Septic Shock induced by Plasmid dsDNA and Truncated mRNA has common Sensing Mechanism to Endotoxin in mRNA Jabs
Pfizer mRNA jabs are toxic soup containing Live E. coli Bacteria, fragments of Synthetic DNA and Truncated mRNA as well as super toxic Endotoxin. How does your body react?
Many people have followed the excellent work of Dr Kevin McKernan analyzing samples of mRNA jabs foisted on billions of people worldwide to prove that the contamination includes fragments of the DNA grown inside E. coli bacteria from which the mRNA designed to code for a Stealth version of the Covid19 virus Spike Protein is made.
Kevin is a world leader in the field and has encouraged others with the knowledge, expertise, equipment and access to jab samples to repeat his work, and has been rewarded with international collaboration to do just that.1
Health Impacts of the Jab contamination
As my subscribers are aware, I have concentrated on the known Mechanisms of Endotoxin damage to all organ systems of the Human body caused by Cytokine Storm, the often Lethal Inflammatory reaction to detection of intrusion of foreign material from Bacteria, Viruses or other pathogens. This relies on recognition of Pathogen-Associated Molecular Patterns (PAMPS).
So I was interested in a key common link to Septic Shock, associated Blood Clotting and other effects in poisoning by foreign DNA, RNA and Endotoxin, published in 2009.2
The authors used a synthetic Poly(dA:dT) DNA to demonstrate it triggers Type I Interferons through RNA Sensor RIG-I. They used relatively short 20-, 40-, 77-, 163-, 245-nucleotide dsDNA molecules.
Type I interferons (IFNs) are cytokines released upon mRNA jab Endotoxin binding to Toll-Like Receptor 4 (TLR4).
The RIG-I investigators found that RNA polymerase III3 plays an essential role in detecting foreign DNA (non-self nucleic acids) which transcribes the dsDNA into double-stranded RNA (dsRNA) containing a 5′-triphosphate moiety that causes the devastating toxic consequences.
RIG-I (and Mda5 to be discussed later) engages the Mitochondrial Adaptor Protein IPS-1 (also known as MAVS, Cardif or VISA) which triggers downstream signaling and activation of the kinase IKKα-IKKβ–transcription factor NF-κB pathway or the Kinase TBK1–transcription factor IRF3 pathway, which promote the transcription of genes encoding inflammatory cytokines and type I interferon, respectively.
Consulting the US government Comparative Toxicogenomics Database (CTD), I found that RNA Sensor RIG-I (which has a plethora of synonyms) that helps detect and cause inflammatory reaction to foreign dsRNA has its top interaction with Endotoxin (LipoPolySaccharide, LPS) as found in Pfizer Process 2 poojabs. RNA sensor RIG-I is linked to 1,781 Diseases at CTD.
Because Moderna and Pfizer are incapable of cleaning up their products, they must be withdrawn immediately and it is obvious that all mRNA jabs under development using bacterial culture are inherently unsafe.
Katalin Karikó and Drew Weismann target TLR3
As part of the decades long plan4 to produce mRNA jabs, Katalin Karikó of BioNTech and Pfizer fame studied how the Human body responds to foreign dsRNA and mRNA and they deliberately targeted Toll-Like Receptor 3 (TLR3) in Dendritic cells in 2004.5
They used anti-TLR3 monoclonal antibodies and looked at the expression of CD83, CD80 and CD86 modified cells. They demonstrated that the transfection agent Lipofectin, a mixture of two Cationic Lipids, N-[1-(2,3-DiOleyloxy)propyl]-n,n,n-TriMethylAmmonium chloride (DOTMA) and DiOleoyl PhosphotidylEthanolamine (DOPE) alone had no effect.
They used poly(I):C6 which is a mismatched double-stranded RNA with one strand being a polymer of Inosinic acid, the other a polymer of Cytidylic acid, and compared the inflammatory response in HEK293 cells to mRNA by measuring IFN-β as shown in their Figure 5.
Note that in the hands of the Pfizer BioNTech jab developer, Endotoxin from Escherichia coli 055:B5 (purchased from Sigma) was at least 10 times more toxic weight for weight than the dsRNA.
dsRNA of 90 base pairs captured in TEM with TLR3
Activation of TLR3 induces secretion of type I interferons and pro-inflammatory cytokines, such as TNF-α, IL-1, and IL-6, triggering immune cell activation and recruitment.
More recent elegant work using cryogenic TEM crystallography, has shown that double stranded RNA can interact directly with TLR3, showing there is much more to uncover with atomic precision about the Cytokine Storm following foreign genome invasion.7
Ablasser A, et al. 2009. RIG-I-dependent sensing of poly(dA:dT) through the induction of an RNA polymerase III–transcribed RNA intermediate. https://www.nature.com/articles/ni.1779
https://en.wikipedia.org/wiki/RNA_polymerase_III
Karikó K, et al. 2004. mRNA Is an Endogenous Ligand for Toll-like Receptor 3. https://www.jbc.org/article/S0021-9258(19)64193-1/fulltext
https://en.wikipedia.org/wiki/Polyinosinic:polycytidylic_acid
Sakaniwa A, et al. 2013. TLR3 forms a laterally aligned multimeric complex along double-stranded RNA for efficient signal transduction. https://www.nature.com/articles/s41467-023-35844-2