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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.

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Feb 11, 2023Liked by Brian Mowrey

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?

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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?

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Feb 11, 2023Liked by Brian Mowrey

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

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Feb 10, 2023Liked by Brian Mowrey

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.

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Feb 10, 2023Liked by Brian Mowrey

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?

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Feb 9, 2023·edited Feb 9, 2023Liked by Brian Mowrey

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.

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Feb 9, 2023Liked by Brian Mowrey

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).

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Feb 8, 2023Liked by Brian Mowrey

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.

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Feb 8, 2023Liked by Brian Mowrey

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.

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Feb 8, 2023·edited Feb 8, 2023Liked by Brian Mowrey

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.

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Feb 8, 2023·edited Feb 8, 2023Liked by Brian Mowrey

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.

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Feb 8, 2023Liked by Brian Mowrey

🤯 Thanks for this - I’m going to need some time to process this - looking forward to the organizing pneumonia part as well.

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Feb 8, 2023Liked by Brian Mowrey

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...

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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.

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Feb 8, 2023Liked by Brian Mowrey

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

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