Just what, actually, *is* "Covid-19 pneumonia"? Interpreting the significance of IgG4 for future infections is helped by understanding severe disease to begin with.
A couple of passages in the Pillai video caught my attention:
31:55-32:30: "And it is this suboptimal immune response which, in an infection like Covid-19, might be causing this deep underbelly of viral variants to emerge. And this is why we should worry about the disease, worry about more people getting immunity from severe infection rather than vaccination. So vaccination is going to control infection rapidly if you are infected, whereas if you get severe immunity [through infection], true, you will eventually get an immune response, eventually if you survive you may be protected for at least some years, but you may generated more viral variants, which is a danger."
Taken at face value, this statement (i.e. that only severe cases drive the production of variants) does not seem to be a very good argument for mass-vaccination, but I strongly suspect that this sort of observation was heard as 'vaccinate everyone cuz who knows if you're going to have a bad case and feed the variant monster'. I distinctly remember that idea showing up in the mainstream press. It would have been helpful if Pillai had been more precise, but I suspect he (like just about every other 'expert' vaccinologist) was on board with the 'vaccinate everyone' program.
34:07-34:42 "...we can either, with good treatments perhaps survive, which is happening more and more today, or we might succumb. And that's one of the things that, even today there is a mortality, and the mortality is tending to happen more in people who were not vaccinated, who did not have any preexisting immunity, and form this entire cycle of going through severe inflammation and then basically altering adaptive immunity, allowing inflammation to persist..."
Again, Pillai seems to be simplifying the picture so as to support mass vaccination. Why were we not provided with *any* age and comorbidity stratified risk/benefit analyses (not in this video, of course, but in general) as with any other pharmaceutical (and especially with radically new ones like these).
39:18-40:00 "...as we develop adaptive immunity in the population, this [i.e. severe outcomes] is not going to be as bad. Even if suppose there was no vaccine, all of us are the descendants of survivors... If there was no vaccine we would eventually have survivors who had low mild immune response and they would procreate and then the whole world would be filled with people who maybe have no genetic susceptibilities and are better protected. That is possible. But now and fortunately for us we have vaccination and maybe more of our species will not be culled out by this virus, and we have antibodies being generated so it'll become milder..."
But why not allow infections to run their course in those not at risk? Pillai seems to be implying that natural immunity is always sub-par compared to what he assumes to be a durable and non-problematic vaccine-induced immunity. This side of his presentation (which doesn't affect the main point of your post, Brian) hasn't aged very well, has it? I'm struck with how much this reflects that cultural meme 'vaccines always good', and since this is a 'vaccine', it must be good, and hell, why not good for everyone? What could go wrong? Alongside an obviously high level of technical expertise there seem to be some glaring blind spots too, including a great deal of hubris about how we can tinker with the immune system in a very complex physical environment. Just my lay observation.
While your criticisms are valid, I did find it interesting that Pillai was offering a theory for "why vaccines stop variants" that I hadn't encountered before and was better than all the other ones (which just repeat viral load results from the earliest breakthrough infections, which are negated by later papers). Mostly my answer to his argument would be that it's just a theory. We haven't actually demonstrated that chronic infections cause variants (as opposed to being "inbred virus" factories with genomes that are not fit enough to cause new infections).
On the other hand, let's say he was totally right, well, that's certainly not a good thing in the IgG4 tolerance era, then. Yet he strangely doesn't bring it up in the new paper. So either he was being honest / correct about variants in late 2021 or he is being honest / correct now, but it can't be both.
The evolutionary argument made no sense. Wouldn't "all the survivors" primarily be people with prompt antiviral immune response? You could have this second selection pressure on the other group, sure. But they would be the smaller group, because so many died. Except most of them are past reproduction age anyway. There's no such thing as selection pressure for being young.
Modern immunology was essentially pre-compromised when it came to vaccines. The "traditional" ones stopped being traditional decades ago, so there was already a conspiracy of silence at work with not speaking out about the recklessness of injecting all kids for every normal childhood illness. When the Salk polio vaccine was being developed, there was loads of pushback and criticism of the speed from within the National Institute itself (which was vindicated by the Cutter incident). The precautionary principle in vaccines doesn't exist anymore, that's a bygone era.
Two of the manufactures of the mRNA gene therapy mistakenly called a vaccine (hereinafter referred to as the #ClotShot) claim that the Spike protein has been coded in the pre-fusional conformation and cannot change to the fusional conformation, I believe.
Does this suggest that it cannot cause the syncytial magic that the real thing (not Coca Cola) does?
Could it be that the problem with the #ClotShot is the sialic acid bits on it that cause the agglutination that everyone is worried about? Or is it, as suggested by Brian elsewhere that the problem is toleration plus a real dose of SARS-CoV-2 viremia?
Correct, can't cause syncytia (or at best would be extremely poor at it). However the S1 unit is still free to fly off and circulate wherever it wants to.
Sorry to keep spamming with comments, but here is another thing I don't understand.
If cytokine storms are not what is happening with SARS-CoV-2 but it can still cause DAD because of infection and syncytia, then how is the mRNA gene-therapy treatment reducing severe disease?
Because the limits of IgG antibodies are a bit overblown. They can seep a bit into the respiratory tract, especially lower lungs, and especially before IgG4 kicks in they can tag infected cells for destruction. All of this limits viral replication and destruction in the lungs. The issue is whether this protection wanes since IgG seepage goes down as serum levels wane (even though the latter is going to automatically ramp back up when B Cells encounter spike). In my estimate, severe efficacy should be durable and there was never any need for more than 1 dose (so the best number of doses after 0 was 1), and even if there is a "need" it doesn't matter because the tolerance paradox renders extending that protection futile.
Delta was caused by two lethal antibodies: REGN10987 and B38. The technology is cmRNA, not mRNA. Uracil has been replaced 100% by Pseudouridine, a chiral isomer. Here is how it works: the immune system will be sabotaged to produce isomeric (binding) abs in response to the misfolded proteins in very large quantities, and at the same time produce less "normal" abs (including the two lethal abs described above). This is how they were able to claim "reducing severe disease". However, now the vaccination campaign has to deal with the isomeric lethal version of REGN10987 and B38, with isomeric IgG4 abs, with the fact that the effect only lasts a mere few days (not weeks, not months).
Avian flu (M. avium + M. influenzae + M. tuberculosis)
MPV non-coding RNA sequences and G-quadruplex structures (non-coding RNA and M. tuberculosis)
I could easily prove to you, using multiple references, that Sars-Cov-2 and MPV are mycobacterium (M. avium, M. influenzae, M. tuberculosis and a variant of M. leprae). But that would be beyond the scope of this thread. Let us keep then our discussion in the realm of viruses. RNA has four nucleobases. And yet, the cmRNA vaccines have replaced one of those nucleobases (Uracil) with a nucleoside (Pseudouridine, which is a chiral isomer). Is Sars-Cov-2 an isomeric pathogenic agent? No, it is not. Why then have these vaccines been offered to the public AS IF we are dealing with an isomeric Sars-Cov-2 (coded with Pseudouridine)? What if indeed an isomeric version of Sars-Cov-2 comes along, what is going to happen, given the prodigious quantities of isomeric abs which have been produced by the immune systems during the vaccination campaign? The antibodies resulting from the cmRNA vaccines are isomeric, they have nothing to do with the pathogenic agent called Sars-Cov-2.
In this video Pillai tells us how the brave investigators saved children from Diphtheria by developing an injectable anti-toxin and I immediately thought about another of your postings:
Is anyone looking at those sudden celeb deaths (SCDS) to see if they have antibodies against the M protein, the N protein etc, or do they only have signs of antibodies against the S protein? Did they ever test positive to SARS-CoV-2?
Also, do their hearts show indications of myocyte syncytia?
Now that Fauci et al are admitting that the mRNA gene therapy treatment does not offer much benefit it seems they are all front-loaded risk and little benefit. I suspect that even oldies (older than me at least) could obtain much more benefit from dosing up on D3, C and Zinc.
I still am not sure why I did not get laid low by one of the variants of SARS-CoV-2 but suspect it was the high levels of D3 I consume. However, it may also be because I am an unrepentant anti-Vaxxer and I simply frightened the virus away. I kid. I do think some vaccines are worth it.
The IgG4 abs are isomeric antibodies. Pseudouridine is a chiral isomer of Uridine. In the cmRNA vaccines Uracil has been replaced 100% by Pseudouridine.
The misfolded proteins are isomeric, and so are the antibodies (including IgG4). Spike proteins had been discovered some 90 years ago by Wilhelm Reich, he called them T-Bacilli.
There is no such thing as mRNA technology, but only cmRNA (chemically modified RNA, where Uracil has been replaced by Pseudouridine, a CRISPR-RNA level modification). The hapless "scientists" who were overjoyed when they had observed that the immune system did not destroy the cmRNA as it did with mRNA, had no idea what they were dealing with. The immune system most certainly had recognized Pseudouridine, the chiral isomer, but did not destroy it right away because humanity had met before with a pathogen which was coded with Pseudouridine (transgenerational epigenetics).
So, we have TWO pandemics running in parallel: M. avium (Sars-Cov-2 is a mycobacterium) and M. influenzae (Omicron), and an isomeric Sars-Cov-2 coded with Pseudouridine from the cmRNA vaccines. What is going to happen next? Coronaflu (Omicron with beta sheet prions and/or avian flu) and Coronapox (the reassortment of Sars-Cov-2 and MPV).
Bacterial secondary infection is a myth? But weren't a very large % of alleged "Covid-19 deaths" found to have bacterial infections?
Further, in my personal experience, every time I got sick during the "pandemic" (once, when around someone that claimed to have tested positive), I had a bacterial infection (strep throat). This same individual that tested positive was prescribed antibiotics, so they must have spotted some sort of bacterial infection.
That's discussed in my new post. The drops weren't that big and were regardless of "Covid-19" inpatients, who were prescribed loads of antibiotics. So the drops were due to people avoiding healthcare for other stuff, eg, surgeries of all types are a big driver of antibiotic prescription in seniors and so that went away for 2 years.
Have you looked into what separates people that get serious covid-19 and those that don't get very sick from it? Since it corresponds so strongly with age, that makes me think it's not really from former coronavirus (common cold) infections, but it's the innate immunity. One of Couey's videos had some guy on it claiming that interferon deficiency was found in like 20% of deaths from the virus. I've also seen evidence that, more than vitamin D deficiency itself, being genetically prone to poor functioning vitamin D receptor is highly associated increased severity.
The idea that vaccinating could solve the problem just doesn't make sense when we found out (quickly) that merely having the immune system of a young child was more than adequate protection.
Well, the question becomes if the vaccine pulls off the Steve Buscemi How Do You Do Fellow Kids routine. In the paxlovid trial in the placebo group the people with early natural antibodies were mostly hunky dory while those without, not https://unglossed.substack.com/i/52792651/assay-what - and so synthetic immunity provides the same protection as a functioning early natural response.
Given that placebo severe outcomes are all in the "no early antibodies" group, and that paxlovid averts severe outcomes, the whole danger of the virus is that it suppresses /evades this early response in at-risk adults. So adults with front-loaded immune responses imitate the agile young.
This doesn't mean it is right to inject older adults with experimental gene therapy but it sheds light on how severe outcomes result from silenced immune response.
I'm glad Brian is out there providing this type of analysis but honestly, I'm just too retarded to follow this one. Usually when he gets this technical I can take the time to read, reread, then research what he's saying and I'm generally able to get a good grasp but I'm tapping out today.
When we focus the microscope at Covid-19 only depth, we lose track of the big picture view;
"And yet now, emerging IgG4 tolerance is largely predicted by vaccine skeptics to be bad (exactly as I said in July when first reviewing Irrgang, et al.7). Well, which is it?"
Does it matter whether it's good, or bad for Covid-19 in particular? The jabs manage to invoke a very strong IgG4 response - a rare condition for our immune systems to be in. If this happens to help protect from phase II (the Artist previously known as Cytokine Storm) ground glass opacities, but also potentiates a raft of new knowns and unknowns... should we have done it? No. There is no defense for these shots... It was an insanely dangerous experiment, the implications of which are learning about week by week.
Macrolides have antiviral properties. Whether their protective effects were anti-bacterial, anti-viral, or both at a mechanistic level doesn't negate their value in early treatment protocols. Their withdrawal from use was pure evil.
"It has been shown that AZM has significant antiviral properties. In contrast with CQ or HCQ, its antiviral activity has been shown in vitro and/or in vivo on a large panel of viruses: Ebola, Zika, respiratory syncytial virus, influenzae H1N1 virus, enterovirus, and rhinovirus [4,5,6,7,8,9,10,11,12,13]. Its activity against respiratory syncytial virus has been demonstrated in a randomized study in infants [10]. Azithromycin exhibited a synergistic antiviral effect against SARS-CoV-2 when combined with HCQ both in vitro [11] and in a clinical setting [13]. Of note, the pre-print version of the article from Andreani et al. [14] also reported a significant antiviral effect of AZM alone on SARS-CoV-2. The mechanisms of the antiviral effect of AZM support a large-spectrum antiviral activity. Azithromycin appears to decrease the virus entry into cells [2, 8]. In addition, it can enhance the immune response against viruses by several actions."
It was always about suppression of highly effective early treatment protocols, and forcing us into a novel transfection with unknown long term consequences. My commentary always keeps this view in mind.
Right, and this is why I have been careful with the evidence for "negative efficacy" in general. So as not to contribute to sabotaging the cost/benefit argument by pretending there is no benefit, at the cost of thousands of substack like button smashes. I'll continue to take that stance.
But, the IgG4 horse is out of the barn now, there's no stopping it from doing whatever it is going to do.
Isn't it likely though that efficacy against severe disease, which may have been positive earlier, has shifted dramatically across the timespan of the variant parade? And wasn't this evolutionary parade predictable early on?
As I examined in SVAH pt 1 and 2, predicted based on what? RNA viruses besides flu are indifferent to immunization (e.g. polio and measles), and no actual evidence for coronavirus antibody evasion actually seem to exist, even though it would seem easy to put something together with some mice or cows etc. (project GOF bovine cov now!). So it was an assumption. Does seem to be coming about after BA.1/2 have saturated the world with natural immunity, but almost none of the mutations before this summer were strong evidence of immune escape pressure. Just L452R which shows up in chronic infections and also appeared in Delta early on in India, and Gamma and Beta E484K, and these didn't emerge in the post-vaccine context.
It's probably no longer possible to discern severe efficacy now that the unvaccinated all have natural immunity and so many uber-boosters are still virus virgins.
Uh oh, I feel like I'm being personally attacked here! 👀👀
But seriously, I think this is an interesting idea. Cytokine storm was something that I used often but actually didn't spend time to look deeper into, so it's possible that it took on a life of its own and was widely used even when the evidence wasn't there. I'm curious if RAS dysfunction may be related to the hyper correction and overreaction.
The innate system part certainly appears to be true. I believe when looking up some microbiome stuff and interferon-related stuff a few months back several articles mentioned an attenuation of the interferon response from COVID.
I'm still of the mindset that there are likely to be some cases of bacterial pneumonia as antibiotics may lead to nosocomial infections. However, from what I've seen I doubt it's at the widespread levels being reported. I'd be interested to see what you say in that section.
Another great article, really helps fill some gaps in knowledge about this area of Covid. It's interesting about interferons, because the asian doctors used them in their protocol for original SARS and did the same for SARS COV2 with encouraging results. However the WHO trialled this in the SOLIDARITY trial but wrote it off, because in the trials they failed to initiate treatment early enough, sound familiar?
I'm suprised no-one in the comments has mentioned ivermectin yet, this was part of the protocol the great doctor Joe Veron used to treat severe Covid patients with much success, so I wonder what the mechanism of action was?
Also Satoshi Omura the discoverer of the natural form of ivermectin, the avermectivn bacteria, was in favour of using ivermectin for treatment too. I had a video link but it's been taken down by Vimeo.
On steroids I have an good friend who knew someone with severe Covid who got to the point they could barely breath, in desparation they tried an asthama inhaler which completely turned them around, such that 30mins later they were knocking back a stiff drink :-) When hearing this I looked and found some trial results which only showed modest benefit, further reducing my faith in medical mainstream to conduct useful trials...
That... is a very interesting incident with the inhaler. It does sound like they were having an inflammatory issue unless it was simply muscle constriction. The hypoxia in most SARS-CoV-2 / Covid-19 doesn't seem to typically have been as violent.
My understanding of Covid-19 science is that we have little understanding of what "severe covid" is.
In a similar vein, we barely understand what "long Covid" is, argue over definitions, and avoid systematic look, allowing nonsense to proliferate, while a significant percentage of the population becomes effectively unable or unwilling to work.
So we are shooting in the dark here.
Do people have ground glass opacity and lung fibrosis because of overexpression of the virus, or immune overreaction, or both?
What exactly makes people more likely to have heart arrhythmia after Covid? What is the mechanism?
Nobody knows.
You are looking in the right direction, no doubt. However the answer may not yet be definitively known.
Such is the state of covid science, they are more interested in receiving grants than saving people.
You would hope that our govt would spent a billion or two on understanding "how Covid works", "how Covid spreads", and "what is long Covid" and "why are people dying suddenly at increased rates".
Nothing is happening and instead good substackers like you are trying to solve puzzles for which we may not even have the data necessary for a definitive answer.
A relative of mine had Ground Glass Opacities in the lungs 2-3 weeks post Vax. He never had covid, never tested positive, never exhibited covid like symptoms, ie Fever, flu, head cold, sore throat. At first it was fatigue, then trouble breathing, then mild sepsis and a diagnosis of "covid lung" and pneumonia. He never really got an explanation and ended up with long term heart and lung scarring. He is doing better but did not recover 100%. What would you say about this case?
Terrible consequences of a "vaccine"! This needs to be studied. I've an aunt who spent a month in hospital with sepsis post removal of a callous from her foot. She's heavily vaxxed. I've started hearing about sepsis post mRNA shots. What is that all about?
The hypoxia is important in this regard. When you send blood to the lungs, it should only go to parts that have oxygen - there's a vasoconstriction reflex (HPV) that shunts blood away from areas without O2 (due to pneumonia etc.). I didn't understand the importance of V/Q mismatch at first until I was discussing the problem in comments here https://unglossed.substack.com/p/the-virus-and-hpv - you have to keep blood from going to air-less lung regions or your pulmonary circuit will "draw from a partly empty well" and you can never hit 90+% O2.
So we know that the virus is destroying the lungs and sabotaging the HPV reflex, and that is why people experience shortness of breath. The lungs can't be subtracted from the disease. And both DAD and "organizing pneumonia" as part 2 will discuss are essentially features of tissue injury.
Many other things, e.g. coagulation and Long Covid, those are additional mysteries, yes - but the pneumonia isn't as mysterious or complicated as it is taken to be.
You might want to look into the role of afucosylated antibodies that are formed early in the initial antibody response and that increase cellular destruction
Also, some respected clinicians like Marik and Korey swear by high dose steroids in serious disease
Right, but Kory also published clear evidence for acute DAD followed by Organizing Pneumonia as manifestations of tissue injury - that is why I link to his paper at the bottom of this post https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7509945/ - so this will be discussed further in Part 2. But as I've said in other replies, if you have injury, of course immune modulation can be helpful - that doesn't mean the immune system caused the injury. And naturally, it wouldn't obviate the fact that cytokine storm in infections is basically a modern "hypothesis" which cytokine levels in SARS-CoV-2 infections failed to support.
Thank you for the link - I am aware of the afucosylated antibodies paper but eager to see what your post discusses
Do you find the treatment plan of Dr. Chetty relevant to the discussion? My laymen understanding was treatment was based on stopping the cytokine response that happened in a percentage of patients one week after symptoms
What I would say is that when I have looked at studies of US hospital treatment protocols, which are still unfortunately usually regarding 2020, steroid use is usually 80% of patients and the death rate is still very high - it is the early phase of infection that seems to be the most important, tamping the injury in the first place.
But as Pete Lincoln stated above, it was a question of dose. To say that 80% of patients were treated with steroids and many still died does not take into account the fact that early protocols used much too low a dose. I recall Kory talking about this.
A couple of passages in the Pillai video caught my attention:
31:55-32:30: "And it is this suboptimal immune response which, in an infection like Covid-19, might be causing this deep underbelly of viral variants to emerge. And this is why we should worry about the disease, worry about more people getting immunity from severe infection rather than vaccination. So vaccination is going to control infection rapidly if you are infected, whereas if you get severe immunity [through infection], true, you will eventually get an immune response, eventually if you survive you may be protected for at least some years, but you may generated more viral variants, which is a danger."
Taken at face value, this statement (i.e. that only severe cases drive the production of variants) does not seem to be a very good argument for mass-vaccination, but I strongly suspect that this sort of observation was heard as 'vaccinate everyone cuz who knows if you're going to have a bad case and feed the variant monster'. I distinctly remember that idea showing up in the mainstream press. It would have been helpful if Pillai had been more precise, but I suspect he (like just about every other 'expert' vaccinologist) was on board with the 'vaccinate everyone' program.
34:07-34:42 "...we can either, with good treatments perhaps survive, which is happening more and more today, or we might succumb. And that's one of the things that, even today there is a mortality, and the mortality is tending to happen more in people who were not vaccinated, who did not have any preexisting immunity, and form this entire cycle of going through severe inflammation and then basically altering adaptive immunity, allowing inflammation to persist..."
Again, Pillai seems to be simplifying the picture so as to support mass vaccination. Why were we not provided with *any* age and comorbidity stratified risk/benefit analyses (not in this video, of course, but in general) as with any other pharmaceutical (and especially with radically new ones like these).
39:18-40:00 "...as we develop adaptive immunity in the population, this [i.e. severe outcomes] is not going to be as bad. Even if suppose there was no vaccine, all of us are the descendants of survivors... If there was no vaccine we would eventually have survivors who had low mild immune response and they would procreate and then the whole world would be filled with people who maybe have no genetic susceptibilities and are better protected. That is possible. But now and fortunately for us we have vaccination and maybe more of our species will not be culled out by this virus, and we have antibodies being generated so it'll become milder..."
But why not allow infections to run their course in those not at risk? Pillai seems to be implying that natural immunity is always sub-par compared to what he assumes to be a durable and non-problematic vaccine-induced immunity. This side of his presentation (which doesn't affect the main point of your post, Brian) hasn't aged very well, has it? I'm struck with how much this reflects that cultural meme 'vaccines always good', and since this is a 'vaccine', it must be good, and hell, why not good for everyone? What could go wrong? Alongside an obviously high level of technical expertise there seem to be some glaring blind spots too, including a great deal of hubris about how we can tinker with the immune system in a very complex physical environment. Just my lay observation.
While your criticisms are valid, I did find it interesting that Pillai was offering a theory for "why vaccines stop variants" that I hadn't encountered before and was better than all the other ones (which just repeat viral load results from the earliest breakthrough infections, which are negated by later papers). Mostly my answer to his argument would be that it's just a theory. We haven't actually demonstrated that chronic infections cause variants (as opposed to being "inbred virus" factories with genomes that are not fit enough to cause new infections).
On the other hand, let's say he was totally right, well, that's certainly not a good thing in the IgG4 tolerance era, then. Yet he strangely doesn't bring it up in the new paper. So either he was being honest / correct about variants in late 2021 or he is being honest / correct now, but it can't be both.
The evolutionary argument made no sense. Wouldn't "all the survivors" primarily be people with prompt antiviral immune response? You could have this second selection pressure on the other group, sure. But they would be the smaller group, because so many died. Except most of them are past reproduction age anyway. There's no such thing as selection pressure for being young.
Modern immunology was essentially pre-compromised when it came to vaccines. The "traditional" ones stopped being traditional decades ago, so there was already a conspiracy of silence at work with not speaking out about the recklessness of injecting all kids for every normal childhood illness. When the Salk polio vaccine was being developed, there was loads of pushback and criticism of the speed from within the National Institute itself (which was vindicated by the Cutter incident). The precautionary principle in vaccines doesn't exist anymore, that's a bygone era.
Two of the manufactures of the mRNA gene therapy mistakenly called a vaccine (hereinafter referred to as the #ClotShot) claim that the Spike protein has been coded in the pre-fusional conformation and cannot change to the fusional conformation, I believe.
Does this suggest that it cannot cause the syncytial magic that the real thing (not Coca Cola) does?
Could it be that the problem with the #ClotShot is the sialic acid bits on it that cause the agglutination that everyone is worried about? Or is it, as suggested by Brian elsewhere that the problem is toleration plus a real dose of SARS-CoV-2 viremia?
Correct, can't cause syncytia (or at best would be extremely poor at it). However the S1 unit is still free to fly off and circulate wherever it wants to.
Sorry to keep spamming with comments, but here is another thing I don't understand.
If cytokine storms are not what is happening with SARS-CoV-2 but it can still cause DAD because of infection and syncytia, then how is the mRNA gene-therapy treatment reducing severe disease?
Because the limits of IgG antibodies are a bit overblown. They can seep a bit into the respiratory tract, especially lower lungs, and especially before IgG4 kicks in they can tag infected cells for destruction. All of this limits viral replication and destruction in the lungs. The issue is whether this protection wanes since IgG seepage goes down as serum levels wane (even though the latter is going to automatically ramp back up when B Cells encounter spike). In my estimate, severe efficacy should be durable and there was never any need for more than 1 dose (so the best number of doses after 0 was 1), and even if there is a "need" it doesn't matter because the tolerance paradox renders extending that protection futile.
Delta was caused by two lethal antibodies: REGN10987 and B38. The technology is cmRNA, not mRNA. Uracil has been replaced 100% by Pseudouridine, a chiral isomer. Here is how it works: the immune system will be sabotaged to produce isomeric (binding) abs in response to the misfolded proteins in very large quantities, and at the same time produce less "normal" abs (including the two lethal abs described above). This is how they were able to claim "reducing severe disease". However, now the vaccination campaign has to deal with the isomeric lethal version of REGN10987 and B38, with isomeric IgG4 abs, with the fact that the effect only lasts a mere few days (not weeks, not months).
Avian flu (M. avium + M. influenzae + M. tuberculosis)
MPV non-coding RNA sequences and G-quadruplex structures (non-coding RNA and M. tuberculosis)
I'm confused. Why are you talking about Mycobacterium? This is about a virus.
I could easily prove to you, using multiple references, that Sars-Cov-2 and MPV are mycobacterium (M. avium, M. influenzae, M. tuberculosis and a variant of M. leprae). But that would be beyond the scope of this thread. Let us keep then our discussion in the realm of viruses. RNA has four nucleobases. And yet, the cmRNA vaccines have replaced one of those nucleobases (Uracil) with a nucleoside (Pseudouridine, which is a chiral isomer). Is Sars-Cov-2 an isomeric pathogenic agent? No, it is not. Why then have these vaccines been offered to the public AS IF we are dealing with an isomeric Sars-Cov-2 (coded with Pseudouridine)? What if indeed an isomeric version of Sars-Cov-2 comes along, what is going to happen, given the prodigious quantities of isomeric abs which have been produced by the immune systems during the vaccination campaign? The antibodies resulting from the cmRNA vaccines are isomeric, they have nothing to do with the pathogenic agent called Sars-Cov-2.
In this video Pillai tells us how the brave investigators saved children from Diphtheria by developing an injectable anti-toxin and I immediately thought about another of your postings:
https://www.youtube.com/watch?v=t2AO1CMLV9A
I'll give it a watch. Does he also mention it in the talk I have highlighted, I wonder? Someone brought it up in my recent content consumption
Is it possible that what is happening with the #ClotShot and myocarditis is the following:
1. The ClotShot causes an IgG class switch to the tolerance class IgG4,
2. The person catches the latest variant of concern but they simply tolerate it, and it proliferates and causes myocyte syncytia etc.
Right, that's what I proposed for sudden cardiac deaths as number 3 of 3 possible etiologies https://unglossed.substack.com/i/80639846/ii-non-recovery-means-sudden-deaths-are-not-arrhythmia
Hmmm, I probably read that but did not understand at the time.
Is anyone looking at those sudden celeb deaths (SCDS) to see if they have antibodies against the M protein, the N protein etc, or do they only have signs of antibodies against the S protein? Did they ever test positive to SARS-CoV-2?
Also, do their hearts show indications of myocyte syncytia?
I don't think anyone is looking into any deaths in the US. Even the German post-vax myocarditis death study didn't look for antigen or antibodies etc.
Now that Fauci et al are admitting that the mRNA gene therapy treatment does not offer much benefit it seems they are all front-loaded risk and little benefit. I suspect that even oldies (older than me at least) could obtain much more benefit from dosing up on D3, C and Zinc.
I still am not sure why I did not get laid low by one of the variants of SARS-CoV-2 but suspect it was the high levels of D3 I consume. However, it may also be because I am an unrepentant anti-Vaxxer and I simply frightened the virus away. I kid. I do think some vaccines are worth it.
The IgG4 abs are isomeric antibodies. Pseudouridine is a chiral isomer of Uridine. In the cmRNA vaccines Uracil has been replaced 100% by Pseudouridine.
https://pubmed.ncbi.nlm.nih.gov/9217014/
Conformational isomerism of IgG antibodies
https://www.researchgate.net/figure/The-schematic-layout-of-the-IgG-subclasses-and-isomers-thereof-A-The-IgG-subclasses_fig2_267814149
https://www.researchgate.net/publication/267814149_IgG_Subclasses_and_Allotypes_From_Structure_to_Effector_Functions
The misfolded proteins are isomeric, and so are the antibodies (including IgG4). Spike proteins had been discovered some 90 years ago by Wilhelm Reich, he called them T-Bacilli.
There is no such thing as mRNA technology, but only cmRNA (chemically modified RNA, where Uracil has been replaced by Pseudouridine, a CRISPR-RNA level modification). The hapless "scientists" who were overjoyed when they had observed that the immune system did not destroy the cmRNA as it did with mRNA, had no idea what they were dealing with. The immune system most certainly had recognized Pseudouridine, the chiral isomer, but did not destroy it right away because humanity had met before with a pathogen which was coded with Pseudouridine (transgenerational epigenetics).
So, we have TWO pandemics running in parallel: M. avium (Sars-Cov-2 is a mycobacterium) and M. influenzae (Omicron), and an isomeric Sars-Cov-2 coded with Pseudouridine from the cmRNA vaccines. What is going to happen next? Coronaflu (Omicron with beta sheet prions and/or avian flu) and Coronapox (the reassortment of Sars-Cov-2 and MPV).
Bacterial secondary infection is a myth? But weren't a very large % of alleged "Covid-19 deaths" found to have bacterial infections?
Further, in my personal experience, every time I got sick during the "pandemic" (once, when around someone that claimed to have tested positive), I had a bacterial infection (strep throat). This same individual that tested positive was prescribed antibiotics, so they must have spotted some sort of bacterial infection.
Only small rates of coinfections, in part because antibiotics were given out to almost all inpatients - I'll go ahead and post that part now
But isn't it very common for bacterial infections to follow the flu also?
And weren't antibiotics not given out initially? Denis Rancourt showed that antibiotic prescriptions dropped considerably at the beginning, in 2020.
That's discussed in my new post. The drops weren't that big and were regardless of "Covid-19" inpatients, who were prescribed loads of antibiotics. So the drops were due to people avoiding healthcare for other stuff, eg, surgeries of all types are a big driver of antibiotic prescription in seniors and so that went away for 2 years.
Have you looked into what separates people that get serious covid-19 and those that don't get very sick from it? Since it corresponds so strongly with age, that makes me think it's not really from former coronavirus (common cold) infections, but it's the innate immunity. One of Couey's videos had some guy on it claiming that interferon deficiency was found in like 20% of deaths from the virus. I've also seen evidence that, more than vitamin D deficiency itself, being genetically prone to poor functioning vitamin D receptor is highly associated increased severity.
The idea that vaccinating could solve the problem just doesn't make sense when we found out (quickly) that merely having the immune system of a young child was more than adequate protection.
Well, the question becomes if the vaccine pulls off the Steve Buscemi How Do You Do Fellow Kids routine. In the paxlovid trial in the placebo group the people with early natural antibodies were mostly hunky dory while those without, not https://unglossed.substack.com/i/52792651/assay-what - and so synthetic immunity provides the same protection as a functioning early natural response.
Given that placebo severe outcomes are all in the "no early antibodies" group, and that paxlovid averts severe outcomes, the whole danger of the virus is that it suppresses /evades this early response in at-risk adults. So adults with front-loaded immune responses imitate the agile young.
This doesn't mean it is right to inject older adults with experimental gene therapy but it sheds light on how severe outcomes result from silenced immune response.
I'm glad Brian is out there providing this type of analysis but honestly, I'm just too retarded to follow this one. Usually when he gets this technical I can take the time to read, reread, then research what he's saying and I'm generally able to get a good grasp but I'm tapping out today.
When we focus the microscope at Covid-19 only depth, we lose track of the big picture view;
"And yet now, emerging IgG4 tolerance is largely predicted by vaccine skeptics to be bad (exactly as I said in July when first reviewing Irrgang, et al.7). Well, which is it?"
Does it matter whether it's good, or bad for Covid-19 in particular? The jabs manage to invoke a very strong IgG4 response - a rare condition for our immune systems to be in. If this happens to help protect from phase II (the Artist previously known as Cytokine Storm) ground glass opacities, but also potentiates a raft of new knowns and unknowns... should we have done it? No. There is no defense for these shots... It was an insanely dangerous experiment, the implications of which are learning about week by week.
Macrolides have antiviral properties. Whether their protective effects were anti-bacterial, anti-viral, or both at a mechanistic level doesn't negate their value in early treatment protocols. Their withdrawal from use was pure evil.
https://link.springer.com/article/10.1007/s40261-020-00933-3
"It has been shown that AZM has significant antiviral properties. In contrast with CQ or HCQ, its antiviral activity has been shown in vitro and/or in vivo on a large panel of viruses: Ebola, Zika, respiratory syncytial virus, influenzae H1N1 virus, enterovirus, and rhinovirus [4,5,6,7,8,9,10,11,12,13]. Its activity against respiratory syncytial virus has been demonstrated in a randomized study in infants [10]. Azithromycin exhibited a synergistic antiviral effect against SARS-CoV-2 when combined with HCQ both in vitro [11] and in a clinical setting [13]. Of note, the pre-print version of the article from Andreani et al. [14] also reported a significant antiviral effect of AZM alone on SARS-CoV-2. The mechanisms of the antiviral effect of AZM support a large-spectrum antiviral activity. Azithromycin appears to decrease the virus entry into cells [2, 8]. In addition, it can enhance the immune response against viruses by several actions."
It was always about suppression of highly effective early treatment protocols, and forcing us into a novel transfection with unknown long term consequences. My commentary always keeps this view in mind.
Right, and this is why I have been careful with the evidence for "negative efficacy" in general. So as not to contribute to sabotaging the cost/benefit argument by pretending there is no benefit, at the cost of thousands of substack like button smashes. I'll continue to take that stance.
But, the IgG4 horse is out of the barn now, there's no stopping it from doing whatever it is going to do.
Isn't it likely though that efficacy against severe disease, which may have been positive earlier, has shifted dramatically across the timespan of the variant parade? And wasn't this evolutionary parade predictable early on?
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0250780
Published: April 28, 2021
Title: Risk of rapid evolutionary escape from biomedical interventions targeting SARS-CoV-2 spike protein
As I examined in SVAH pt 1 and 2, predicted based on what? RNA viruses besides flu are indifferent to immunization (e.g. polio and measles), and no actual evidence for coronavirus antibody evasion actually seem to exist, even though it would seem easy to put something together with some mice or cows etc. (project GOF bovine cov now!). So it was an assumption. Does seem to be coming about after BA.1/2 have saturated the world with natural immunity, but almost none of the mutations before this summer were strong evidence of immune escape pressure. Just L452R which shows up in chronic infections and also appeared in Delta early on in India, and Gamma and Beta E484K, and these didn't emerge in the post-vaccine context.
It's probably no longer possible to discern severe efficacy now that the unvaccinated all have natural immunity and so many uber-boosters are still virus virgins.
Thank you Brian, On what basis do you make this statement;
" and so many uber-boosters are still virus virgins."
That was the subject of my catch up series https://unglossed.substack.com/p/it-will-always-be-catch-up-effect - A preprint after those posts affirmed the same thing in Nordic countries https://www.medrxiv.org/content/10.1101/2023.01.19.23284764v1
Uh oh, I feel like I'm being personally attacked here! 👀👀
But seriously, I think this is an interesting idea. Cytokine storm was something that I used often but actually didn't spend time to look deeper into, so it's possible that it took on a life of its own and was widely used even when the evidence wasn't there. I'm curious if RAS dysfunction may be related to the hyper correction and overreaction.
The innate system part certainly appears to be true. I believe when looking up some microbiome stuff and interferon-related stuff a few months back several articles mentioned an attenuation of the interferon response from COVID.
I'm still of the mindset that there are likely to be some cases of bacterial pneumonia as antibiotics may lead to nosocomial infections. However, from what I've seen I doubt it's at the widespread levels being reported. I'd be interested to see what you say in that section.
Correct - I personally blame you for creating the cytokine storm myth! How could you!
I knew it! You thought you were subtle with all of your tiny jabs and allusions, but I am onto you my good sir!!
🤯 Thanks for this - I’m going to need some time to process this - looking forward to the organizing pneumonia part as well.
Thanks!
Another great article, really helps fill some gaps in knowledge about this area of Covid. It's interesting about interferons, because the asian doctors used them in their protocol for original SARS and did the same for SARS COV2 with encouraging results. However the WHO trialled this in the SOLIDARITY trial but wrote it off, because in the trials they failed to initiate treatment early enough, sound familiar?
https://www.bnnbloomberg.ca/treat-covid-19-early-to-save-patients-lives-sars-veteran-urges-1.1509497
https://emcrit.org/pulmcrit/combination/
I'm suprised no-one in the comments has mentioned ivermectin yet, this was part of the protocol the great doctor Joe Veron used to treat severe Covid patients with much success, so I wonder what the mechanism of action was?
https://abc13.com/ivermectin-covid-treat-dr-joseph-varon-united-memorial-medical-center/10976044/
Also Satoshi Omura the discoverer of the natural form of ivermectin, the avermectivn bacteria, was in favour of using ivermectin for treatment too. I had a video link but it's been taken down by Vimeo.
On steroids I have an good friend who knew someone with severe Covid who got to the point they could barely breath, in desparation they tried an asthama inhaler which completely turned them around, such that 30mins later they were knocking back a stiff drink :-) When hearing this I looked and found some trial results which only showed modest benefit, further reducing my faith in medical mainstream to conduct useful trials...
That... is a very interesting incident with the inhaler. It does sound like they were having an inflammatory issue unless it was simply muscle constriction. The hypoxia in most SARS-CoV-2 / Covid-19 doesn't seem to typically have been as violent.
My understanding of Covid-19 science is that we have little understanding of what "severe covid" is.
In a similar vein, we barely understand what "long Covid" is, argue over definitions, and avoid systematic look, allowing nonsense to proliferate, while a significant percentage of the population becomes effectively unable or unwilling to work.
So we are shooting in the dark here.
Do people have ground glass opacity and lung fibrosis because of overexpression of the virus, or immune overreaction, or both?
What exactly makes people more likely to have heart arrhythmia after Covid? What is the mechanism?
Nobody knows.
You are looking in the right direction, no doubt. However the answer may not yet be definitively known.
Such is the state of covid science, they are more interested in receiving grants than saving people.
You would hope that our govt would spent a billion or two on understanding "how Covid works", "how Covid spreads", and "what is long Covid" and "why are people dying suddenly at increased rates".
Nothing is happening and instead good substackers like you are trying to solve puzzles for which we may not even have the data necessary for a definitive answer.
It seems to me that “ground glass opacity” is a radiologic indicator of one gazillion different entities.
A relative of mine had Ground Glass Opacities in the lungs 2-3 weeks post Vax. He never had covid, never tested positive, never exhibited covid like symptoms, ie Fever, flu, head cold, sore throat. At first it was fatigue, then trouble breathing, then mild sepsis and a diagnosis of "covid lung" and pneumonia. He never really got an explanation and ended up with long term heart and lung scarring. He is doing better but did not recover 100%. What would you say about this case?
This vaccine is often times worse than Covid - and invites Covid instead of repelling it
Terrible consequences of a "vaccine"! This needs to be studied. I've an aunt who spent a month in hospital with sepsis post removal of a callous from her foot. She's heavily vaxxed. I've started hearing about sepsis post mRNA shots. What is that all about?
The hypoxia is important in this regard. When you send blood to the lungs, it should only go to parts that have oxygen - there's a vasoconstriction reflex (HPV) that shunts blood away from areas without O2 (due to pneumonia etc.). I didn't understand the importance of V/Q mismatch at first until I was discussing the problem in comments here https://unglossed.substack.com/p/the-virus-and-hpv - you have to keep blood from going to air-less lung regions or your pulmonary circuit will "draw from a partly empty well" and you can never hit 90+% O2.
So we know that the virus is destroying the lungs and sabotaging the HPV reflex, and that is why people experience shortness of breath. The lungs can't be subtracted from the disease. And both DAD and "organizing pneumonia" as part 2 will discuss are essentially features of tissue injury.
Many other things, e.g. coagulation and Long Covid, those are additional mysteries, yes - but the pneumonia isn't as mysterious or complicated as it is taken to be.
You might want to look into the role of afucosylated antibodies that are formed early in the initial antibody response and that increase cellular destruction
Also, some respected clinicians like Marik and Korey swear by high dose steroids in serious disease
https://pete843.substack.com/p/igg4-abs-tregs-afucosylated-antibodies
Right, but Kory also published clear evidence for acute DAD followed by Organizing Pneumonia as manifestations of tissue injury - that is why I link to his paper at the bottom of this post https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7509945/ - so this will be discussed further in Part 2. But as I've said in other replies, if you have injury, of course immune modulation can be helpful - that doesn't mean the immune system caused the injury. And naturally, it wouldn't obviate the fact that cytokine storm in infections is basically a modern "hypothesis" which cytokine levels in SARS-CoV-2 infections failed to support.
Thank you for the link - I am aware of the afucosylated antibodies paper but eager to see what your post discusses
Do you find the treatment plan of Dr. Chetty relevant to the discussion? My laymen understanding was treatment was based on stopping the cytokine response that happened in a percentage of patients one week after symptoms
https://rumble.com/vsokj8-dr.-shankara-chetty-successfully-treated-4000-covid-19-patients-0-deaths.html
What I would say is that when I have looked at studies of US hospital treatment protocols, which are still unfortunately usually regarding 2020, steroid use is usually 80% of patients and the death rate is still very high - it is the early phase of infection that seems to be the most important, tamping the injury in the first place.
But as Pete Lincoln stated above, it was a question of dose. To say that 80% of patients were treated with steroids and many still died does not take into account the fact that early protocols used much too low a dose. I recall Kory talking about this.