Thank you so much for this post! I've been trying to wrap my head around OAS, and I've written about it previously and why I felt as if the mentions of OAS were being misattributed, including the UK data. I think your perspective is far better in your analysis, as I just posited that it may have been due to viral removal before antigen presentation since the N protein is sequestered within the virus, although that is definitely a parochial perspective.
I think this really just highlights that there's so much nuance and complexity to really discuss here and that we should be hesitant when we are adamant about a position. I'm really bad with virology and certain aspects of molecular biology. I find I much prefer to examine medicinal chemistry and pharmacology, so a lot of this tends to really go over my head and takes plenty of time to examine.
As much as I consider everything that goes on ridiculous, I do think we need to remain rational and not counter the craziness going on with our own misreadings and misinterpretations of the data, so thanks for your analysis!
Right, it's certainly plausible that early breakthrough infections are essentially abortive when it comes to whatever stage of infection would normally be followed by N seroconversion. And October, when the text appeared in the UKHSA document, was still very much "early breakthrough infection study season." But if the reader wasn't following MSM science journalism at the time, they wouldn't know that, and the writer could just say "Oh look it says 'recent', that means recent."
And studies of "post-Barnstable-era" breakthrough antibody kinetics *still* haven't really arrived. But post-Barnstable is when 99% of breakthrough infections occurred and is thus the only reality relevant for most of the injected.
Meanwhile, N-antibodies are shooting up among UK donors for the last months while the UKHSA comment saying N antibodies aren't rising is still scare-quoted everywhere.
That's a nice one. In general I agree that the innate immune system is better weaponry for the young and shouldn't be traded in for an antibody.
But beyond that, it's going out on quite a few limbs. I mentioned the limits with the Netherlands study in the "Neg" footnotes - https://unglossed.substack.com/p/neg#footnote-6 - so at the point where that post is speculating that the pseudouridine encourages an anti-fungal immune response and this is all tied up with why the overall response is tolerance instead of sensitization... it's all very hypothetical territory.
The Oregon cardiac deaths paper is pretty trippy. It seems that most (80%) of the "Covid +" who go on to have cardiac mortality also had cardiac history. But who knows... maybe some of the infected are dying 180 days after "recovery"...
Hi Brian, have discovered you courtesy of Mark L. Noticed Berenson has posted referring to this paper on monkey studies on boosting with omicron specific mRNA. The conclusion appears to be they are less effective than the original Wuhan strain booster at producing effective antibodies. Given the subject of this post I'd be interested to hear your thoughts on the study and it's findings:
Not to be macabre with the macaques, but the study is way too limited. What’s the biology of mRNA transfection with an Omicron protein vs a Wuhan protein to begin with, not in the context of a booster? Changes to the spike amino acid recipe can affect cellular output in different hosts, based on a million different factors.
And does mRNA + spike production + immune response on macaques really say anything about the outcomes for humans? The authors are in la-la-land when they say macaques have been well established as correlates for protection. Nothing is a correlate for protection for Omicron. Lastly, only eight test subjects? I look at the pre-boost antibody levels and those eight monkeys are already very skewed in antibody output. So did the high-pre-booster-antibody monkeys fall in the Wuhan booster or the Omicron booster set?
And what would the results of a non-boosted Omicron challenge? Oops, the study has no non-boosted macaques to work with, sorry. Geez, why couldn’t they just let these poor 8 monkeys go about their lives instead of pretending there was anything left to gain from infecting and sacrificing them without a large enough population to control for anything.
All that aside, in so far as the study suggests anything it’s that prior sensitization to the “wuhan spike” doesn’t impede immune response against Omicron in any meaningful way during actual infection.
See also my comments on the mouse / hamster vax study posted by Betty Lee.
Indeed. Despite my criticisms I don't find the outcome "tailored boosters not any better than vanilla boosters" implausible. Which means, infection efficacy will be fleeting, judging by the situation in Israel (0 infection efficacy in the under 60s for either triple-dosed or double-dosed)
IMPORTANT question - can you pls debunk or give your take on this study so that I can sleep through the night once more without thinking I'm going to get infected with disability-inducing omicron 3 times a year? LOL. Appreciate you! "Interestingly, we found that mice previously immunized with A.1-specific vaccines failed to elevate neutralizing antibody titers against B.1.1.529 following B.1.1.529-targeted boosting, suggesting pre-existing immunity may impact the efficacy of B.1.1.529- targeted boosters." - OAS? https://www.biorxiv.org/content/10.1101/2022.01.31.478520v1
That's a fun one. First, it wouldn't require any new study to demonstrate that vaccination with a homologous antigen -let's use X' - to a previously vaccinated antigen - X - probably won't result in a lot of antibodies against X'. This is the relevance of OAS in terms of vaccination. It's extrapolating this problem to the real world where things fall apart. Immunology has moved beyond antibodies since 1960. We know that injected vaccination can't provide the mucosal immunity that results from real infection in the first place, so the idea that "can't keep updating antibodies against mutations" is a problem supposes that we shouldn't want vaccinated people to go out and get infected in real life and update their mucosal immune response that way. Why not? Don't we want them to have mucosal immunity at some point? The point of OAS is "how can we make endlessly updating vaccines" not "are endlessly updated vaccines necessary, given real-world immune response after 'infection boosting'." There is no evidence that suggests the answer to the second question is yes, so why are we asking the first question to begin with?
Does this study support any extension of the vaccination relevance of OAS into real life? No.
If we look at Figure 2B, where the grey bars are double A.1 vaxxed + Omicron boosted and the red are double HA influenza vaxxed (control) + Omicron boosted, there's no "increase" in ELISA-measured binding against Omicron Receptor Binding Domain because A.1 already had higher anti-Omicron-RBD binding than the HA group ends up having.
Then the neutralization assay (C). Discard the bars, the dots are what matter. 2 of 5 HA influenza vaxxed + Omicron boosted don't pass this test either. This suggests the authors didn't calibrate the neutralization assay very well. A more sensitive assay might reveal more neutralizers in the A.1 vaxxed groups. Even so, neutralization assays are not real life.
Onto the hamsters, where theres 1-dose A.1 vaxxed, 1-dose Omicron vaxxed, and controls. A.1 vaxxed are a bit outperformed by the Omicron vax, but overall still do much "better" than the controls in terms of where the authors are able to find viral antigen or RNA on day 4. Better is in scare quotes because Omicron did not cause lesions or weight loss on any hamsters, it was totally mild (while earlier experiments with "Wuhan-strains" produced lesions) and focused on upper respiratory tract. But the A.1 vaxxed hamsters, again, had only 1 of 6 viral antigen in lung detection vs 5 of 6 in controls and 4 of 6 epitheilial viral antigen vs 2 of 6 omicron vaxxed and 6 of 6 controls. A.1 vaxxed still benefited against Omicron.
Again as I mention in footnote 2, injected vaccines might still be a net negative via "more plausible mechanisms" but it's not clear-cut. If Wuhan-spike-mRNA-transfection had 0 adverse events, then you would have to weigh protection against viremia with "maybe more reinfections over the course of a lifetime" and you might come up with "better for some." If you believe that the immune system is smart and knows what it's doing, you can see why either outcome could be true: The immune system should only encounter the virus in natural context, to not be confused, or the immune system will self-correct after "natural boosting" post injection.
I have a question. What exactly do high antibody levels mean anyway? I've had numerous Epstein-Barr virus blood tests done in the past few years. Without exception, the IgM is negative (since I first got mono at 17), but the IgG is super high (often going over 750), the EBNA is high, and the early antigen (EA) is positive. Some say this patten is indicative of reactivated Epstein-Barr but when I had a blood PCR test done last year, it was negative. So why is my body producing high levels of EBV antibodies? (Unless the virus is not in my bloodstream?)
Ideally, high antibodies should only correspond to recent exposure - either reinjection in the case of vaccines or a viral challenge that gets past innate suppression - with fadeout afterward. I think it also makes sense that during an actual secondary injection / infection, circulating antibodies are going to be "tied up" with the virus or destroyed bits from T-Cell-lysed cells.
Persistent high antibodies are a hallmark of autoimmunity, or so I understand the conventional wisdom to assert. So if long-lived plasma cells take up residence in a center of inflammation, they can just kick out their programmed antibodies around the clock; these antibodies could create a feedback loop leading to more inflammation, on and on until tolerance mechanisms sort things out. This is an inherent danger with any viral / bacterial infection because there's cellular destruction, inflammation, and novel antigens with potential resemblance to self-peptides (due to viral structures designed to interact with our cellular receptors, or bacterial structures designed to mimic the host biology, etc), all being thrown at the immune system at once. In fact the only reason we don't get Guillain-Barré or similar disorders after every infection is because the immune system usually pulls off the miracle of NOT crossing any wires. But when such outcomes occur, the immune system eventually gets the clue that it's not fighting an actual virus, most likely because there's too much antigen stimulation without the appropriate PAMP pathway markers, and tolerance kicks in.
Dormant viruses, in my intuition, don't mix well with autoimmune sensitization because the virus "expects" the immune system to keep it in check, and will replicate too fast if the immune sensitization drops, and this replication then re-sensitizes overactive immune response at the inflammatory centers. Spirochaete bacteria can lead to the same paradox. So you can end up with either lifelong asymptomatic presence - a sort of harmony - or lifelong autoimmunity in either scenario.
Interesting debate going here on OAS. You make some good points, it seems. Doesn't the real world data, such as we have, make it pretty certain that the vaxxed are indeed getting Omicron at higher rates? If not OAS, what is it?
I really would love if we could get granular, high quality data on who exactly is getting infected and when across all categories. Unvaxxed naive, vaxxed naive, unvaxxed natural immunity, vaxxed natural immunity, boosted naive and NI, how long since last dose, when were previous infections, etc.
Raw "negative efficacy" would not support OAS. OAS implies that something is "bad" (i.e. sinful) in real life about the inability to trick the immune system into making antibodies against A' after tricking it to make antibodies against A. Mere higher susceptibility to A' wouldn't be OAS: since you can't make antibodies to A' before infection, saying "reduced ability to make antibodies to A' causes the infection that has to precede making antibodies to A'" is logically incoherent.
So what would negative efficacy imply? Antibodies against A enhance infection by A' - which is more like Antibody Dependent Enhancement. Vanden Bossche has offered a very plausible mechanism, which I recycled for a post in https://unglossed.substack.com/p/neg
Now that almost everybody has been either exposed to many different variants or vaccinated, everybody has some imprinting (either natural or via vaccine).
Two questions:
1. If we were able to predict next variant A' (which we obviously can't) and vaccinate against that variant before it hit (now we can produce antibodies A' *before* we get infected) , wouldn't OAS mean that previously vaccinated would be more susceptible?
2. But the same thing also applies for people that were naturally infected.
Imprinting happens there as well. Right? This is what happens with flu. Immune system is imprinted with the first flu you encounter.
Let’s assume natural immunity against A is superior to artificial immunity against A’ because mucosal /cellular immune programming + related antigen recognition.
Are people juiced up with A’ antibodies better off than people juiced up with A antibodies (who now can’t have their artificial programming rewritten) in challenge with A’? Well, actually, maybe not - maybe a bit of difference leads to an enriched or more robust “immune correction” while still protecting against viremia. The funny thing is that OAS isn’t even sure which answer confirms the “sin” - a Eugyppius can fire off a post saying either result is proof of OAS!
Yes, and the more I look into both OAS and ADE the murkier it is.
And let's face it, because the data is so crappy (either by design or by incompetence) it's hard enough to see through the fog
if you are genuinely trying to uncover the truth. If you are just searching for confirmation of your prior belief or your hypothesis, then it's great because you can show pretty much anything.
It's also interesting that OAS might have occurred with H1N1
And these mRNA (and adenovirus) vaccines were developed and sold with the premise that we know exactly what happens in our body and what those developed antibodies will do.
Feb 4, 2022·edited Feb 4, 2022Liked by Brian Mowrey
Hmmm, I thought - in layman's terms - OAS (immune imprinting) basically meant that your first immune response to a pathogen set the tone for future immune responses to the same or similar pathogen. A suboptimal original immune response, in the case of the mRNA vaccine because it was specific to the S protein instead of the whole virus. This might result in a decreased ability to stave off subsequent symptomatic infections but shouldn't compromise the immune system's ability to combat severe illness so much. ADE, on the other hand, results in your immune system's inability to generate antibodies that are capable of recognizing and attacking the mutated virus. This essentially clears the way for the mutated variant to replicate unchecked, which results in a much greater vulnerability to both infection and severe illness.
The data we're seeing, mostly from other countries thus far, on Omicron seems to be suggesting an affinity for infecting vaccinated / boosted individuals relative to the unvaccinated, but not necessarily leading to more severe illness than in the vaccinated. So why wouldn't that be a greater signal of OAS than ADE? I mean, assuming OAS was actually a thing (I know you don't).
Because negative efficacy ≠ OAS. OAS is totally narrowly focused on generation of novel antibodies and has nothing to say about anything we know about immunity after 1960 - but it still retains "relevance" for vaccination. Lower-than-naive antigenic sensitivity to homologous versions of an antigen mean vaccination cannot generate antibodies to the homologous version. But *does* lower-than-naive antigenic sensitivity to homologous versions of previously-sensitized antigens have a real world relevance, even for the vaccinated? Neither "antibodies can mess up infection in other ways" nor "vaccine-induced immune response fails to induce the full suite of cellular memory immunity that we've come to discover after OAS was theorized" satisfy OAS. It's like asking whether nuclear fission "is alchemy."
Just one point I wanted to make.... I don't think my simplification was implying that negative efficacy = OAS. Rather, it's breaking efficacy down into the individual components of infection, illness and death and then assigning them to possible differentiating signals . Or maybe what you're saying is that no matter which of those components you select, it doesn't or can't be a signal of OAS. It's probably that. Thanks for the response.
Brian, greatly appreciate your balanced and sensible perspective as always. I don't know how you do it but you seem to truly be able to keep an open mind and not be blinded by confirmation bias. Your point about the samples being taken before seroconversion would normally complete throws a lot of doubt on the results.
That said, there does seem to be a decent amount of evidence suggesting that Omicron is more likely to infect a person with a lapsed 2 dose regimen - the population adjusted case rates - although this evidence is also full of possible confounders. But the anecdotal data certainly isn't positive. It will be interesting to see how this experiment plays out as (presumably) people stop getting these shots and normal life hopefully resumes.. will there be a long term pattern of greater illness in that population?
I see my concerns were sent up the chain. The brass seems to think the main issue in need of addressing was the small sample size... Perhaps they didn't actually read the memo. "the maqaque booster trials show the same effect [it literally doesn't, more self-brainwashing], and the idea extends far beyond sars-2 vaccines to the whole history of Influenza vaccination, and [literally that's it, that's the only 'history']"
I think most of the evidence that would fit that description is looking at "if infected" rates, which penalize the recently injected for renewed infection efficacy against Delta (though this actually makes the boosted look worse than the lapsed, as in https://unglossed.substack.com/p/funeral-for-a-fact#footnote-3)
As I mentioned in a comment below, I earlier pointed out that the unvaccinated are also having a surge of reinfections over in Israel, possibly at a higher rate than the Covid-vaccinated, possibly merely because the unvaccinated+infected in Israel were infected earlier / more often on average than the vaxxed - https://unglossed.substack.com/p/reinfections-in-israel
I do find it anecdotally convincing (including the Nathan Thompson video https://rumble.com/vnaocj-immune-system-lab-results-after-1st-and-2nd-jab.html) and plausible on a theoretical level that the injected are walking around with suppressed / sabotaged immune systems, possibly for months after the last dose, leading to more "getting sick" - but how does this balance out with the hugely jacked-up anti-spike antibodies prompted by boosters (https://jamanetwork.com/journals/jama/fullarticle/2786096), with IgG antibodies likely oozing into the mucosa to provide a temporary, artificial mucosal "neutralizing" effect? I think that short-term infection efficacy against Omicron from boosters is prima facie plausible.
If you attempt to ask a question that is not like "I read your article and it is genius" you get shot down as not having read his article. (see his comment session. It is a cemetery of open discussion. )
I think deattenuation happens on a much faster timeframe. For the Sabin live polio vaccine virus, for example, it probably deattenuates by the time it replicates enough in the recipient to be shed back out. This is why Sabin can cause poliomyelitis if caught second-hand by someone who isn't vaccinated - it essentially "is" polio. It doesn't take years or decades. Just a few cellular passages.
Maybe the timeline is actually slower. The SARS-CoV-2 variant Alpha (and probably Delta) featured amped-up Orf9b production which inproves TOM70 intracellular immunity suppression - https://www.nature.com/articles/s41586-021-04352-y - this is likely a recovered anti-immunity trait that was lost (became clonally "recessive") during cellular passage in the lab, but it still took months to reemerge in real life. But young people still did fine against Alpha / Delta, it wasn't a super-weapon. In the end, a "deattenuated" SARS-CoV-2 just means... a regular coronavirus, with the regular coronavirus intracellular immune evasion toolkit, which is probably really extensive and exquisite and cool. The pathogenicity of SARS-CoV-2 stems from apparent inflammatory or autoimmune responses triggered by weird accessory epitopes on the spike, or maybe weird senescence-alteration effects on monocytes - but not its essential "virulence." So I'm sanguine about potential increases to that virulence. I think they might happen (just as flu sometimes becomes more virulent, defying the trope that viruses "want to get milder"), but they won't dramatically alter our experience of the virus.
I'm a bit puzzled by that blog too. In the latest entry it seems he is talking about prion disease? He's kind of vague and only about 10% of the entry is relevant, the rest is summarized as "I'm angry because people won't listen to me". I don't know if prion disease is likely or at what incidence it would be expected.
My general thinking about prions is that they sound super scary, like ICE-9 or gray goo.. but in reality this must be something that we have evolved to deal with over the last billion years. To my thinking there must be some people who are susceptible to prion problems, and this is relatively rare, and everyone else has some mechanism that addresses the issue. The fact that it's been 2 years of this evil CCP bioweapon that is going to kill everyone on earth, but nothing really has showed up yet, makes be doubt this story. If we have learned one thing from this disaster, it's that our immune systems are amazingly complex and amazingly effective.
Really the same story with OAS. VEI does happen, but it's a fairly rare scenario, because our immune systems have evolved to avoid it. Vaccinating with a super narrow antigen in the midst of a pandemic is probably pushing our luck, and something like VEI may still come to pass, but on the other hand our immune systems are pretty awesome so maybe it's not very likely!
What's a lot more likely than irreparable harm from a "novel" CoV that's mostly natural? A lot of other kinds of problems stemming from injecting yourself with toxic crap that's TRULY novel (e.g. PEG and metylpseudouridine).. cancer, clots, autoimmune, neurological problems, etc.
Feb 3, 2022·edited Feb 3, 2022Liked by Brian Mowrey
The prion disease *may* be an issue for some vaccinated people because multiple natural barriers have been bypassed through means of injection - the jab. And such cases have been heard including the Astrazeneca researcher. In the normal course of virus exposure however interface (nose) will most likely have a very limited number of folded proteins circulating and all of them will be cleaned by our immune system way before they get to a nerve and all of them result of our Immune system apoptosing infected cells. Or ?
Right, if you want a hard-core bioweapon super-virus, well... Adenovirus, Coronavirus, Varicella zoster, Measles... All of these would sound apocalyptic if their mechanisms were described on the news as belonging to a "novel" virus. Yeah, maybe someone could edit the code in varicella zoster to remove the dormancy timer, and kill 9/10ths of the planet before the virus re-co-evolves with its host, I guess - but in general it's a lot easier to kill everyone with an injection than a virus.
Hi Brian. I must say that you have made a tremendous effort and wrote a very interesting article. I must admit that I have not analyzed every chart of it but you definitely have a point about NOT measuring antibodies at the right time, etc.
That said, I disagree with you on the main conclusion that there is no OAS. OAS for covid vaccinated exists, in my opinion.
The best proof of it is in real world observable events, and in statistics of thousands, not in measuring antibodies in a few convalescent guys. The observable events are
- Existing reinfections with a short recovery interval among the vaccinated
- UKHSA pretty much said that there is OAS when they admitted that the vaxed develop strong S antibodies after breakthrough infections, but do NOT develop N antibodies. This is the textbook definition of OAS.
I wrote a bunch of articles about it but the most recent one is:
I am open to changing my mind and I am not married to the concept of OAS.
But what else other than OAS can explain reinfections of the vaccinated that occur relatively often? My article has a few such testimonies pulled off reddit.
Right, and I'm in favor of considering anecdotal evidence in general. But at the moment, since the anecdotal evidence doesn't have any support in my own personal experience and since the Goldberg et al. study shows low rates of post-breakthrough reinfection, my vibe is that the anecdotes are rare outliers. And Omicron is driving reinfections for the unvaccinated just as much, if not more, than the Covid-vaccinated - https://unglossed.substack.com/p/reinfections-in-israel - likely due to the altered tropism in favor of the upper respiratory tract, circumventing resident T Cells leftover from "Wuhan-strain" infections. Realistically, it will be months before there are any studies providing data on post-Omicron reinfection rates, for either the naive / recovered / vaccinated.
Thanks. Both in the UK, whose data I used, and in Israel, they rely on PCR tests only (no record of symptoms). As many of my readers pointed out this is going to significantly muddle the picture for analysis. The first test could be a false positie, or the second. I am myself not sure how to deal with it. It is important.
Right - before Omicron, the low rate of reinfection was itself an effective "control" against false positives. It essentially didn't matter if the positive PCR was "false," since having a positive PCR conferred a ~.1 likelihood of later positive PCR. So you could say reinfections were rare, because it would be true even if all reinfections were false.
Now that Omicron "second positives" (reinfections) happen at the same rate as first positives, there's no way to decipher if they are false positives or true reinfections. For the moment I'm inclined to bet on the latter.
My own definition of a "real Covid case" is a positive test, accompanies with a fever. I understand why this is inconvenient for health authorities to measure.
The question I ask as a non-technical layperson in this field is not is OAS real but is there a need to get jabbed versus following something like FLCCC protocols? When I read an article like the below or see a summary of CDC/NIH flip flops and lies, you know something is not right.
OAS/AAS/BAS/CAS who cares! Is it safe and effective?
As I mention in footnote 2, there are plausible "non-OAS" concerns for whether vaccination sabotages the immune response that follows infection. But then you also have to ask if this tradeoff is still a net benefit for vulnerable groups - if the vaccine protects them against viremia. I think NO, because the vaccine essentially causes the same harms as viremia, by dispersing the script for spike throughout the body.
More complicated are the treatment protocols - they don't cause the harms that the vaccines do, but do they, by reducing symptoms, temper the immune response a bit, and is this possibly a net negative for some (i.e., if lifetime reinfections are higher after FLCCC treatment, are younger people better off roughing out the virus now? - this is my instinct, and partly why I didn't use any treatment during my likely-Omicron infection two weeks ago).
There's lots and lots of complexities to the issue - everything about immunity involves a built-in equilibrium, in which there's no free lunch, but deficiencies tend to self-correct over time. The OAS trope totally denies the latter reality which is why it gets my blood boiling.
Right, though it's still "asymptomatic as suppressed by the innate immune system" instead of asymptomatic as suppressed by drugs that made the virus attack less aggressively. Memory immunity is a learning algorithm - so just because some people learn without as much "struggle," doesn't mean you can go ahead and hide the harder part of the math book from them without messing up their test scores, to veer off into total cartoon-biology-mode.
It would depend on whether the innate system is enhanced by the treatment protocol yeah? If it gets past that then whether the body works quickly or slowly shouldn't be a problem in terms of generating memory immunity - I would have thought?
I don't understand biology or the protocols well enough to see where the assistance is delivered - at the mucosal / innate level or below.
Well, if we're talking ivermectin then we're in theoretical "binds against literally everything from polyprotein to RdRp to spike" land, with in vitro "5000-fold reduction" of production of viral RNA, as summarized in the retracted Zaidi / Dehgani-Mobaraki review, though whether that happens in vivo is unknown.
If we're just talking about boosting innate immunity, I still have my qualms but they're in my super-luddite "no pain no gain" mental territory.
Stupid question: If my understanding is correct, it's possible that blood analysis shows zero antibodies although you have capability of creating those antibodies
(via memory cells). Right? Otherwise our bodies would be full of antibodies for all sorts of diseases.
In the studies like this where you have a blood sample (and possibly no antibodies, but possibly B memory cells), does adding virus/bacteria trigger antibody production
Neutralization assays only use the plasma - meaning that the B Cells are subtracted. So to begin with, they don't really say anything about real life memory immune response, where stimulated memory B Cells divide and mature and start kicking out thousands of antibodies per second. You can really plug your own model for infection and immunity in here, since there's so much we actually don't know. In my model, antibody ramp-up isn't likely to stop reinfection, only to ward off viremia (virus shedding into bloodstream) - but exactly *because* of this deficiency, the immune system is going to be stimulated anew - so, likely increased/improved mucosal immunity / resident T Cells after "breakthrough" infection, leading to higher resilience against symptomatic / PCR-detected reinfection down the line. For Omicron I've speculated that the altered tropism forces the Covid-vaccinated and naturally infected alike to replay this learning experience, and now there will be higher defenses in the upper respiratory tract.
Interesting -- we'll probably have to wait until next winter to really see what happens after Omicron. As you pointed out, 1-2 months is not enough time
I just watched this very interesting interview with the pathologist Dr. Ryan Cole on Epoch TV today. He discusses an uptick in cancers, but also talks about Omicron and explains how it is not a variant of Omicron and why, and this explains why people with natural immunity are not protected from Omicron and can get it. My son is one. He had early Covid in Nov. 2019, is unvaxxed, but got Omicron 3 weeks ago. It was more like a flu...bad enough, but not too bad.
I'll have to switch to paid to watch it. But I referenced the altered tropism (to favor the upper respiratory tract) of Omicron as a plausible explanation for immune evasion during my own bout with the virus, I wonder if that is what he mentions as well
Bahahahahahahah oh god I did a double take, thinking I had already clicked an article of this title like 10 minutes ago. lolnope it's a punny bastard punnishing a pundit. I'll read it now.
Thank you so much for this post! I've been trying to wrap my head around OAS, and I've written about it previously and why I felt as if the mentions of OAS were being misattributed, including the UK data. I think your perspective is far better in your analysis, as I just posited that it may have been due to viral removal before antigen presentation since the N protein is sequestered within the virus, although that is definitely a parochial perspective.
I think this really just highlights that there's so much nuance and complexity to really discuss here and that we should be hesitant when we are adamant about a position. I'm really bad with virology and certain aspects of molecular biology. I find I much prefer to examine medicinal chemistry and pharmacology, so a lot of this tends to really go over my head and takes plenty of time to examine.
As much as I consider everything that goes on ridiculous, I do think we need to remain rational and not counter the craziness going on with our own misreadings and misinterpretations of the data, so thanks for your analysis!
Right, it's certainly plausible that early breakthrough infections are essentially abortive when it comes to whatever stage of infection would normally be followed by N seroconversion. And October, when the text appeared in the UKHSA document, was still very much "early breakthrough infection study season." But if the reader wasn't following MSM science journalism at the time, they wouldn't know that, and the writer could just say "Oh look it says 'recent', that means recent."
And studies of "post-Barnstable-era" breakthrough antibody kinetics *still* haven't really arrived. But post-Barnstable is when 99% of breakthrough infections occurred and is thus the only reality relevant for most of the injected.
Meanwhile, N-antibodies are shooting up among UK donors for the last months while the UKHSA comment saying N antibodies aren't rising is still scare-quoted everywhere.
Pieces coming together while bio-logical coherence breaks further apart?
https://www.rintrah.nl/suppression-of-the-innate-immune-system-the-main-cause-of-the-pandemic-of-the-fully-vaccinated/
That's a nice one. In general I agree that the innate immune system is better weaponry for the young and shouldn't be traded in for an antibody.
But beyond that, it's going out on quite a few limbs. I mentioned the limits with the Netherlands study in the "Neg" footnotes - https://unglossed.substack.com/p/neg#footnote-6 - so at the point where that post is speculating that the pseudouridine encourages an anti-fungal immune response and this is all tied up with why the overall response is tolerance instead of sensitization... it's all very hypothetical territory.
The Oregon cardiac deaths paper is pretty trippy. It seems that most (80%) of the "Covid +" who go on to have cardiac mortality also had cardiac history. But who knows... maybe some of the infected are dying 180 days after "recovery"...
Hi Brian, have discovered you courtesy of Mark L. Noticed Berenson has posted referring to this paper on monkey studies on boosting with omicron specific mRNA. The conclusion appears to be they are less effective than the original Wuhan strain booster at producing effective antibodies. Given the subject of this post I'd be interested to hear your thoughts on the study and it's findings:
https://www.biorxiv.org/content/10.1101/2022.02.03.479037v1?
to paste from another thread:
Not to be macabre with the macaques, but the study is way too limited. What’s the biology of mRNA transfection with an Omicron protein vs a Wuhan protein to begin with, not in the context of a booster? Changes to the spike amino acid recipe can affect cellular output in different hosts, based on a million different factors.
And does mRNA + spike production + immune response on macaques really say anything about the outcomes for humans? The authors are in la-la-land when they say macaques have been well established as correlates for protection. Nothing is a correlate for protection for Omicron. Lastly, only eight test subjects? I look at the pre-boost antibody levels and those eight monkeys are already very skewed in antibody output. So did the high-pre-booster-antibody monkeys fall in the Wuhan booster or the Omicron booster set?
And what would the results of a non-boosted Omicron challenge? Oops, the study has no non-boosted macaques to work with, sorry. Geez, why couldn’t they just let these poor 8 monkeys go about their lives instead of pretending there was anything left to gain from infecting and sacrificing them without a large enough population to control for anything.
All that aside, in so far as the study suggests anything it’s that prior sensitization to the “wuhan spike” doesn’t impede immune response against Omicron in any meaningful way during actual infection.
See also my comments on the mouse / hamster vax study posted by Betty Lee.
Thanks! The human trial results should be interesting.
Indeed. Despite my criticisms I don't find the outcome "tailored boosters not any better than vanilla boosters" implausible. Which means, infection efficacy will be fleeting, judging by the situation in Israel (0 infection efficacy in the under 60s for either triple-dosed or double-dosed)
IMPORTANT question - can you pls debunk or give your take on this study so that I can sleep through the night once more without thinking I'm going to get infected with disability-inducing omicron 3 times a year? LOL. Appreciate you! "Interestingly, we found that mice previously immunized with A.1-specific vaccines failed to elevate neutralizing antibody titers against B.1.1.529 following B.1.1.529-targeted boosting, suggesting pre-existing immunity may impact the efficacy of B.1.1.529- targeted boosters." - OAS? https://www.biorxiv.org/content/10.1101/2022.01.31.478520v1
That's a fun one. First, it wouldn't require any new study to demonstrate that vaccination with a homologous antigen -let's use X' - to a previously vaccinated antigen - X - probably won't result in a lot of antibodies against X'. This is the relevance of OAS in terms of vaccination. It's extrapolating this problem to the real world where things fall apart. Immunology has moved beyond antibodies since 1960. We know that injected vaccination can't provide the mucosal immunity that results from real infection in the first place, so the idea that "can't keep updating antibodies against mutations" is a problem supposes that we shouldn't want vaccinated people to go out and get infected in real life and update their mucosal immune response that way. Why not? Don't we want them to have mucosal immunity at some point? The point of OAS is "how can we make endlessly updating vaccines" not "are endlessly updated vaccines necessary, given real-world immune response after 'infection boosting'." There is no evidence that suggests the answer to the second question is yes, so why are we asking the first question to begin with?
Does this study support any extension of the vaccination relevance of OAS into real life? No.
If we look at Figure 2B, where the grey bars are double A.1 vaxxed + Omicron boosted and the red are double HA influenza vaxxed (control) + Omicron boosted, there's no "increase" in ELISA-measured binding against Omicron Receptor Binding Domain because A.1 already had higher anti-Omicron-RBD binding than the HA group ends up having.
Then the neutralization assay (C). Discard the bars, the dots are what matter. 2 of 5 HA influenza vaxxed + Omicron boosted don't pass this test either. This suggests the authors didn't calibrate the neutralization assay very well. A more sensitive assay might reveal more neutralizers in the A.1 vaxxed groups. Even so, neutralization assays are not real life.
Onto the hamsters, where theres 1-dose A.1 vaxxed, 1-dose Omicron vaxxed, and controls. A.1 vaxxed are a bit outperformed by the Omicron vax, but overall still do much "better" than the controls in terms of where the authors are able to find viral antigen or RNA on day 4. Better is in scare quotes because Omicron did not cause lesions or weight loss on any hamsters, it was totally mild (while earlier experiments with "Wuhan-strains" produced lesions) and focused on upper respiratory tract. But the A.1 vaxxed hamsters, again, had only 1 of 6 viral antigen in lung detection vs 5 of 6 in controls and 4 of 6 epitheilial viral antigen vs 2 of 6 omicron vaxxed and 6 of 6 controls. A.1 vaxxed still benefited against Omicron.
Again as I mention in footnote 2, injected vaccines might still be a net negative via "more plausible mechanisms" but it's not clear-cut. If Wuhan-spike-mRNA-transfection had 0 adverse events, then you would have to weigh protection against viremia with "maybe more reinfections over the course of a lifetime" and you might come up with "better for some." If you believe that the immune system is smart and knows what it's doing, you can see why either outcome could be true: The immune system should only encounter the virus in natural context, to not be confused, or the immune system will self-correct after "natural boosting" post injection.
I have a question. What exactly do high antibody levels mean anyway? I've had numerous Epstein-Barr virus blood tests done in the past few years. Without exception, the IgM is negative (since I first got mono at 17), but the IgG is super high (often going over 750), the EBNA is high, and the early antigen (EA) is positive. Some say this patten is indicative of reactivated Epstein-Barr but when I had a blood PCR test done last year, it was negative. So why is my body producing high levels of EBV antibodies? (Unless the virus is not in my bloodstream?)
Ideally, high antibodies should only correspond to recent exposure - either reinjection in the case of vaccines or a viral challenge that gets past innate suppression - with fadeout afterward. I think it also makes sense that during an actual secondary injection / infection, circulating antibodies are going to be "tied up" with the virus or destroyed bits from T-Cell-lysed cells.
Persistent high antibodies are a hallmark of autoimmunity, or so I understand the conventional wisdom to assert. So if long-lived plasma cells take up residence in a center of inflammation, they can just kick out their programmed antibodies around the clock; these antibodies could create a feedback loop leading to more inflammation, on and on until tolerance mechanisms sort things out. This is an inherent danger with any viral / bacterial infection because there's cellular destruction, inflammation, and novel antigens with potential resemblance to self-peptides (due to viral structures designed to interact with our cellular receptors, or bacterial structures designed to mimic the host biology, etc), all being thrown at the immune system at once. In fact the only reason we don't get Guillain-Barré or similar disorders after every infection is because the immune system usually pulls off the miracle of NOT crossing any wires. But when such outcomes occur, the immune system eventually gets the clue that it's not fighting an actual virus, most likely because there's too much antigen stimulation without the appropriate PAMP pathway markers, and tolerance kicks in.
Dormant viruses, in my intuition, don't mix well with autoimmune sensitization because the virus "expects" the immune system to keep it in check, and will replicate too fast if the immune sensitization drops, and this replication then re-sensitizes overactive immune response at the inflammatory centers. Spirochaete bacteria can lead to the same paradox. So you can end up with either lifelong asymptomatic presence - a sort of harmony - or lifelong autoimmunity in either scenario.
Interesting debate going here on OAS. You make some good points, it seems. Doesn't the real world data, such as we have, make it pretty certain that the vaxxed are indeed getting Omicron at higher rates? If not OAS, what is it?
I really would love if we could get granular, high quality data on who exactly is getting infected and when across all categories. Unvaxxed naive, vaxxed naive, unvaxxed natural immunity, vaxxed natural immunity, boosted naive and NI, how long since last dose, when were previous infections, etc.
Raw "negative efficacy" would not support OAS. OAS implies that something is "bad" (i.e. sinful) in real life about the inability to trick the immune system into making antibodies against A' after tricking it to make antibodies against A. Mere higher susceptibility to A' wouldn't be OAS: since you can't make antibodies to A' before infection, saying "reduced ability to make antibodies to A' causes the infection that has to precede making antibodies to A'" is logically incoherent.
So what would negative efficacy imply? Antibodies against A enhance infection by A' - which is more like Antibody Dependent Enhancement. Vanden Bossche has offered a very plausible mechanism, which I recycled for a post in https://unglossed.substack.com/p/neg
Now that almost everybody has been either exposed to many different variants or vaccinated, everybody has some imprinting (either natural or via vaccine).
Two questions:
1. If we were able to predict next variant A' (which we obviously can't) and vaccinate against that variant before it hit (now we can produce antibodies A' *before* we get infected) , wouldn't OAS mean that previously vaccinated would be more susceptible?
2. But the same thing also applies for people that were naturally infected.
Imprinting happens there as well. Right? This is what happens with flu. Immune system is imprinted with the first flu you encounter.
Let’s assume natural immunity against A is superior to artificial immunity against A’ because mucosal /cellular immune programming + related antigen recognition.
Are people juiced up with A’ antibodies better off than people juiced up with A antibodies (who now can’t have their artificial programming rewritten) in challenge with A’? Well, actually, maybe not - maybe a bit of difference leads to an enriched or more robust “immune correction” while still protecting against viremia. The funny thing is that OAS isn’t even sure which answer confirms the “sin” - a Eugyppius can fire off a post saying either result is proof of OAS!
Yes, and the more I look into both OAS and ADE the murkier it is.
And let's face it, because the data is so crappy (either by design or by incompetence) it's hard enough to see through the fog
if you are genuinely trying to uncover the truth. If you are just searching for confirmation of your prior belief or your hypothesis, then it's great because you can show pretty much anything.
It's also interesting that OAS might have occurred with H1N1
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3165229/
but it's remarkable that we really don't know much and for sure.
It's also clear that many vaccines are a product of guess as opposed to deep and solid understanding:
https://www.nature.com/articles/nm1216
And these mRNA (and adenovirus) vaccines were developed and sold with the premise that we know exactly what happens in our body and what those developed antibodies will do.
Hmmm, I thought - in layman's terms - OAS (immune imprinting) basically meant that your first immune response to a pathogen set the tone for future immune responses to the same or similar pathogen. A suboptimal original immune response, in the case of the mRNA vaccine because it was specific to the S protein instead of the whole virus. This might result in a decreased ability to stave off subsequent symptomatic infections but shouldn't compromise the immune system's ability to combat severe illness so much. ADE, on the other hand, results in your immune system's inability to generate antibodies that are capable of recognizing and attacking the mutated virus. This essentially clears the way for the mutated variant to replicate unchecked, which results in a much greater vulnerability to both infection and severe illness.
The data we're seeing, mostly from other countries thus far, on Omicron seems to be suggesting an affinity for infecting vaccinated / boosted individuals relative to the unvaccinated, but not necessarily leading to more severe illness than in the vaccinated. So why wouldn't that be a greater signal of OAS than ADE? I mean, assuming OAS was actually a thing (I know you don't).
Because negative efficacy ≠ OAS. OAS is totally narrowly focused on generation of novel antibodies and has nothing to say about anything we know about immunity after 1960 - but it still retains "relevance" for vaccination. Lower-than-naive antigenic sensitivity to homologous versions of an antigen mean vaccination cannot generate antibodies to the homologous version. But *does* lower-than-naive antigenic sensitivity to homologous versions of previously-sensitized antigens have a real world relevance, even for the vaccinated? Neither "antibodies can mess up infection in other ways" nor "vaccine-induced immune response fails to induce the full suite of cellular memory immunity that we've come to discover after OAS was theorized" satisfy OAS. It's like asking whether nuclear fission "is alchemy."
I said layman's terms! LOL.
Just one point I wanted to make.... I don't think my simplification was implying that negative efficacy = OAS. Rather, it's breaking efficacy down into the individual components of infection, illness and death and then assigning them to possible differentiating signals . Or maybe what you're saying is that no matter which of those components you select, it doesn't or can't be a signal of OAS. It's probably that. Thanks for the response.
Brian, greatly appreciate your balanced and sensible perspective as always. I don't know how you do it but you seem to truly be able to keep an open mind and not be blinded by confirmation bias. Your point about the samples being taken before seroconversion would normally complete throws a lot of doubt on the results.
That said, there does seem to be a decent amount of evidence suggesting that Omicron is more likely to infect a person with a lapsed 2 dose regimen - the population adjusted case rates - although this evidence is also full of possible confounders. But the anecdotal data certainly isn't positive. It will be interesting to see how this experiment plays out as (presumably) people stop getting these shots and normal life hopefully resumes.. will there be a long term pattern of greater illness in that population?
I see my concerns were sent up the chain. The brass seems to think the main issue in need of addressing was the small sample size... Perhaps they didn't actually read the memo. "the maqaque booster trials show the same effect [it literally doesn't, more self-brainwashing], and the idea extends far beyond sars-2 vaccines to the whole history of Influenza vaccination, and [literally that's it, that's the only 'history']"
I think most of the evidence that would fit that description is looking at "if infected" rates, which penalize the recently injected for renewed infection efficacy against Delta (though this actually makes the boosted look worse than the lapsed, as in https://unglossed.substack.com/p/funeral-for-a-fact#footnote-3)
As I mentioned in a comment below, I earlier pointed out that the unvaccinated are also having a surge of reinfections over in Israel, possibly at a higher rate than the Covid-vaccinated, possibly merely because the unvaccinated+infected in Israel were infected earlier / more often on average than the vaxxed - https://unglossed.substack.com/p/reinfections-in-israel
I do find it anecdotally convincing (including the Nathan Thompson video https://rumble.com/vnaocj-immune-system-lab-results-after-1st-and-2nd-jab.html) and plausible on a theoretical level that the injected are walking around with suppressed / sabotaged immune systems, possibly for months after the last dose, leading to more "getting sick" - but how does this balance out with the hugely jacked-up anti-spike antibodies prompted by boosters (https://jamanetwork.com/journals/jama/fullarticle/2786096), with IgG antibodies likely oozing into the mucosa to provide a temporary, artificial mucosal "neutralizing" effect? I think that short-term infection efficacy against Omicron from boosters is prima facie plausible.
Ok, off topic but what do you think of the doom and gloom theory of the Soritkin blog ? https://harvard2thebighouse.substack.com/p/a-grin-without-a-cat he is convinced that the virus will deattenuate from its present form to a full, true widowmaker.
I really would like to see a post on that.
He brings up this article often https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5787669/pdf/nihms925368.pdf
If you attempt to ask a question that is not like "I read your article and it is genius" you get shot down as not having read his article. (see his comment session. It is a cemetery of open discussion. )
I think deattenuation happens on a much faster timeframe. For the Sabin live polio vaccine virus, for example, it probably deattenuates by the time it replicates enough in the recipient to be shed back out. This is why Sabin can cause poliomyelitis if caught second-hand by someone who isn't vaccinated - it essentially "is" polio. It doesn't take years or decades. Just a few cellular passages.
Maybe the timeline is actually slower. The SARS-CoV-2 variant Alpha (and probably Delta) featured amped-up Orf9b production which inproves TOM70 intracellular immunity suppression - https://www.nature.com/articles/s41586-021-04352-y - this is likely a recovered anti-immunity trait that was lost (became clonally "recessive") during cellular passage in the lab, but it still took months to reemerge in real life. But young people still did fine against Alpha / Delta, it wasn't a super-weapon. In the end, a "deattenuated" SARS-CoV-2 just means... a regular coronavirus, with the regular coronavirus intracellular immune evasion toolkit, which is probably really extensive and exquisite and cool. The pathogenicity of SARS-CoV-2 stems from apparent inflammatory or autoimmune responses triggered by weird accessory epitopes on the spike, or maybe weird senescence-alteration effects on monocytes - but not its essential "virulence." So I'm sanguine about potential increases to that virulence. I think they might happen (just as flu sometimes becomes more virulent, defying the trope that viruses "want to get milder"), but they won't dramatically alter our experience of the virus.
I loved this answer. Good points.
I'm a bit puzzled by that blog too. In the latest entry it seems he is talking about prion disease? He's kind of vague and only about 10% of the entry is relevant, the rest is summarized as "I'm angry because people won't listen to me". I don't know if prion disease is likely or at what incidence it would be expected.
My general thinking about prions is that they sound super scary, like ICE-9 or gray goo.. but in reality this must be something that we have evolved to deal with over the last billion years. To my thinking there must be some people who are susceptible to prion problems, and this is relatively rare, and everyone else has some mechanism that addresses the issue. The fact that it's been 2 years of this evil CCP bioweapon that is going to kill everyone on earth, but nothing really has showed up yet, makes be doubt this story. If we have learned one thing from this disaster, it's that our immune systems are amazingly complex and amazingly effective.
Really the same story with OAS. VEI does happen, but it's a fairly rare scenario, because our immune systems have evolved to avoid it. Vaccinating with a super narrow antigen in the midst of a pandemic is probably pushing our luck, and something like VEI may still come to pass, but on the other hand our immune systems are pretty awesome so maybe it's not very likely!
What's a lot more likely than irreparable harm from a "novel" CoV that's mostly natural? A lot of other kinds of problems stemming from injecting yourself with toxic crap that's TRULY novel (e.g. PEG and metylpseudouridine).. cancer, clots, autoimmune, neurological problems, etc.
The prion disease *may* be an issue for some vaccinated people because multiple natural barriers have been bypassed through means of injection - the jab. And such cases have been heard including the Astrazeneca researcher. In the normal course of virus exposure however interface (nose) will most likely have a very limited number of folded proteins circulating and all of them will be cleaned by our immune system way before they get to a nerve and all of them result of our Immune system apoptosing infected cells. Or ?
Right, if you want a hard-core bioweapon super-virus, well... Adenovirus, Coronavirus, Varicella zoster, Measles... All of these would sound apocalyptic if their mechanisms were described on the news as belonging to a "novel" virus. Yeah, maybe someone could edit the code in varicella zoster to remove the dormancy timer, and kill 9/10ths of the planet before the virus re-co-evolves with its host, I guess - but in general it's a lot easier to kill everyone with an injection than a virus.
Hi Brian. I must say that you have made a tremendous effort and wrote a very interesting article. I must admit that I have not analyzed every chart of it but you definitely have a point about NOT measuring antibodies at the right time, etc.
That said, I disagree with you on the main conclusion that there is no OAS. OAS for covid vaccinated exists, in my opinion.
The best proof of it is in real world observable events, and in statistics of thousands, not in measuring antibodies in a few convalescent guys. The observable events are
- Existing reinfections with a short recovery interval among the vaccinated
- UKHSA pretty much said that there is OAS when they admitted that the vaxed develop strong S antibodies after breakthrough infections, but do NOT develop N antibodies. This is the textbook definition of OAS.
I wrote a bunch of articles about it but the most recent one is:
https://igorchudov.substack.com/p/ukhsa-explains-endless-reinfections
I am open to changing my mind and I am not married to the concept of OAS.
But what else other than OAS can explain reinfections of the vaccinated that occur relatively often? My article has a few such testimonies pulled off reddit.
Right, and I'm in favor of considering anecdotal evidence in general. But at the moment, since the anecdotal evidence doesn't have any support in my own personal experience and since the Goldberg et al. study shows low rates of post-breakthrough reinfection, my vibe is that the anecdotes are rare outliers. And Omicron is driving reinfections for the unvaccinated just as much, if not more, than the Covid-vaccinated - https://unglossed.substack.com/p/reinfections-in-israel - likely due to the altered tropism in favor of the upper respiratory tract, circumventing resident T Cells leftover from "Wuhan-strain" infections. Realistically, it will be months before there are any studies providing data on post-Omicron reinfection rates, for either the naive / recovered / vaccinated.
Thanks. Both in the UK, whose data I used, and in Israel, they rely on PCR tests only (no record of symptoms). As many of my readers pointed out this is going to significantly muddle the picture for analysis. The first test could be a false positie, or the second. I am myself not sure how to deal with it. It is important.
Right - before Omicron, the low rate of reinfection was itself an effective "control" against false positives. It essentially didn't matter if the positive PCR was "false," since having a positive PCR conferred a ~.1 likelihood of later positive PCR. So you could say reinfections were rare, because it would be true even if all reinfections were false.
Now that Omicron "second positives" (reinfections) happen at the same rate as first positives, there's no way to decipher if they are false positives or true reinfections. For the moment I'm inclined to bet on the latter.
My own definition of a "real Covid case" is a positive test, accompanies with a fever. I understand why this is inconvenient for health authorities to measure.
not trying to refute anything in this article (because I can't) but here is another:
https://palexander.substack.com/p/original-antigenic-sin-mortal-antigenic
The question I ask as a non-technical layperson in this field is not is OAS real but is there a need to get jabbed versus following something like FLCCC protocols? When I read an article like the below or see a summary of CDC/NIH flip flops and lies, you know something is not right.
OAS/AAS/BAS/CAS who cares! Is it safe and effective?
https://www.canadiancovidcarealliance.org/media-resources/the-pfizer-inoculations-for-covid-19-more-harm-than-good-2/
As I mention in footnote 2, there are plausible "non-OAS" concerns for whether vaccination sabotages the immune response that follows infection. But then you also have to ask if this tradeoff is still a net benefit for vulnerable groups - if the vaccine protects them against viremia. I think NO, because the vaccine essentially causes the same harms as viremia, by dispersing the script for spike throughout the body.
More complicated are the treatment protocols - they don't cause the harms that the vaccines do, but do they, by reducing symptoms, temper the immune response a bit, and is this possibly a net negative for some (i.e., if lifetime reinfections are higher after FLCCC treatment, are younger people better off roughing out the virus now? - this is my instinct, and partly why I didn't use any treatment during my likely-Omicron infection two weeks ago).
There's lots and lots of complexities to the issue - everything about immunity involves a built-in equilibrium, in which there's no free lunch, but deficiencies tend to self-correct over time. The OAS trope totally denies the latter reality which is why it gets my blood boiling.
If following a treatment protocol is the same as mild or asymptomatic infection, they may be ok?:
https://www.cell.com/cell/fulltext/S0092-8674(20)31008-4?rss=yes
Robust T Cell Immunity in Convalescent Individuals with Asymptomatic or Mild COVID-19
Right, though it's still "asymptomatic as suppressed by the innate immune system" instead of asymptomatic as suppressed by drugs that made the virus attack less aggressively. Memory immunity is a learning algorithm - so just because some people learn without as much "struggle," doesn't mean you can go ahead and hide the harder part of the math book from them without messing up their test scores, to veer off into total cartoon-biology-mode.
It would depend on whether the innate system is enhanced by the treatment protocol yeah? If it gets past that then whether the body works quickly or slowly shouldn't be a problem in terms of generating memory immunity - I would have thought?
I don't understand biology or the protocols well enough to see where the assistance is delivered - at the mucosal / innate level or below.
Well, if we're talking ivermectin then we're in theoretical "binds against literally everything from polyprotein to RdRp to spike" land, with in vitro "5000-fold reduction" of production of viral RNA, as summarized in the retracted Zaidi / Dehgani-Mobaraki review, though whether that happens in vivo is unknown.
If we're just talking about boosting innate immunity, I still have my qualms but they're in my super-luddite "no pain no gain" mental territory.
If there was OAS, what would you expect to see (both in terms of case/hospitalization/death data say in the UK and at individual level over time)?
Stupid question: If my understanding is correct, it's possible that blood analysis shows zero antibodies although you have capability of creating those antibodies
(via memory cells). Right? Otherwise our bodies would be full of antibodies for all sorts of diseases.
In the studies like this where you have a blood sample (and possibly no antibodies, but possibly B memory cells), does adding virus/bacteria trigger antibody production
in this blood sample?
Neutralization assays only use the plasma - meaning that the B Cells are subtracted. So to begin with, they don't really say anything about real life memory immune response, where stimulated memory B Cells divide and mature and start kicking out thousands of antibodies per second. You can really plug your own model for infection and immunity in here, since there's so much we actually don't know. In my model, antibody ramp-up isn't likely to stop reinfection, only to ward off viremia (virus shedding into bloodstream) - but exactly *because* of this deficiency, the immune system is going to be stimulated anew - so, likely increased/improved mucosal immunity / resident T Cells after "breakthrough" infection, leading to higher resilience against symptomatic / PCR-detected reinfection down the line. For Omicron I've speculated that the altered tropism forces the Covid-vaccinated and naturally infected alike to replay this learning experience, and now there will be higher defenses in the upper respiratory tract.
Interesting -- we'll probably have to wait until next winter to really see what happens after Omicron. As you pointed out, 1-2 months is not enough time
to say anything but speculate.
re: reinfections
https://igorchudov.substack.com/p/uk-reinfections-show-huge-undercount
An interesting alternative opinion, thanks! We need more debate on this to seek the actual truth.
https://nakedemperor.substack.com/
It’s a shame he bounced you from his substack. This kind of back and forth is necessary. Thank you.
Dissent, debate... only losers bother with that stuff!
Lol.
I just watched this very interesting interview with the pathologist Dr. Ryan Cole on Epoch TV today. He discusses an uptick in cancers, but also talks about Omicron and explains how it is not a variant of Omicron and why, and this explains why people with natural immunity are not protected from Omicron and can get it. My son is one. He had early Covid in Nov. 2019, is unvaxxed, but got Omicron 3 weeks ago. It was more like a flu...bad enough, but not too bad.
https://www.theepochtimes.com/dr-ryan-cole-alarming-cancer-trend-suggests-covid-19-vaccines-alter-natural-immune-response_4250442.html?&utm_medium=AmericanThoughtLeaders&utm_source=Others&utm_campaign=ATL-Dr.%20Ryan%20Cole&utm_content=2-1-2022&fbclid=IwAR1b1OipQfsDq-OSKezX0XG-Wt1G1BugHr60SQRbT4C8xsOgBN0XLZNbIkQ
I'll have to switch to paid to watch it. But I referenced the altered tropism (to favor the upper respiratory tract) of Omicron as a plausible explanation for immune evasion during my own bout with the virus, I wonder if that is what he mentions as well
You probably know, but paying for Epoch is totally worth it. One of the very few trustworthy general news organizations.
Bahahahahahahah oh god I did a double take, thinking I had already clicked an article of this title like 10 minutes ago. lolnope it's a punny bastard punnishing a pundit. I'll read it now.