‘The BNT162b2 mRNA vaccine against SARS-CoV-2 reprograms both adaptive and innate immune responses’

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by Jessica Rose 

A brand new medRxiv pre-print study entitled: “The BNT162b2 mRNA vaccine against SARS-CoV-2 reprograms both adaptive and innate immune responses” has graced our world. This paper is so important and it provides evidence to support what many prominent immunologists and vaccinologists have been saying for a long time, including myself. These COVID-19 mRNA injectable products are causing, yes, causing, immune system dysregulation – and not just in the context of the adaptive system, but in the context of the innate system. Not only that, but these findings provide very good reasons as to why we are seeing resurgences of latent viral infections and other adverse events reported in VAERS (and other adverse event reporting systems) and perhaps more importantly, why we should under no circumstances inject this crap into our children. Children are fine in the context of COVID-19 (for the 80 millionth time – this is well documented) and this is due to their extraordinary innate immune response systems.

Let’s rip into some background in immunology, shall we?

Figure 2 shows many of the different cell types involved in the adaptive and the innate immune system branches. Most of you probably know about T cells and B cells. I would bet that many more of you have not heard of my personal favorite killer, the Natural Killer (NK) cell. They kill infected cells and are of utmost importance to a healthy and functioning immune system. The cell types involved in the innate immune response system emit special molecules in response to invaders. These special molecules primarily comprise defensins, collectins, c-reactive proteins, lipopolysaccharide (endotoxin) binding proteins, and complement factors. These responses are non-specific and target invading pathogens and even cancer cells.

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Figure 2: The big picture of adaptive versus innate immune cells.

In a nutshell, in this article, what they found was that the BNT162b2 (Pfizer/BioNTech) injectable products are modulating the production of inflammatory cytokines by innate immune cells upon stimulation with both specific (SARS-CoV-2) and non-specific (viral, fungal and bacterial) stimuli whereby the response of innate immune cells to TLR4 and TLR7/8 ligands was weaker after BNT162b2 injection, while fungi-induced cytokine responses were stronger.

In conclusion, the mRNA BNT162b2 vaccine induces complex functional reprogramming of innate immune responses, which should be considered in the development and use of this new class of vaccines.

Yes. It should be. And it should have been.

So what is inside the nutshell? Let’s back it up a bit, shall we? What is acquired/adaptive immune responses and more importantly, what are innate immune responses? I did say we were going to rip into immunology. Our immune system’s first line of defense is called the innate immune system. It comprises the skin (chock full of epidermal dendritic cells or Langerhans cells), mucous and mucosal epithelium, immune cells such as natural killer cells, basophils, dendritic cells, mast cells, and macrophages and many molecular mediators such as cytokines, interleukins, c-reactive proteins and complement factors. The complement system (Figure 2) is an immutable system vital to the proper functioning of antibodies and phagocytic cells (cells that eat stuff), clearance of invaders and damaged cells, inflammatory response promotion and membrane attack complex (MAC) formation (Figure 2). Membrane attack complex. Cool name for a band.

Figure 2: The complement cascade

The mucus layer covering the mucosal epithelium acts as a first physical and biochemical barrier. An additional layer of physical protection against microorganisms is provided by a tightly interlaced cell-to-cell network of epithelial cells and intraepithelial lymphocytes. Various antimicrobial peptides produced by the epithelium and secreted into the mucosal lumen can directly kill the invading pathogenic bacteria.1

Every single ‘invader’ such as bacteria or viruses has molecules on their surfaces known as Pathogen-Associated Molecular Patterns (PAMPs) that are detectable by cognate molecules on immune cell surfaces call Pattern Recognition Receptors (PRRs). One type of PRR is Toll-like Receptors (TLRs). These TLRs come in many types and bind to specific types of molecules. TLR-7, for example, binds single-stranded RNA (ssRNA). Hmm. Where have I seen that before? Oh right! SARS-nCoV-2 is an ssRNA virus. Interesting. There are also cell receptors called RIG-I-like receptors (RLRs) that sense viral RNA.2

If a PAMP is detected by a PRR, an intracellular signaling cascade commences which results in the production of such inflammatory mediators as Nitric Oxide, histamine, TNF-alpha, IL-1 (a prototypic inflammatory cytokine), and others as part of a pro-inflammatory reaction to quell invaders. Perhaps of primary note is that via TLR signaling – a prolific PRR type – Nuclear Factor kappa B (NF-kB) activation ensues. What is NF-kB?

NF-kB3 plays a key role in regulating the immune response to infection. Incorrect regulation of NF-kB has been linked to cancerinflammatory and autoimmune diseasesseptic shockviral infection, and improper immune development.

In the presence of danger, the immune system responds via these fantastic on/off switches and mechanisms, to eliminate said dangers. This is the natural way of things and it is a constant ebb and flow of immune system regulatory magic.

Let’s assume the role of the coronavirus and see what our life would be like in the case of say, a child. You should know, once again, that children have very strong innate immune systems. The links attached refer to excellent works by Dr. Robert Malone and Dr. Francis Christian on this subject. So I’m a coronavirus and some arshole just sneezed me all over the face of a child standing next to me. The person who sneezed is one of those people who wears a mask incessantly on their chin and then sneezes all over everyone whilst symptomatic. So the child has me (Dr. Coronavirus or Dr. CV, for short) all over its face. And just so you know, there are many of me. So I find my way in a misty droplet into the sweet nasal cavity of this child where I encounter lots of mucousy membranes and sheets of epithelial cells. Lots of mucous. Mucosaliscious. I imagine it would be like running through a tunnel full of spider webs like Frodo Baggins did when he was trying to escape ‘she who needs to feed’ in order to get to the Mordor volcano to destroy the ring of power. So it’s kind of hard to get through. The nose. Sort of.

Ok, so most of me get stuck in the booger path in the child’s nose. But nasal epithelial cells are chock full of ACE-2 receptors. I can bind them and thus can easily get inside the nice and warm cozy cells. There are also CD147 receptors here! So, a few of me manage to get ‘past’ this mucousy hurdle and bind to yummy epithelial cells via ACE-2 and CD147 receptors, which to me, are like red and yellow-colored lollipops of delight leading me into the place where I can call home and settle down and reproduce. But wait, before we get into that, since I am lurking around looking for receptors to bind, I am also encountering a lot of cells. These cells start telling me that they need to see my green pass if I want to keep lurking. No, wait, no not my green pass, my PAMPs, so that they can find out how dangerous I am. I am new to this neck of the woods so they’re more than a little curious about my lurking. So they probe me with their PRR/TLR tools. Oh, man! This is not pleasant at all! Being frisked by dendritic cells is like being manhandled by an octopus on a mission. So even though I have no idea, the by-product of their frisk is the inevitable launch of an army of things hell-bent on removing me from this kid. All of a sudden I’m surrounded by tenticular cells and they’re throwing TNF-alpha and IL-1 Molotov cocktails at me! And it’s starting to get really hot in here and I’m like, man, this is not a hospitable environment. What did I do to deserve this? I’m just an innocent virus ultimately looking for a place to… breed.

Luckily, I have made a home in some cells. I am bound to others about to gain entry. But, the immune defenses don’t stop on the outside of cells; they continue on the inside. I thought I had found a nice warm and cuddly cell to settle down in and reproduce in. I have to think again! All of a sudden the PH is, way too high! This feels awful! They’re trying to kill me, man! And eventually, they destroy me before I can get out. One of them sicked this crazy MAC on me and it poked holes in my home cell that I had managed to get into. They also used all sorts of internal and external armaments to make sure they cleared me out. And they did!

How do I know that? Because I am speaking from virus heaven.

So that’s the imaginary journey of the SARS-nCoV-2 virus and the potent response of a child’s innate immune system to my presence. Not enough cells get infected fast enough for an infection to ensue. The kid never gets to a disease state and in most cases, symptoms are excessively mild or non-existent.

Alas, not enough of me was able to ‘infect’ enough cells to result in enough of me being produced to result in a ‘symptomatic infection’ party. Innate immune system: 1. Coronavirus me: 0.

But what if I am reincarnated as mRNAs’ssss. And let’s go really sci-fi and imagine I am reincarnated as mRNAssss’s wrapped in a Lipid Nano Particle (LNP) bubble. And what if, I happened to be injected into someone’s arm muscle. What lives I am having! So what would be my fate? Well, surely, since I am injected intramuscularly with a pretty heavy gauge needle (22–25-gauge 5/8 inch (16 mm)), I get inserted pretty deep and in copious amounts into muscle tissue. I witnessed many muscle cells screaming in pain! I can’t really see anything yet because of this fat bubble I am in. But all of a sudden I feel us moving! So fast! The injector didn’t aspirate to check if I was being injected into the muscle as planned! It’s like riding the rapids of the cardiovascular system! Or something. Then suddenly we stop. There’s some kind of blurry kidney-shaped thing outside. It seems like the LNP has slimed its way into a cell. And I think we were just dumped out of the LNP into this cell. Well, ok. This is great news! Since we have been reincarnated into mRNAs, we can simply find ribosomes and start translating ourselves into the butterfly proteins we’ve always wanted to be! And there will be so many of us! Butterflies a swarmin’ in the body of a person! We have to act fast though, lest we be… degraded, however. I guess this is why we were wrapped in an LNP.

Later on that day…

So we are spike proteins now! Hallelujah. We can do so many things! But we have to be careful: there are cells everywhere looking to eat us and turn us into alphabet soup. These so-called antigen-presenting cells just love to gobble up foreign proteins like us and regurgitate our entrails and mount them on Major Histocompatibility Complex (MHC) I and II molecules. If they do that, then those T cells and B cells can detect our ground-up guts mounted on these complexes and then build an army of cells that can recognize us and kill us! We do not want that. We want to exist. We seem to be doing alright in that desire. We also have to make sure that we don’t end up killing this person we got injected into! That wouldn’t help anyone, now would it. We can embed ourselves into monocytes4 and other cells like epithelial cells5 due to their proclivity to express ACE-26. But there’s a problem here. Through no fault of our own, we are causing some serious micro-clotting issues all over this person’s body by binding all these ACE-2 and CD147 receptors. The inflammatory mediators produced in response to our presence are in overdrive and the entire system is on fire! Hyperinflammation abound! The normal systems that regulate the anti-inflammatory response seem to be on vacation and it just won’t seem to stop. And it’s all because of little old me! Since I was designed to be pretty durable with my extra prolines and my pseudouridines, I am not easily get-ridable. [Word on the street says that my prolines aren’t preventing me from binding ACE-2 at all.] That would explain why so many of me are stuck in monocytes. Teehee. By the way, I forgot to mention, while I was inside the cell as mRNA, there were these TLR-7 molecules that seemed to find me very attractive. They detected some of me and in some cells, causing a chain reaction that obliterated us and the cell.7 TLR-7 is actually really important in the context of COVID-19 clearance.8

Perhaps the most successful part of our journeys, however, has been the avoidance of those pesky innate immune mediators in that kid’s nose. Phew, what a bullet we dodged there, right? So we got catapulted all over the body, triggered the T and B cells to respond accordingly with their specificness all along the way, but we avoided all of that other stuff. That’s some weird under-the-radar stuff right there.

Until this body flushes me out (which could take 15 months (see reference #4) unless they inject me again!) I am probably going to cause some systemic problems while I am here. These problems include the dysregulation of the innate immune system, the (subsequent) induction of a hyper-inflamed environment and so many thrombotic events.

I think we can get into the paper now. This article was meant to be about the paper, not an immunology lesson. But it seems these things are simply not mutually exclusive.

So dysregulated inflammation plays an important role in the pathogenesis and severity of COVID-19.9 There are studies that show that long-term innate immune responses can be either increased (trained immunity) or down-regulated (innate immune tolerance) after certain vaccines (such as Bacillus Calmette-Guérin (BCG) and the measles, mumps, and rubella (MMR) vaccines) or infections, so this is not a new thing.10 The way that the authors determined that the innate responses were being modulated in the context of the COVID-19 (the BNT162b2 one) injectables, was by checking out if the levels of certain measurable immune mediators produced in response to TLR stimulation using other viruses, bacteria, and fungi antigens, were ‘off’. Trained immunity (the one with decreases) is often measured by looking at the rustled-elevated-inflammatory cytokine (like monocyte-derived cytokines TNF-alpha, IL-1beta, and IL-1Ra) leaves. When the TLR-3 and TLR-7 receptors were tickled, the amount of TNF-alpha production was way lower (significantly so for TLR-7) following dose 2 of the Pfizer stuff.

TNF-alpha production following stimulation with the TLR7/8 agonist R848 of peripheral blood mononuclear cells from volunteers was significantly decreased after the second [injection].

They also tickled the system with yeast (fungus) and found that the responses (specifically for IL-1beta – a fever-inducing interleukin) were higher following dose 1. The production of the anti-inflammatory cytokine IL-1Ralpha11 (the yin to the IL-1 yang) was reduced in response to a bacterial antigen (lipopolysaccharide (LPS)) and to yeast after the second injection – more evidence that there’s a shift to a stronger inflammatory response to fungal stimuli after injection. They also found that Interleukin-6 (IL-6) responses were similarly decreased, which is interesting because IL-6 induces the liver to produce a c-reactive protein that activates the complement system which helps antibodies out and promotes inflammation which means that doesn’t this mean that we should see less inflammation? So many questions. So very few answers.

Dysregulated continual synthesis of IL-6 plays a pathological effect on chronic inflammation and autoimmunity.12

You don’t say.

So that’s what they found in the paper, in a very small nutshell. Figure 3 shows the design and some of the results of their essays. It basically shows fold-changes in Interferon-gamma (IFN-gamma) (these guys activate macrophages and induce MHC-II molecule expression) and TNF-alpha in response to stimulation of blood cells from injected people using TLR stimulation with various pathogens.

Figure 3: Figure 1. TNF-α and IFN-α production in response to heterologous stimuli in PBMCs isolated from vaccinated subjects. (A) Description of the study: vaccination and blood collection days. (B-G)

The bottom line here is this. We know that innate responses are vital to a healthy and optimally functioning immune system. They are vitally integrated with and into the adaptive responses as these two branches work in impeccable, complex harmony. We also know that there are cases where vaccines have caused dysregulation of innate responses in humans. We also know that something is very, very wrong with these COVID-19 injectable products with regards to persistent hyper inflammation and a plethora of systemic and physiologically-comprehensive adverse events including death from micro-emboli formation and clotting. We also know that these authors have now provided evidence to support that these COVID-19 injectable products are modulating innate responses and that this isn’t limited to problems with COVID-19. Problems with fungi, other viruses, and bacteria can be anticipated. VAERS has hundreds of thousands of reports of adverse events related to fungal infections, plagues of herpes zoster occurrences (shingles) indicating weakened immunity, cancers coming out of remission, and the list goes on. And most of these reports are made for adults.

Here’s the thing…

Since children have extraordinary capabilities with regards to dealing with COVID-19 via their innate immune system responses, what will happen to them if these are not only bypassed by these injections but knocked down by them?

Figure 4: The kids are alright. Leave them alone.

Please listen to the mighty baby. The kids are alright. Leave them alone. You might not get how these circles back the kids, but it does. Thanks for reading this to the end. And don’t inject kids with this stuff. You might mess them up and they don’t need it.

1

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Rehwinkel J, Gack MU. RIG-I-like receptors: their regulation and roles in RNA sensing. Nat Rev Immunol. 2020 Sep;20(9):537-551. DOI: 10.1038/s41577-020-0288-3. Epub 2020 Mar 13. PMID: 32203325; PMCID: PMC7094958.

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Liu T, Zhang L, Joo D, Sun SC. NF-κB signaling in inflammation. Signal Transduct Target Ther. 2017;2:17023-. doi:10.1038/sigtrans.2017.23.

4

Bruce K. Patterson, Edgar B. Francisco, Ram Yogendra, Emily Long, Amruta Pise, Hallison Rodrigues, Eric Hall, Monica Herrara, Purvi Parikh, Jose Guevara-Coto, Xaiolan Chang, Jonah B Sacha, Rodrigo A Mora-Rodríguez, Javier Mora. Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post-Acute Sequelae of COVID-19 (PASC) Up to 15 Months Post-Infection. bioRxiv 2021.06.25.449905; doi: https://doi.org/10.1101/2021.06.25.449905.

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Xu H, Zhong L, Deng J, et al. High expression of ACE2 receptor of 2019-nCoV on the epithelial cells of the oral mucosa. Int J Oral Sci. 2020;12(1):8. Published 2020 Feb 24. doi:10.1038/s41368-020-0074-x.

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Fu J, Zhou B, Zhang L, Balaji KS, Wei C, Liu X, Chen H, Peng J, Fu J. Expressions and significances of the angiotensin-converting enzyme 2 genes, the receptor of SARS-CoV-2 for COVID-19. Mol Biol Rep. 2020 Jun;47(6):4383-4392. DOI: 10.1007/s11033-020-05478-4. Epub 2020 May 14. PMID: 32410141; PMCID: PMC7224351.

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National Center for Biotechnology Information (2021). PubChem Pathway Summary for Pathway WP4868, Source: WikiPathways. Retrieved December 16, 2021, from https://pubchem.ncbi.nlm.nih.gov/pathway/WikiPathways:WP4868.

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Li SW, Wang CY, Jou YJ, et al. SARS Coronavirus Papain-Like Protease Inhibits the TLR7 Signaling Pathway through Removing Lys63-Linked Polyubiquitination of TRAF3 and TRAF6. Int J Mol Sci. 2016;17(5):678. Published 2016 May 5. doi:10.3390/ijms17050678.

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Tahaghoghi-Hajghorbani S, Zafari P, Masoumi E, Rajabinejad M, Jafari-Shakib R, Hasani B, Rafiei A. The role of dysregulated immune responses in COVID-19 pathogenesis. Virus Res. 2020 Dec;290:198197. DOI: 10.1016/j.virusres.2020.198197. Epub 2020 Oct 16. PMID: 33069815; PMCID: PMC7561578.

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Alberto Mantovani, M.D., and Mihai G. Netea, M.D.. Trained Innate Immunity, Epigenetics, and Covid-19. NEJM 383;11 nejm.org September 10, 20201078.

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Arend WP. Interleukin-1 receptor antagonist. Adv Immunol. 1993;54:167-227. doi: 10.1016/s0065-2776(08)60535-0. PMID: 8379462.

12

Tanaka T, Narazaki M, Kishimoto T. IL-6 in inflammation, immunity, and disease. Cold Spring Harb Perspect Biol. 2014;6(10):a016295. Published 2014 Sep 4. doi:10.1101/Csh Perspect.a016295.