I was recently presented that Indiana study by someone, and they used it to try to claim some benefit from being vaxxed. I noticed quickly that it was not comparing vaxxed vs unvaxxed, but vaxxed vs unvaxxed with "documented SARS-CoV-2 infection between November 29, 2020, and February 9, 2022"
I wondered why they didn't compare unvaxxed vs vaxxed. If you look at figure 1, you'll see the "neither vaccinated nor infected" group is n=4.2 million
the "infected individuals" is n=736 thousand; vaxxed is 2.8 million.
Right off the bat, I saw a massive issue with the study. By this date (Feb 2022) according to the CDC, over half (57.7%) of Americans had already been exposed to the virus:
Many did not even know; if they did, it's unlikely this was ever documented. Because the person I was talking to and myself are both in our late 20s, I was focusing mainly on this age group. At most, probably about 1% of those in our age group that get exposed to SARS-CoV-2 ever seek medical assistance over it. Generally, it's not a big deal and lasts a few days if that. personally, I have never gotten sick from it, but allegedly 94% of Americans have been exposed by now, so maybe I was just asymptomatic.
Either way, the people that have a record of infection that medical professionals can access will, on average, be much different than the rest of the population. They are outright selecting for susceptibility to disease with this analysis. So it doesn't seem like a very good analysis to argue in favor of "real-world benefits of vaccination."
It's also extremely suspicious that they did not compare the vaxxed & unvaxxied without documented previous infection. They had the data, so why not do it? Maybe the results would not have been what they wanted to publish.
It is an extremely weird, bad, study, frankly Berenson ought to be fined several millions of dollars for causing me to have even looked at it.
The idea of comparing all vaccinees to natural infections is literally bonkers. The requirement of previous encounter with the database possibly puts an unhealthy user bias on both the vaccine and virus side. One really wonders what the authors are thinking. I just want someone to hit me on the head and cut to the next scene like in a Bond movie.
Brian, I have recommended your stack, I find very interesting and informative. We may not agree all of the time but you are very smart, detailed, high quality. Thanks for your work.
Brian, I have recommended your stack, I find very interesting and informative. We may not agree all of the time but you are very smart, detailed, high quality. Thanks for your work.
It's unfortunate that some people mistake our situation as a high school debate, won or lost by pedantic statistical or rhetorical nuances. It's not. We're in an information war, with millions of lives already lost and many millions more still at risk. If Berenson tells his readers the vax causes excess mortality, a widely proven conclusion, it's not really important whether his basis includes extraneous points that might be incorrect. We really need to focus on the objective of making it stop. We can work out the details later.
The government and medical industry drove the herd to fear the virus. We need to drive the herd to fear the government and medical complex. It's not a rational process. It's how information war is waged. Everybody gets dirty. If we try to keep it clean, we'll continue ue to lose.
Next Christmas will be merrier. Lots of humbug this year.
Perfectly clear this should not have been given to many, classically to any, certainly not as any precondition of getting rid of ineffective and illegal restrictions on people’s liberty
People say "Accelerating the evolution of SARS-COV-2." a lot without actually discussing the mechanisms and the probabilities.
There are a relatively small number of proteins involved and changes to the N protein genes or the RdRp genes are not likely to lead to a viable virus. Changes to the S protein genes such that it could bind to a wider range of receptors might make it more virulent but no one is demonstrating that such a possible change exists.
Since the current S protein seems pretty specific to ACE2 and maybe TMPRSS2 and these things depend heavily on folding of proteins it seems unlikely they could bind to another receptor.
What else could change? Maybe they will develop a whole new machinery for RNA copy fidelity and packaging of only perfect proteins. I am not holding my breath.
Ah, yes, @tradsperger here is referring to clause 73§3:C of the human immune system operation manual, which as everyone knows clearly states what enables and prohibits Herd Immunity ™, hence why such confident statements are not pure imagination, sarcasm.
When it comes to evaluating the efficacy of the mRNA inoculations, the one thing I have not seen done in any of these relatively small scale studies is to reconcile the results to the broader epidemiological data.
Kyle Beattie's big data analysis showing that the mRNA inoculation campaigns actually increased the incidence of COVID cases pretty much demolishes the notion that the inoculations are an effective defense.
Similarly, when the rates of community spread increases after the inoculation ratio in a population passes 50% also cuts against the possibility of the inoculations being effective.
I see nothing in Beattie's method that addresses causation. You already know you are looking at a data set where there are more cases and deaths in 2021. So you are going to plug in "vaccines" to that and somehow show that they caused what you already know happens in the system? How? You have no control system where the rise in cases/deaths doesn't happen. Can Beattie show that Taylor Swift downloads don't show the same "causation" as a negative control?
Beattie used Bayesian analysis to statistically impute causation. It's not direct evidence, but Bayesian analysis is a valid analytical method. In the absence of direct evidence it can be compelling.
I don't really do statistics. But, Wikipedia says Popper said that Bayesian analysis 'presupposes what it attempts to justify' which sounds exactly like my take on the paper to begin with, so I don't get the vibe that it is an appropriate approach to prove the vaccine caused something we know in advance already happened everywhere no matter what.
So you are saying that earlier on, the shots/boosters were actually preventing people from catching covid. And so their covid rate was genuinely lower than the unvaccinated. But now the shots are wearing off, and the unvaccinated have ever more natural immunity, so the unvaccinated are doing better?
And the reason the chart from the paper doesn't show this, is because it doesn't go far enough back, to where the shots were actually helping prevent infection? And if went much further back, the infection rate would be lower (early on) for the vaccinated, and higher (early on) for the unvaccinated?
I'm confused, because I thought the shots never were tested to prevent infection, and never did (except for the original Wuhan strain).
They have an efficacy window of 3 months. Circulating IgG leaks into the mucosa so as long as your IgG levels are jacked up to crazy levels, you have a sort of artificial mucosal immunity. Even if the trials didn't test this (because there was no random screening, PCR was only issued after symptoms were reported) various real-world studies have found the same short term infection efficacy.
One way we could "see" this efficacy is by noticing when it wore off. Like in the Israel dashboard in summer, 2021, the per-100k infection rates suddenly ticked upward for the double-dosed as infection efficacy went away. But that was the same time boosters were rush-authorized. So the signal was instantly hidden, but it seems from the Bar-On studies that most people transitioned from double-dosed to triple-dosed without any bump in infections. So they safely got back into the efficacy boat until the next boosters, and then the same thing repeated.
I'll say I was still surprised when the BA.5 survey paper came out, and previous reported infection rates were still lower in the boosted (of course there are biases in a survey). I thought the BA.1/2 wave would have evened the playing-field. But it doesn't seem that way.
I am not 100% convinced by this argument. The study period was Sept-Nov 2022. I would have thought that anyone with 1 or 2 shots only, would have gotten them at least 1 year prior to the study period, so would have at least 9 months of exposure after 3 months of protection. Shouldn't efficacy have reverted to nearly 0 by this time? Yet it shows 2 shots as doubling your odds of infection.
It also doesn't look good for the shots if 3 months of protection is balanced out by 9+ months of 2x risk! Am I missing something?
Also - an unrelated note, I don't know if you saw this https://hiddencomplexity.substack.com/p/about-the-igg4-trend article on IgG4. I'm not sure I understood it completely but he seems to be saying in one of the linked sub-articles ( https://hiddencomplexity.substack.com/p/chimeric-nature-of-galectin-3-and ) that IgG4, in addition to potential problems with tolerating the virus, also causes changes to the activity of Galectin-3 which apparently can cause all sorts of problems with fibrosis and formation of connective tissue in the wrong places ("IgG4 Related Disease"?).. which made me think of those rubbery clots.
I guess that maybe we can add a few more new worst case scenarios to the list :(
Looking into the galectin thing, there appears to be some confusion in Schroder, Bieneman regarding the GTNGTKR paper and what it was saying about galectin. GTNGKR is a loop, not a fold; in general the similarity between the NTD of coronaviruses and galectin may simply and unremarkably reflect that both are designed to bind to sugars; and in SARS-CoV-2 once again the fold quality is lost.
This is why I am wary of small-author-number papers, to be a bit snobby.
But the link is highly appreciated as I was previously ignorant of NL63's similarity to SARS-CoV-1/2
"According to the results of searches performed with the DALI protein structure database search server (2), whereas MHV NTD and human galectins share the same fold, the SARS-CoV and NL63-CoV C-domains each represent a novel fold (Fig. 2A and B). Interestingly, despite their different structures, NL63-CoV and SARS-CoV C-domains bind to overlapping regions on their common receptor, human angiotensin-converting enzyme 2 (ACE2) (Fig. 3A and B) (9). We previously hypothesized that SARS-CoV and NL63-CoV C-domains diverged from a common ancestor into different structures and then converged functionally to recognize the same ACE2 receptor (8, 9). In this report, we present evidence to support this hypothesis and expand the evolutionary discussion to include all three coronavirus genera." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302248/
What the SLFS model has going for it is that the events being tracked only happen to outliers. The following implication of which... actually isn't depicted in the model, because a full simulation would have millions of squares obviously. Anyway it doesn't matter whether most double-injected (1x course of blue paint) stopped having blue paint a long time ago, it only matters that, ok, here were a few that got blue paint later in the game. So they're still in the "double-injected" group but they don't reflect the group. But, the group has these outliers who are short on natural immunity going into the study period and so the outliers cause the group as a whole to rack up more "hits" for the virus.
In particular, if anyone got the vaccine on a will-they-wont-they mandate holdout last-minute timing, they would be less likely to have a BA.1 wave infection, which is what confers the best protection ("last infected in BA.4/5" aren't protected because it actually consists of people infected right before or during the study, which is why it starts out at 0 at-risk *Edit: Just before, not during, these ones were all infected in the 90 day window before the study start.)
Oh, thank you. I thought that the short-lived efficacy of the vaccine was against "severe illness and death"(TM) due to lots of antibodies being pumped out. I didn't realize there was actual (short lived) protection against infection due to mucosal immunity. If that is true, maybe people who would die if they caught covid, really should be vaccinated. I do know a number of really old people who have had all four shots (and some the bivalent as well) and they seem okay, other than several of them having blood clots. I think they have no natural immune systems to speak of, so maybe the shot is a benefit to them.
And if covid really does do terrible things to T cells and dendritic cells and that leads to cancer and RSV, doesn't it make sense to get the shot every three months to get the mucosal immunity? If that's the sort of thing you care about? The people I know who are now getting fast growing, sudden cancer are all vaccinated, but not every three months.
Most of the people I know who are ultra boosted (with bivalent) are still hunkered down. It is the people I know who have had three shots who have decided that it's all over and they can go out to eat. They've mostly caught covid. They look terrible, but I don't know if it is due to the shot or due to the covid or due to being toyed with by psychopaths. There are so many variables.
I can't wish you a typical Merry Christmas since the 17th century Christian sect that I have worshipped with for the last four years (there are still holdouts, mostly in Ohio) considers every day to be Christmas. And that the celebration is internal, and not to be external. And that tomorrow will merely be "the day the world calls Christmas." However, I wish you the internal spiritual experience of the true holiday, on every day.
Severe/death efficacy should be long-lasting, as B Cells will do their job and ramp up antibodies when the virus shows up. There's no big danger for either the naturally or artificially immune if their antibodies go down, when it comes to severe outcomes.
Does that mean old people should take the shots? I don't think so. Antibodies are protective, but we could just give them to people when they are infected. There's no reason to use mRNA to turn people into factories for things that we can literally... produce in a factory.
Moreover, no matter which risk group you look at, severe outcomes and death still only affect a minority of infected people. So severe efficacy can never benefit most recipients. And anyone it doesn't benefit is just left with whatever the harms are from the shots. Even if the cost-benefit for some groups might seem positive, you are harming some people to protect others - human sacrifice, essentially.
Now, as for infection efficacy, that one is temporary because the super-high IgG antibody levels are going to fade and then you have no more mucosal immunity. Whereas for natural infection, tissue-resident memory T Cells go into your respiratory tract and you have "immunity" as properly understood - you don't get sick again. The big question, imo, was always whether the injections interfered with this. At this point I don't think they do.
As far as the virus's effect on T Cells, that is again going to be an individual phenomenon and not imply that everyone needs protection from the shots. Also, here, I think it is pretty safe to bet that the shots would show at least just as much, probably more general immunosuppression. In fact I'm at least toe-in-the-water on Team VAIDS, I think things like this https://unglossed.substack.com/p/would-die-for-pseudo-u and this https://twitter.com/alexmeshkin/status/1585261482253565953 in the Covid-vaccinated speak for themselves.
Overall, the CBA for the elderly is a difficult and nuanced subject. That's why I oppose attempts to just skirt the discussion with "look! chart! negative efficacy! OAS! No need to make hard calls here!" which are really fantasies.
OK, a quick search reveals that there are papers out there talking about IgG antibodies in the mucosa. I guess I should not have expected any different. If the body can get IgA antibodies into the mucosa why would it not be able to get IgG antibodies into the mucosa?
Because the mechanism (Fc receptor mediated transcytosis) occurs minimally in the upper respiratory tract. It occurs in a larger scale in the lower airways and GI mucosa. Look up neonatal Fc receptor mediated transcytosis.
IgA is more expected since B Cells take up residence and secrete it long term. Temporary IgG leakage makes sense since, besides the observed short-term efficacy of the Covid-19 injections, how else would one explain classic observations of injected flu vaccine efficacy against symptomatic infection, esp. in 1958 when H2 arrived so there wasn't any pre-existing sterilizing immunity.
"The Asian vaccine was estimated to cause a three-fold reduction—that is, 66% protection—in the number of influenza cases as compared with the numbers in the [influenza-B-vaccine receiving] control group occurring nine days after [the second dose] and thereafter. Within the first eight days after [the second dose; and so, before additional seroconversion could take place] no differences were found [echoing 1943, when Francis and Salk’s injection appeared to work despite being delivered mid-wave]. The polyvalent influenza A vaccine [comprised of previously circulating strains] behaved just like the control influenza B vaccine, so it can be concluded that the stimulus of the up-to-date Asian antigen was necessary for protection. Recent published accounts of trials of Asian vaccines in the USA have given figures of effectiveness in the range of 40-67%."
I think I understand the argument you are making but I suspect I need to read the paper to determine how they are measuring infections. Is it more PCR tests where anyone challenged with the virus, regardless of immunity, might yield a positive result, or was it based on actual symptoms?
Also, I would like to know how they measure that 30%. In the original Pfizer trials they used Relative Risk Reduction of getting one symptom and the control group had about a 0.84% risk of experiencing one symptom with the trial group having something like a 0.04% risk of experiencing one symptom.
I am not interested in a vaccine that reduces my risk of developing one symptom from below one percent to even further below one percent.
In this paper are they at least using ARR?
Also, what would allow them to draw more robust conclusions? Another 51,000 people who were never vaccinated and who could be matched on when they last had the virus?
It's adjusted Cox HR. The raw HR was only .87. The absolute benefit of the boosters is going to be pretty small since there aren't that many "cases" (positive antigen *edit: PCR, not antigen, I always confuse "NAAT" for "RAT," tests) to go around anyway.
The headline by-dose and by-prior-infection plots are Simon and Makuch / Kaplan Meier HR. HR should be the same as a person-days RR calculation in both cases since the slopes are steady. But I don't really know, it's statistics stuff.
Interesting thought Brian. When seeing "negative efficacy" data I immediately become hesitant because one would have to reason why such a phenomenon would occur, and that may end up resulting from OAS in some regard (although we've criticized it).
I think your argument is an interesting one. It at least makes sense that the more distant we get from Wuhan/D614G SARS-COV2 that we should expect a lag to occur, now catching up. It would be interesting to see what effect the bivalent boosters would have in the discussion, but apparently the uptake for these boosters have been far lower than people thought, and fortunately I think that even a bad respiratory season may not lead to more boosting due to fatigue.
As to Berenson, Berenson is indicative of someone that doesn't really read into studies and just takes the information at face value. Maybe it's a consequence of his old life as s journalist. When reading news reports on studies it's clear that the reporter just repeats verbatim what the study states, and then relies on other doctors/scientists to quote in their reports. It's like reporters spend so much time doing everything BUT reading the actual study.
Also, Merry Christmas to you and your family Brian! Thanks for the information and analysis you've provided the past year!
"So much time but reading the study" - Well, probably my approach on this one as well. I was already familiar with Shrestha's setup so I just made some assumptions and started putting fish in squares, haha. BUT DOES BERENSON EVEN PUT FISH IN SQUARES? WHAT IS ANYONE PAYING HIM FOR?
OAS of course makes no sense since it's a (false suggestion of a) dose-dependent relationship. But OAS is just an incoherent stand-in for "drugs really ARE sinful" in Berenson's mind.
My own pretty worthless unscientific observation is that my vaxxed/boosted friends, family, and acquaintances didn't seem to catch the virus until after they got the 3rd shot. Now they're going for number 4 and all around me I see vaxxed out sick with whatever it's called now.
But my unvaxxed self, friends and family are not untouchable either. Eldest son (a shot virgin) had Delta last December and just now is getting over another milder case of the crud. So much depends on physique, age and behavior.
Merry Christmas, Brian! Thanks for your articles, they're always worth pondering.
I always value anecdotes. For myself, a never-Wuhan-er (probably asymptomatically immunized before the first lockdown thanks to being very active in the Bay), my January Omi bout has gotten me through the so-called tripledemic with just occasional scratchy throats, despite once again being active, going to the gym, etc. I do wish people were still ashamed to cough. I wanted that part of the whole thing to last. Now they do it without even thinking about it again. I just don't like coughing.
I and many people I know of differing levels of vaccination (me being one of the unvaccinated) got caught up in the wave of Omicron. There's a ton of context that tends to get missed out in the discussion. I understand that there are serious concerns over the vaccines, but it can be a bit frustrating when we find information to fit the narrative rather than examine things for what we see.
Interestingly, given the timing of the booster I would be curious if your situation coincided with Omicron as well and it being the most escapiest of escaping variants relative to the prior ones.
"Support for this “catch-up” explanation for the higher infection rate " - this makes a lot of sense, I didn't think of that. Thank you!
Glad I left berenson's stack long ago, I don't miss it.
I was recently presented that Indiana study by someone, and they used it to try to claim some benefit from being vaxxed. I noticed quickly that it was not comparing vaxxed vs unvaxxed, but vaxxed vs unvaxxed with "documented SARS-CoV-2 infection between November 29, 2020, and February 9, 2022"
I wondered why they didn't compare unvaxxed vs vaxxed. If you look at figure 1, you'll see the "neither vaccinated nor infected" group is n=4.2 million
the "infected individuals" is n=736 thousand; vaxxed is 2.8 million.
Right off the bat, I saw a massive issue with the study. By this date (Feb 2022) according to the CDC, over half (57.7%) of Americans had already been exposed to the virus:
https://www.cbsnews.com/news/covid-majority-americans-children-adults-infected/
Many did not even know; if they did, it's unlikely this was ever documented. Because the person I was talking to and myself are both in our late 20s, I was focusing mainly on this age group. At most, probably about 1% of those in our age group that get exposed to SARS-CoV-2 ever seek medical assistance over it. Generally, it's not a big deal and lasts a few days if that. personally, I have never gotten sick from it, but allegedly 94% of Americans have been exposed by now, so maybe I was just asymptomatic.
Either way, the people that have a record of infection that medical professionals can access will, on average, be much different than the rest of the population. They are outright selecting for susceptibility to disease with this analysis. So it doesn't seem like a very good analysis to argue in favor of "real-world benefits of vaccination."
It's also extremely suspicious that they did not compare the vaxxed & unvaxxied without documented previous infection. They had the data, so why not do it? Maybe the results would not have been what they wanted to publish.
It is an extremely weird, bad, study, frankly Berenson ought to be fined several millions of dollars for causing me to have even looked at it.
The idea of comparing all vaccinees to natural infections is literally bonkers. The requirement of previous encounter with the database possibly puts an unhealthy user bias on both the vaccine and virus side. One really wonders what the authors are thinking. I just want someone to hit me on the head and cut to the next scene like in a Bond movie.
😅 I hope you get your millions!
Brian, I have recommended your stack, I find very interesting and informative. We may not agree all of the time but you are very smart, detailed, high quality. Thanks for your work.
Thank you for these kind remarks!
Brian, I have recommended your stack, I find very interesting and informative. We may not agree all of the time but you are very smart, detailed, high quality. Thanks for your work.
It's unfortunate that some people mistake our situation as a high school debate, won or lost by pedantic statistical or rhetorical nuances. It's not. We're in an information war, with millions of lives already lost and many millions more still at risk. If Berenson tells his readers the vax causes excess mortality, a widely proven conclusion, it's not really important whether his basis includes extraneous points that might be incorrect. We really need to focus on the objective of making it stop. We can work out the details later.
How does Berenson's headline, "URGENT... higher risk... getting Covid" accelerate the end of society being politically hostage to a virus?
The government and medical industry drove the herd to fear the virus. We need to drive the herd to fear the government and medical complex. It's not a rational process. It's how information war is waged. Everybody gets dirty. If we try to keep it clean, we'll continue ue to lose.
Next Christmas will be merrier. Lots of humbug this year.
Quid custodiet ipsos custodes
I get it
Not ok nevertheless
Perfectly clear this should not have been given to many, classically to any, certainly not as any precondition of getting rid of ineffective and illegal restrictions on people’s liberty
People say "Accelerating the evolution of SARS-COV-2." a lot without actually discussing the mechanisms and the probabilities.
There are a relatively small number of proteins involved and changes to the N protein genes or the RdRp genes are not likely to lead to a viable virus. Changes to the S protein genes such that it could bind to a wider range of receptors might make it more virulent but no one is demonstrating that such a possible change exists.
Since the current S protein seems pretty specific to ACE2 and maybe TMPRSS2 and these things depend heavily on folding of proteins it seems unlikely they could bind to another receptor.
What else could change? Maybe they will develop a whole new machinery for RNA copy fidelity and packaging of only perfect proteins. I am not holding my breath.
Heh, lots of people are jumping on the bandwagon:
https://www.rintrah.nl/unprecedented-global-respiratory-disease/
Ah, yes, @tradsperger here is referring to clause 73§3:C of the human immune system operation manual, which as everyone knows clearly states what enables and prohibits Herd Immunity ™, hence why such confident statements are not pure imagination, sarcasm.
When it comes to evaluating the efficacy of the mRNA inoculations, the one thing I have not seen done in any of these relatively small scale studies is to reconcile the results to the broader epidemiological data.
Kyle Beattie's big data analysis showing that the mRNA inoculation campaigns actually increased the incidence of COVID cases pretty much demolishes the notion that the inoculations are an effective defense.
https://newsletter.allfactsmatter.us/p/how-many-red-flags-are-enough
Similarly, when the rates of community spread increases after the inoculation ratio in a population passes 50% also cuts against the possibility of the inoculations being effective.
https://newsletter.allfactsmatter.us/p/no-return-to-normal-in-sight
Which means any study that only just now shows the inoculations to be ineffective is way behind the curve. That has already been proven in abundance.
I see nothing in Beattie's method that addresses causation. You already know you are looking at a data set where there are more cases and deaths in 2021. So you are going to plug in "vaccines" to that and somehow show that they caused what you already know happens in the system? How? You have no control system where the rise in cases/deaths doesn't happen. Can Beattie show that Taylor Swift downloads don't show the same "causation" as a negative control?
Beattie used Bayesian analysis to statistically impute causation. It's not direct evidence, but Bayesian analysis is a valid analytical method. In the absence of direct evidence it can be compelling.
I don't really do statistics. But, Wikipedia says Popper said that Bayesian analysis 'presupposes what it attempts to justify' which sounds exactly like my take on the paper to begin with, so I don't get the vibe that it is an appropriate approach to prove the vaccine caused something we know in advance already happened everywhere no matter what.
So you are saying that earlier on, the shots/boosters were actually preventing people from catching covid. And so their covid rate was genuinely lower than the unvaccinated. But now the shots are wearing off, and the unvaccinated have ever more natural immunity, so the unvaccinated are doing better?
And the reason the chart from the paper doesn't show this, is because it doesn't go far enough back, to where the shots were actually helping prevent infection? And if went much further back, the infection rate would be lower (early on) for the vaccinated, and higher (early on) for the unvaccinated?
I'm confused, because I thought the shots never were tested to prevent infection, and never did (except for the original Wuhan strain).
They have an efficacy window of 3 months. Circulating IgG leaks into the mucosa so as long as your IgG levels are jacked up to crazy levels, you have a sort of artificial mucosal immunity. Even if the trials didn't test this (because there was no random screening, PCR was only issued after symptoms were reported) various real-world studies have found the same short term infection efficacy.
One way we could "see" this efficacy is by noticing when it wore off. Like in the Israel dashboard in summer, 2021, the per-100k infection rates suddenly ticked upward for the double-dosed as infection efficacy went away. But that was the same time boosters were rush-authorized. So the signal was instantly hidden, but it seems from the Bar-On studies that most people transitioned from double-dosed to triple-dosed without any bump in infections. So they safely got back into the efficacy boat until the next boosters, and then the same thing repeated.
I'll say I was still surprised when the BA.5 survey paper came out, and previous reported infection rates were still lower in the boosted (of course there are biases in a survey). I thought the BA.1/2 wave would have evened the playing-field. But it doesn't seem that way.
I am not 100% convinced by this argument. The study period was Sept-Nov 2022. I would have thought that anyone with 1 or 2 shots only, would have gotten them at least 1 year prior to the study period, so would have at least 9 months of exposure after 3 months of protection. Shouldn't efficacy have reverted to nearly 0 by this time? Yet it shows 2 shots as doubling your odds of infection.
It also doesn't look good for the shots if 3 months of protection is balanced out by 9+ months of 2x risk! Am I missing something?
Also - an unrelated note, I don't know if you saw this https://hiddencomplexity.substack.com/p/about-the-igg4-trend article on IgG4. I'm not sure I understood it completely but he seems to be saying in one of the linked sub-articles ( https://hiddencomplexity.substack.com/p/chimeric-nature-of-galectin-3-and ) that IgG4, in addition to potential problems with tolerating the virus, also causes changes to the activity of Galectin-3 which apparently can cause all sorts of problems with fibrosis and formation of connective tissue in the wrong places ("IgG4 Related Disease"?).. which made me think of those rubbery clots.
I guess that maybe we can add a few more new worst case scenarios to the list :(
Looking into the galectin thing, there appears to be some confusion in Schroder, Bieneman regarding the GTNGTKR paper and what it was saying about galectin. GTNGKR is a loop, not a fold; in general the similarity between the NTD of coronaviruses and galectin may simply and unremarkably reflect that both are designed to bind to sugars; and in SARS-CoV-2 once again the fold quality is lost.
This is why I am wary of small-author-number papers, to be a bit snobby.
But the link is highly appreciated as I was previously ignorant of NL63's similarity to SARS-CoV-1/2
"According to the results of searches performed with the DALI protein structure database search server (2), whereas MHV NTD and human galectins share the same fold, the SARS-CoV and NL63-CoV C-domains each represent a novel fold (Fig. 2A and B). Interestingly, despite their different structures, NL63-CoV and SARS-CoV C-domains bind to overlapping regions on their common receptor, human angiotensin-converting enzyme 2 (ACE2) (Fig. 3A and B) (9). We previously hypothesized that SARS-CoV and NL63-CoV C-domains diverged from a common ancestor into different structures and then converged functionally to recognize the same ACE2 receptor (8, 9). In this report, we present evidence to support this hypothesis and expand the evolutionary discussion to include all three coronavirus genera." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302248/
This will be useful.
What the SLFS model has going for it is that the events being tracked only happen to outliers. The following implication of which... actually isn't depicted in the model, because a full simulation would have millions of squares obviously. Anyway it doesn't matter whether most double-injected (1x course of blue paint) stopped having blue paint a long time ago, it only matters that, ok, here were a few that got blue paint later in the game. So they're still in the "double-injected" group but they don't reflect the group. But, the group has these outliers who are short on natural immunity going into the study period and so the outliers cause the group as a whole to rack up more "hits" for the virus.
In particular, if anyone got the vaccine on a will-they-wont-they mandate holdout last-minute timing, they would be less likely to have a BA.1 wave infection, which is what confers the best protection ("last infected in BA.4/5" aren't protected because it actually consists of people infected right before or during the study, which is why it starts out at 0 at-risk *Edit: Just before, not during, these ones were all infected in the 90 day window before the study start.)
Oh, thank you. I thought that the short-lived efficacy of the vaccine was against "severe illness and death"(TM) due to lots of antibodies being pumped out. I didn't realize there was actual (short lived) protection against infection due to mucosal immunity. If that is true, maybe people who would die if they caught covid, really should be vaccinated. I do know a number of really old people who have had all four shots (and some the bivalent as well) and they seem okay, other than several of them having blood clots. I think they have no natural immune systems to speak of, so maybe the shot is a benefit to them.
And if covid really does do terrible things to T cells and dendritic cells and that leads to cancer and RSV, doesn't it make sense to get the shot every three months to get the mucosal immunity? If that's the sort of thing you care about? The people I know who are now getting fast growing, sudden cancer are all vaccinated, but not every three months.
Most of the people I know who are ultra boosted (with bivalent) are still hunkered down. It is the people I know who have had three shots who have decided that it's all over and they can go out to eat. They've mostly caught covid. They look terrible, but I don't know if it is due to the shot or due to the covid or due to being toyed with by psychopaths. There are so many variables.
I can't wish you a typical Merry Christmas since the 17th century Christian sect that I have worshipped with for the last four years (there are still holdouts, mostly in Ohio) considers every day to be Christmas. And that the celebration is internal, and not to be external. And that tomorrow will merely be "the day the world calls Christmas." However, I wish you the internal spiritual experience of the true holiday, on every day.
Severe/death efficacy should be long-lasting, as B Cells will do their job and ramp up antibodies when the virus shows up. There's no big danger for either the naturally or artificially immune if their antibodies go down, when it comes to severe outcomes.
Does that mean old people should take the shots? I don't think so. Antibodies are protective, but we could just give them to people when they are infected. There's no reason to use mRNA to turn people into factories for things that we can literally... produce in a factory.
Moreover, no matter which risk group you look at, severe outcomes and death still only affect a minority of infected people. So severe efficacy can never benefit most recipients. And anyone it doesn't benefit is just left with whatever the harms are from the shots. Even if the cost-benefit for some groups might seem positive, you are harming some people to protect others - human sacrifice, essentially.
Now, as for infection efficacy, that one is temporary because the super-high IgG antibody levels are going to fade and then you have no more mucosal immunity. Whereas for natural infection, tissue-resident memory T Cells go into your respiratory tract and you have "immunity" as properly understood - you don't get sick again. The big question, imo, was always whether the injections interfered with this. At this point I don't think they do.
As far as the virus's effect on T Cells, that is again going to be an individual phenomenon and not imply that everyone needs protection from the shots. Also, here, I think it is pretty safe to bet that the shots would show at least just as much, probably more general immunosuppression. In fact I'm at least toe-in-the-water on Team VAIDS, I think things like this https://unglossed.substack.com/p/would-die-for-pseudo-u and this https://twitter.com/alexmeshkin/status/1585261482253565953 in the Covid-vaccinated speak for themselves.
Overall, the CBA for the elderly is a difficult and nuanced subject. That's why I oppose attempts to just skirt the discussion with "look! chart! negative efficacy! OAS! No need to make hard calls here!" which are really fantasies.
Thank you for your wish, and likewise!
OK, a quick search reveals that there are papers out there talking about IgG antibodies in the mucosa. I guess I should not have expected any different. If the body can get IgA antibodies into the mucosa why would it not be able to get IgG antibodies into the mucosa?
https://pubmed.ncbi.nlm.nih.gov/32015473/
Because the mechanism (Fc receptor mediated transcytosis) occurs minimally in the upper respiratory tract. It occurs in a larger scale in the lower airways and GI mucosa. Look up neonatal Fc receptor mediated transcytosis.
IgA is more expected since B Cells take up residence and secrete it long term. Temporary IgG leakage makes sense since, besides the observed short-term efficacy of the Covid-19 injections, how else would one explain classic observations of injected flu vaccine efficacy against symptomatic infection, esp. in 1958 when H2 arrived so there wasn't any pre-existing sterilizing immunity.
https://unglossed.substack.com/i/51625377/pacific-theatre-asian-flu-vaccine
"The Asian vaccine was estimated to cause a three-fold reduction—that is, 66% protection—in the number of influenza cases as compared with the numbers in the [influenza-B-vaccine receiving] control group occurring nine days after [the second dose] and thereafter. Within the first eight days after [the second dose; and so, before additional seroconversion could take place] no differences were found [echoing 1943, when Francis and Salk’s injection appeared to work despite being delivered mid-wave]. The polyvalent influenza A vaccine [comprised of previously circulating strains] behaved just like the control influenza B vaccine, so it can be concluded that the stimulus of the up-to-date Asian antigen was necessary for protection. Recent published accounts of trials of Asian vaccines in the USA have given figures of effectiveness in the range of 40-67%."
Wait. I am getting the impression that this stuff is more complex than Big Pharma wants us to believe. Maybe I am wrong.
Good point - back to "Vaccine shows immune system wanted poster of the bad guy"!
Merry Christmas.
I think I understand the argument you are making but I suspect I need to read the paper to determine how they are measuring infections. Is it more PCR tests where anyone challenged with the virus, regardless of immunity, might yield a positive result, or was it based on actual symptoms?
Also, I would like to know how they measure that 30%. In the original Pfizer trials they used Relative Risk Reduction of getting one symptom and the control group had about a 0.84% risk of experiencing one symptom with the trial group having something like a 0.04% risk of experiencing one symptom.
I am not interested in a vaccine that reduces my risk of developing one symptom from below one percent to even further below one percent.
In this paper are they at least using ARR?
Also, what would allow them to draw more robust conclusions? Another 51,000 people who were never vaccinated and who could be matched on when they last had the virus?
It's adjusted Cox HR. The raw HR was only .87. The absolute benefit of the boosters is going to be pretty small since there aren't that many "cases" (positive antigen *edit: PCR, not antigen, I always confuse "NAAT" for "RAT," tests) to go around anyway.
The headline by-dose and by-prior-infection plots are Simon and Makuch / Kaplan Meier HR. HR should be the same as a person-days RR calculation in both cases since the slopes are steady. But I don't really know, it's statistics stuff.
Merry Christmas
Interesting thought Brian. When seeing "negative efficacy" data I immediately become hesitant because one would have to reason why such a phenomenon would occur, and that may end up resulting from OAS in some regard (although we've criticized it).
I think your argument is an interesting one. It at least makes sense that the more distant we get from Wuhan/D614G SARS-COV2 that we should expect a lag to occur, now catching up. It would be interesting to see what effect the bivalent boosters would have in the discussion, but apparently the uptake for these boosters have been far lower than people thought, and fortunately I think that even a bad respiratory season may not lead to more boosting due to fatigue.
As to Berenson, Berenson is indicative of someone that doesn't really read into studies and just takes the information at face value. Maybe it's a consequence of his old life as s journalist. When reading news reports on studies it's clear that the reporter just repeats verbatim what the study states, and then relies on other doctors/scientists to quote in their reports. It's like reporters spend so much time doing everything BUT reading the actual study.
Also, Merry Christmas to you and your family Brian! Thanks for the information and analysis you've provided the past year!
"So much time but reading the study" - Well, probably my approach on this one as well. I was already familiar with Shrestha's setup so I just made some assumptions and started putting fish in squares, haha. BUT DOES BERENSON EVEN PUT FISH IN SQUARES? WHAT IS ANYONE PAYING HIM FOR?
OAS of course makes no sense since it's a (false suggestion of a) dose-dependent relationship. But OAS is just an incoherent stand-in for "drugs really ARE sinful" in Berenson's mind.
And Merry Christmas likewise!
My own pretty worthless unscientific observation is that my vaxxed/boosted friends, family, and acquaintances didn't seem to catch the virus until after they got the 3rd shot. Now they're going for number 4 and all around me I see vaxxed out sick with whatever it's called now.
But my unvaxxed self, friends and family are not untouchable either. Eldest son (a shot virgin) had Delta last December and just now is getting over another milder case of the crud. So much depends on physique, age and behavior.
Merry Christmas, Brian! Thanks for your articles, they're always worth pondering.
I always value anecdotes. For myself, a never-Wuhan-er (probably asymptomatically immunized before the first lockdown thanks to being very active in the Bay), my January Omi bout has gotten me through the so-called tripledemic with just occasional scratchy throats, despite once again being active, going to the gym, etc. I do wish people were still ashamed to cough. I wanted that part of the whole thing to last. Now they do it without even thinking about it again. I just don't like coughing.
Merry Christmas as well!
I get pretty irked when people cough open mouthed around others. It was never right, not before nor with nor after covid.
I and many people I know of differing levels of vaccination (me being one of the unvaccinated) got caught up in the wave of Omicron. There's a ton of context that tends to get missed out in the discussion. I understand that there are serious concerns over the vaccines, but it can be a bit frustrating when we find information to fit the narrative rather than examine things for what we see.
Interestingly, given the timing of the booster I would be curious if your situation coincided with Omicron as well and it being the most escapiest of escaping variants relative to the prior ones.
Brian, Merry Christmas. 🎄
Thank you for work, I think you’ve really seal(ed) the deal on the Walrus.
Merry Christmas!
As everyone knows, the Walrus was Paul.
😂😂😂