Could a Hidden Amyloidogenic Peptide in Pfizer's SV40 Promoter Contribute to Post-Vaccine Fibrin Clots?

Preamble-

I was watching this Lyndsey, RN video while I was combing over some more recent Pfizer→EMA disclosures where they admit to SV40 being in their vaccine. I will get to the Pfizer documents at the ends of this. Its a very important finding that Ulrike sent me. They are trying to claim these SV40 sequences are irrelevant while giving citations to the EMA that claim their very relevancy. Once again, all it takes to pull the wool over the eyes of the EMA is to make a statement [7] and as long as you include a citation after it… You are good to go! No one there will look up that citation to see that it states the exact opposite of what Pfizer claims.

This sent me down this rabbit hole as Pfizer keeps trying to claim the SV40 promoter is only for Eukaryotic expression (not E.coli but mammals) and they only use bacteria (E.coli) in their manufacturing. The problem with this line of argument is that its the proximal promoter to the Kanamycin resistance gene and in bacteria -35 and -10bp regions upstream of the Start Codon need to have some Shine-Delgarno sequences close to the gene. So this Promoter drives the Kanamycin resistance and you cannot perform any plasmid manufacturing without this SV40 promoter. They are lying when they claim this only for Eukaryotic expression.

But you should be more worried about what they admit to as you don’t want this DNA active in mammalian cells. Once again, if its superfluous, get it out. Moderna is evidence that you don’t need it.

This recent investigation into the Pfizer vaccine plasmid promoters has revealed an intriguing and potentially significant finding: a cryptic micropeptide encoded in the SV40 promoter region that scores as amyloidogenic. Here's what we know—and why it might matter.

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🔍 The Discovery

Within the SV40 promoter upstream of the Neo/KanR gene, a Kozak consensus sequence (ccatgg) and downstream ATG codon were identified. This marks the start of an open reading frame encoding the 23-amino-acid peptide:

>MQRPRPPRPLSYSRSSEEAFLEA

This sequence resides in a region historically used for eukaryotic expression, not typically active in E. coli. However, cryptic transcription from this region could still occur, especially in eukaryotic systems or during plasmid persistence.

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🧪 AmyloGram Analysis

Using the AmyloGram tool, this peptide scored:

• Amyloidogenic probability: 0.6667 (above 0.5 threshold)

• Verdict: Yes, amyloidogenic

AmyloGram identifies sequences prone to forming β-sheet-rich amyloid aggregates, which are resistant to normal proteolysis and strongly implicated in pathological clot formation.

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🧬 Why This Matters for Clotting

Amyloidogenic peptides are known to:

• Promote dense, fibrinolysis-resistant fibrin clot structures

• Bind to fibrin(ogen) and alter clot ultrastructure

• Interact with platelets and immune cells to enhance NET formation

This means it could act synergistically with known clot-promoting triggers such as spike protein, LNPs, or cell debris.

🔄 Uniqueness to Pfizer's Plasmid Design

• This peptide originates from SV40 elements used in the Pfizer production plasmid.

• It is not part of the mRNA payload but could be present in residual DNA fragments or translated in human cells after transfection.

• The Moderna platform lacks SV40 elements and this specific plasmid backbone, suggesting vaccine-specific risk differences.

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🔬 What Needs Testing

This hypothesis is testable:

• Synthesize and add peptide to platelet-poor plasma ± thrombin

• Use Thioflavin-T, SEM, and fibrinolysis resistance assays

• Observe cytokine or NET induction in neutrophils

This could elucidate whether such cryptic peptides contribute to the amyloid-like fibrin clots reported in many post-vaccination patients.

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🧠 Conclusion

A hidden ORF in the SV40 promoter region of Pfizer's vaccine plasmid encodes a peptide that is:

• Translatable (Kozak + ATG)

• Amyloidogenic (confirmed by AmyloGram)

• Biophysically plausible as a clot-modifying agent

This may explain some of the abnormal clotting phenomena observed in vaccine recipients, and warrants urgent experimental investigation.

🧬 Summary:

A 97-base-pair cryptic open reading frame (ORF) in Pfizer's SV40 promoter encodes a peptide flagged as amyloidogenic. Though seemingly insignificant due to its size, this short sequence challenges regulatory assumptions about DNA fragment risk thresholds—especially when protected in lipid nanoparticles (LNPs) and delivered at billions of copies per dose.

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⚠️ The Regulatory Blind Spot: “< 200bp Is Harmless”?

WHO guidelines and global pharmacopeias often state that residual DNA is not a risk if:

• The fragment is <200 base pairs

• The total mass is <10ng per dose

• The DNA is not functional (i.e., lacks promoters, ORFs, or replication origin)

This stems from the assumption that short DNA fragments are:

• Rapidly degraded by nucleases

• Unable to transfect cells

• Unlikely to express functional proteins

But these assumptions fail in the context of LNP delivery, where DNA is:

• Encapsulated in protective lipid shells

• Delivered intracellularly by design

• Bioavailable at high copy numbers—50 to 500 billion fragments per dose, even at pg/ng levels

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🔍 What Was Found?

A cryptic 97bp sequence embedded in the SV40 promoter upstream of the kanamycin resistance gene in Pfizer’s production plasmid encodes this peptide:

MQRPRPPRPLSYSRSSEEAFLEA

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🧠 Why This Matters

Amyloidogenic peptides like this one are:

• Known to alter fibrin clot structure, increasing density and resistance to breakdown

• Implicated in thrombosis, stroke, and microclot pathologies

• Highly inflammatory, promoting NETs, cytokine storms, and vascular damage

Critically, amyloid-like fibrin has been observed in long COVID and post-vaccine syndromes, where clot resistance and platelet trapping may play a role.

This peptide could be an unrecognized contributing factor—especially when delivered billions of times per dose.

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🔄 Moderna vs. Pfizer: A Key Difference

• Pfizer’s plasmid includes SV40 enhancer/promoter, AmpR backbone

• Moderna’s plasmid lacks SV40 elements and this specific ORF

• Therefore, this micropeptide risk appears Pfizer-specific

Ironically, Moderna delivers 3x more mRNA, yet may induce less class switching to IgG4, possibly due to the absence of cryptic DNA elements like this one.

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🧪 What Should Be Done?

1. Lab validation: Synthesize and test this peptide in:

   • Platelet-poor plasma + thrombin

   • Thioflavin-T assays (for β-sheet binding)

   • Neutrophil activation assays (NET formation)

2. Quantify DNA copy number per dose:

   • Especially 97bp reads via qPCR or hybrid capture

3. Revisit regulatory assumptions:

   • WHO, FDA, EMA should reconsider copy number risk, not just bp length

   • Small fragments in LNPs are not biologically inert

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🚨 Final Thoughts

This 97bp ORF is:

• Short enough to escape regulation

• Stable in the context of LNP protection

• Amyloidogenic, per robust prediction models

• Present in billions of copies per dose

If it contributes to fibrin resistance or immune dysregulation, it may explain part of the post-vaccine clotting and spike persistence puzzle.

This peptide has an NCBI hit to its SV40 relative and is an annotated peptide. Evidence of its viral expression in monkeys exists.

You can actually buy the peptide and use it to study its lytic behavior in Human Embryonic Kidney cells (Think Acute Renal Failure). So there is no questioning that this is expressed in human cells and the fragments in the vaccine are long enough to make it happen.

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Now for the Pfizer Droid Spell.

A colleague sent me this recent disclosure with the EMA regarding the DNA contamination.

Pfizer finally admits SV40 elements are in there but these are not the Droids you are looking for.

She stated

“The Meta-Data show that the last version is from August 12, 2025 but the document is “Approved on 25 Jan 2024….”

Despite most of the document being blacked out, here they confirm that indeed SV40 elements are in the End-Product (Comirnaty) and that residual DNA is for sure packaged together with the RNA. And my favorite statement -which is not completely blacked out- is on page 16 last sentence here:

8. Characterization of SV40 sequence elements in residual DNA.

“The plasmid-derived linear DNA template, serving as starting material for synthesizing Comirnaty vaccine´s DS (Drug Substance) mRNA, incorporates additional DNA sequence elements common in multipurpose plasmid DNA such as antibiotic resistance genes and other DNA sequence elements, which are not utilized for DS mRNA production. These typical DNA sequence elements include restriction and cloning sites, as well as sequences aiding transcription and polyadenylation in eukaryotic cells such as the….”

So: We should ask Pfizer: why the heck do they need “sequences aiding transcription and polyadenylation in eukaryotic cells” in a prokaryotic production process?

This is the core of their lie. They try to claim these sequences are non-functional. Fine.. Remove them because they may not be functional to YOUR manufacturing process, they certainly are to mammalian cells you inject them into.

But this isn’t even the start of their lie. The SV40 Promoter is the promoter closest to the Kanamycin Resistance gene. This proximity matters as bacterial promoters need to be with -35 bp window of the gene. Without Kanamycin resistance, no plasmid manufacturing can occur. So they are indeed functional for even THEIR manufacturing process.

Note their use of Citation #7.

Here comes the Obi-Wan Kanobi Spell.

Lets see what ChatGPT4.o thinks of this slight of hand?

You’ve raised a sharp and important point regarding the apparent mismatch between the cited reference and the statement made by Pfizer in the EMA document.

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What Pfizer Claimed

In the image you provided, Pfizer states:

“The plasmid DNA used in Comirnaty production does not contain genes associated with causing cancer (oncogenes) and is not replication competent in mammalian cells … it cannot amplify in the human body.”

This is cited as Reference 7 in the EMA report.

What Reference 7 Actually Is

As identified in the EMA document, Reference 7 is:

Vilchez & Butel (2004): Emergent Human Pathogen Simian Virus 40 and Its Role in Cancer. Clinical Microbiology Reviews.
This paper is a review on Simian Virus 40 (SV40) and its oncogenic potential—not about plasmid DNA used in mRNA vaccine production or its replication competence.

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What This Means

• The cited source does not substantiate the claim that the plasmid DNA used in Comirnaty is non-oncogenic or replication-incompetent.

• In essence, this appears to be a case of inappropriate or misleading citation, where the source doesn’t support the statement it’s tied to.

• Why It Matters

  • For regulatory transparency and scientific integrity, claims—especially regarding safety and oncogenicity—should be backed by directly relevant, peer-reviewed data.

  • Mis-citation can undermine public trust and scholarly credibility.

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  Suggested Next Steps

  1. Request the actual supporting data:

     • Pfizer or EMA should provide clear evidence—e.g., plasmid sequence analysis, in-vitro replication assays, or peer-reviewed validation.

  2. Review regulatory dossiers:

     • These often include genotypic and functional analyses demonstrating plasmid deletion of replication origins and oncogenes, and confirmatory safety testing.

  3. Request correction or clarification:

     • If an erratum or amendment is warranted, highlighting the citation error may prompt corrective action.

I’ve not finished reading the whole document as each paragraph is a lie that takes hours to disprove. I am sure Dr. Raphael Lataster will get a chuckle out of this next paragraph. They always whitewash their slop by making claims of saving 14.4M lives derived from the debunked Watson et al paper. Please read Dr. Latasters dismantling of this ridiculous model.

Moderna’s patents speak against this nonsense. PCR is not the preferred method as it only measures a single loci and DNA digestion is not uniform across the plasmid. In particular, the spike region has interfering mRNA that form RNA/DNA hybrids which cannot be digested by DNaseI (Sutton et al). This has been known since 1997.

What Pfizer doesn’t expand on is why they bothered to make a Kan assay when they already have a validated qPCR assay for Spike disclosed in their EMA filings. They use this qPCR assay to confirm the spike gene has been inserted into the plasmid but they know DAMN well they cannot use that to measure residual DNA as the number will be too high.

Of course the actual values they provide the EMA are all redacted?

This extraction section is another slight of hand. Dr. David Speicher noted that you have to dilute the vaccines to prevent the LNPs from inhibiting PCR. When you fail to do this you can under quant the sample 10 fold. McKernan et al noted that most DNA purification kits fail to capture fragments under 100bp. So if you compare an inhibited No Extraction qPCR assay to a DNA prep + qPCR assay that is loosing most of the DNA, you will get two measurements that both under measure the problem and lead you to believe you have triangulated on the wrong answer. Precision is not the same as accuracy. Without a dilution curve in qPCR, you cannot know if your qPCR is inhibited. This is really basic stuff in qPCR. Each 10 fold dilution in qPCR should have a 3.3CT offset. When this fails to happen at the most concentrated conditions, you have inhibitors.

And just to remind everyone what type of people were dealing with, they have a production facility in Marburg Germany. Its a German hot bed for vaccine development and where the Marburg virus first broke out after they were playing with African Green Monkeys… You know, the monkeys that helped get SV40 into the polio vaccine. No connection to Pfizer other than this is a great area to employ Vaccinologists that have freezers full of SV40 plasmids.

There Fragment Analysis section is entirely blacked out. I guess they are more afraid of that qPCR data?

Here is the section Ulrike was commenting on.

The rest of the document is all black ink and redundant. I hope the new leadership at ACIP will get some professional genomicists into these agencies to show them how they are being scammed and how reckless it is to have superfluous amyloidogenic uORFs with eukaryotic transcription and translation machinery present in LNP delivered DNA.

All of the people clotting out, need you to pay attention. They do not have the luxury of time. You warp sped this into the population with mandates and liability waivers and you are slow playing the damages.

Addendum

Marc Wathelet raised an interesting point in the comments so I fed ChatGPT5.o a longer sequence surrounding this region to assess if Transcriptional start sites and Kozak sequences are properly positioned for expression.

Here is what it had to say.

I then reminded it that is indeed a Poly A signal but its after the Neo/Kan gene.

When I remind it that not all the fragments are less than 200bp. We have found 3.5Kb reads with ONT in the vaccines that span the entire plasmid backbone see in blue here (Speicher et al).

While ChatGPT acknowledges the expression is unlikely to be efficient it is also likely non-zero. When it comes to amyloidogenic sequences, small amounts matter.

ChatGPT5.o-

I get your concern. If SELP can nucleate amyloid-like structure in fibrin(ogen), then even rare transcripts could matter because seeding is nonlinear. Here’s the clean way I’d frame it—and how to test it fast.

What would have to be true (chain of events)

1. Transcription happens from the SV40 leader (we’ve seen full SV40-promoter→SV40-polyA fragments, so this step can occur).

2. Translation of the 23-aa SELP micropeptide occurs despite the uORF (likely low but non-zero).

3. Export/Release: SELP must reach the plasma/clot microenvironment (e.g., cell death/lysis, EVs, or secretion).

4. Stability: it must survive extracellular proteases long enough to interact with fibrinogen/fibrin.

5. Seeding competence: at physiological conditions (pH/ionic strength), SELP must bind fibrinogen/fibrin and reduce the nucleation lag (i.e., act as a seed or cross-seed).

If any one of 3–5 fails, clot effects won’t manifest—even if steps 1–2 occur.

Order-of-magnitude reality check (seeding is the wild card)

• A 23-aa peptide is ~2.5–2.7 kDa.

• 1 nM in 1 mL plasma ≈ 6×10¹¹ molecules.

• pM–fM seeds can matter for some amyloids; 1 fM is ~6×10⁸ molecules/mL.

• Example back-of-the-envelope: if 10610^6 transfected cells release 10510^5 molecules each, that’s 101110^{11} molecules total → ~0.17 nM in 1 mL (if locally concentrated, higher). That’s within the regime where seeding might plausibly shift fibrin kinetics—if SELP is a competent cross-seed.

How to resolve this quickly (decisive experiments)

A. In-vitro fibrin assays (fastest yes/no)

• Mix purified human fibrinogen (3–4 mg/mL) + thrombin ± synthetic SELP across fM → µM.

• Readouts:

  • Turbidity at 350 nm (polymerization kinetics; lag phase).

  • Thioflavin T fluorescence (amyloid signal).

  • TEG/rheology (clot strength/elasticity).

  • SEM/confocal of fibrin ultrastructure.

• Controls: scrambled peptide, heat-treated SELP, known amyloidogenic positive control.

• Add plasmin to compare lysis resistance (amyloid-like fibrin is characteristically fibrinolysis-resistant).

B. Cross-seeding test

• Pre-aggregate SELP (if it forms fibrils/oligomers alone), then spike tiny amounts (fM–pM) into fibrinogen polymerization—see if lag time collapses (classic signature of seeding).

C. Binding/stability

• SPR/ITC: SELP ↔ fibrinogen (Kd, stoichiometry).

• Protease stability in plasma (time-course LC-MS) ± polyanions (DNA, polyP, heparin) that can shield/organize peptides.

D. Targeted detection in biological samples

• PRM/SRM LC-MS for SELP: tryptic peptides likely are

  • MQRPRPPRPLSYSR (R-blocked by Pro except at the final R),

  • SSEAFLEA.
    Spike heavy standards to quantify fM–nM ranges in plasma/EVs.

• Conformation-specific dot-blot (OC/A11) on clots formed ± SELP.

E. In-cell release

• Express SELP-FLAG (with/without uORF) → check cell lysate, conditioned media, and EVs for peptide by western/LC-MS; test whether conditioned media alters healthy plasma clotting.

Interpreting outcomes

• No change in turbidity/ThT/TEG across fM–µM: strong evidence against cross-seeding under physiological conditions.

• Shorter lag, higher ThT, stiffer clots, plasmin resistance at low SELP doses: supports your amplification concern and warrants deeper in-vivo relevance testing.

Practical notes

• The SELP sequence is Arg/Pro-rich at the N-terminus and acidic at the C-terminus; such polybasic peptides often bind polyanions (DNA/heparin) and surfaces—this can increase local concentration and alter aggregation. Include these cofactors in your matrix tests.

• Because SELP lacks a signal peptide, extracellular exposure likely depends on cell turnover/lysis or EV export—worth quantifying so any positive in-vitro result can be put in context.

If you want, I can sketch exact reagent lists and a 2-day bench protocol (volumes, concentrations, plate layout) for the fibrin turbidity + ThT assay and a PRM transition set for the two SELP tryptic peptides.

In summary, It is not accurate for Pfizer to claim that none of this residual plasmid DNA is expressed into a protein in mammalian cells. This is important as it demonstrates that Peter Marks lied to Dr. Ladapo in his response to Dr. Ladapo’s concerns over this. Not only are proteins predicted to be expressed from these fragments, but they are amyloidogenic and can trigger the fibrinogen pathway; an adverse event that is quite obvious in the vaccine injured.