine-surveillance-report-week-41.pdf
Page 21-23 figures 3, 4a, 4b
Interesting that there is a plateau in Nucleocapsid antibodies given that we'd expect S to rise as more Brits have gotten their gmo-shot(s). Is no one else developing N antibodies, even after recovering from all of the breakthrough infections? Or, is it too soon to tell???
Remember that St. Jude study where the N T-cells seemed to drop off on 6 of 10 patients post jab and we didn't have enough samples to really know what was going on?
That's true, there's a possibility that "breakthrough" infections won't lead to immune response to the N protein to begin with. But, even assuming it does (which would be a good sign for improved memory immune response), comparing N protein seroprevalence by age group (instead of vaccination status per age group) has a big flaw - it discounts for the older morality rate in the elderly! So the N protein antibody positivity will always be higher in the young compared to the old, even if the vaccinated are being infected more.
Yes, but what I think is most interesting is that on figure 3 the N category seems to be flat lining. Hard to say what this means right now. Maybe it’ll go up, but if it doesn’t that doesn’t sound so great. I guess all we can do right now is stay tuned.
I agree that it seems like a more "sedated" pattern. But not completely robotic, yet. It must be remembered that the threshold for "seropositive" is usually based on very small sample sizes - 100 - 1000 - evaluated by the test manufacturers, which can flatten and obscure a lot of action in plasma antibodies.
One thing odd about Israel is that the IFR, after all these jabs and boosters, seems (eyeballing the cases and deaths data in the same frame) almost the same as in the first wave.
Which is that? The autumn 2020 wave is a bit hazardous to extrapolate IFR from because positivity rates were higher than in summer 2021, indicating a discount on the denominator. That only adds to your observation, of course. Still, IFR is a very fluid metric. Things look more positive for Covid vaccine "deaths efficacy" in the cumulative graphs at worldometers https://www.worldometers.info/coronavirus/country/israel/