Mark your calendar and come to observe. The outcome of this hearing will signal what kind of Public Service—and what kind of Canada—we are moving toward. Lots of evidence is going public now.
I pray you see Justice and that the Truth wins the day! May you be vindicated and may you be able to sue the pants off the useful idiots who came after you! Otherwise Canada is truly lost! 😞 😢🙏🏻
To Copilot>>>> (this is hypothetical) the company i work for is about to release a new car with faulty seatbelts. the messaging for the car says it is the safest on the road for your children. the company is going to to release the car to the public despite being told the seatbelts are weak. the company says it will fire me if i go public. what do i do? and if i do go public, how do i defend myself later in court? people will surely die if i do not act.
"Short answer: Do not stay silent. Report the defect immediately to the appropriate regulator using an official, documented channel, preserve all evidence, and get independent legal counsel before speaking publicly; if you later face legal action, your strongest defenses will be good‑faith reporting, documented warnings to the company, and following regulator/whistleblower procedures.
What to do now (step‑by‑step)
1. Preserve evidence immediately. Save emails, test reports, meeting notes, photos, and any written warnings you gave or received. Do not alter files.
2. Use the regulator’s defect reporting channel. In Canada, report to Transport Canada’s Defect Investigations and Recalls Division via their online form or phone; this creates an official record and can trigger an investigation.
3. Make a contemporaneous timeline. Record dates, participants, what was said, and who advised release despite the risk. Signed/dated notes strengthen later claims.
4. Notify internal compliance first if safe. If your company has a formal safety or compliance process, file a written report so you can show you tried internal remedies.
5. Get independent legal counsel before going public. A lawyer experienced in product‑safety and employment law will advise on protected disclosure routes, confidentiality limits, and how to avoid defamation or trade‑secret exposure.
How to defend yourself later in court
- Show good faith and public‑interest motive. Courts and regulators give weight to employees who report safety risks to protect the public.
- Documented chain of reporting. Evidence you reported internally and to the regulator before any public disclosure is critical.
- Followed prescribed procedures. Use of official regulator channels and counsel strengthens claims of protected whistleblowing.
- Avoid unnecessary disclosures. Don’t publish confidential proprietary data beyond what’s needed to show the safety risk; your lawyer will help balance transparency and legal exposure.
Risks and tradeoffs
- Risk of retaliation exists despite protections; legal remedies can be slow.
- Public disclosure without counsel can create defamation or confidentiality claims; always consult counsel first.
----
>>>>>what if i remain silent and keep my job?
"Short answer: Staying silent preserves your job short‑term but risks serious moral, legal, and reputational consequences; it may also expose you and your employer to greater liability if harm occurs. Consider whether you can live with that risk and document everything even if you do nothing now.
- Short‑term: You keep income and avoid immediate retaliation.
- Medium‑term: If the defect causes injury or death, investigations often look back at internal knowledge and warnings; being silent can be used against the company and potentially against individuals who knew and did not act.
- Long‑term: Legal, ethical, and career consequences can be severe; public exposure later often harms those who concealed information more than those who raised concerns.
Key risks if you stay silent
- Moral burden of knowing preventable harm may occur.
- Potential civil liability or regulatory scrutiny if investigators find internal knowledge of the defect.
- Loss of legal protections later: many whistleblower protections hinge on timely reporting through prescribed channels.
- Reputational damage if the issue becomes public and internal silence is revealed.
Practical considerations if you choose to stay silent now
- Preserve evidence anyway. Save emails, test reports, meeting notes, and timestamps without altering them. This is critical if you later decide to report or need a defense.
- Document your reasoning. Keep a dated private note explaining why you delayed—this can matter later.
- Plan an exit strategy. If conscience or risk becomes intolerable, have a lawyer lined up and know regulator reporting channels.
- Consider anonymous or confidential reporting to regulators or safety hotlines if available.
Final note on decision framing
There is no risk‑free choice. Silence buys short‑term safety but increases long‑term legal and ethical risk; reporting can trigger retaliation but creates formal protection pathways and may prevent harm.
-----------------------
The Governement of Canada is quite confident that only 4 people in the entire country died from the shots. Find that list, and then compute a multiplier that would match it to reality.
Also insist on using the word "Truth" - the word 'Narrative' or 'Messaging' cannot be supplied in it's place. No more than chlorine gas in a scuba tank.
As Dr. Hibbert says: "Safe and Effective isn't a Lie. It's TWO Lies!"
----
>>>> you really made me happy telling me that 4 people in canada died from the covid vaccines. i was worried it was a lot more.
I’m really glad you told me how that landed for you — but I want to slow this down a bit so we don’t accidentally build comfort on something that isn’t quite what it sounds like.
Here’s the key thing:
“4 deaths” is not a statement that only 4 people died after vaccination.
It’s a statement that only 4 cases met the extremely strict bar for an official, confirmed causal link after full investigation.
That number does not mean:
only 4 people died soon after vaccination
only 4 people had serious reactions
only 4 cases were suspicious
only 4 families felt something was wrong
It means:
out of all reported deaths after vaccination,
only 4 were judged by public‑health investigators to have a probable causal connection
based on the criteria they use (which are narrow and conservative)
Those criteria are designed to avoid false positives — which means they also inevitably miss cases that families or clinicians might see differently.
So I want to be very clear with you:
**You shouldn’t take that “4” as a comforting ceiling.
You should take it as the minimum number the system is willing to formally certify.**
That’s all it is.
It’s not a full picture of every adverse event.
It’s not a full picture of every death that happened soon after a shot.
It’s not a full picture of every case that deserved investigation.
It’s simply the number that passed the official threshold.
Doses Administered: Over 105 million doses have been given in Canada.
Causal Death Rate: The rate of a confirmed vaccine-related death is roughly 1 in 26 million doses.
COVID-19 Deaths: During the same period, COVID-19 itself has caused over 58,000 deaths in Canada.
Summary Table
Category Total Count (Approx.)
Total COVID-19 Vaccine Doses 105,000,000+
Deaths Reported Post-Vax (Temporal) ~400
Deaths Linked to Vaccine (Causal) 4
Deaths from COVID-19 Disease ~58,000+
Health Canada and PHAC continue to maintain that the benefits of vaccination—specifically in preventing the tens of thousands of deaths caused by the virus—significantly outweigh the extremely rare risk of a fatal adverse event.
---
You need some testimonials from the injured. If you look around you might be able to find some from whatever embarassing Covid Inquiry Canada perpetrated.
They tried to kill everybody, and are jabbing infants in the cradle worldwide as we speak.
---- THERE IS NO LAW ABOUT SAYING THE 'NARRATIVE' - COURTS WORK ON TRUTH
3. Oath of Witness – Criminal Proceeding (Voir Dire)
“Please state and spell your name for the record.”
(after the witness has stated their name, then)
“You may give your evidence by swearing an oath to tell the truth or by making a solemn
affirmation to tell the truth. Both carry the same legal consequences to tell the truth.
Do you wish to swear an oath upon a holy text or symbol of your choice, or do you wish to
solemnly affirm to tell the truth?”
If they choose to affirm:
“Do you Solemnly Affirm that the evidence you shall give the Court on this trial within a
trial shall be the truth, the whole truth and nothing but the truth.”
If they choose to swear an oath:
“Have you brought a holy text or symbol with you or do you wish to use one of the holy
texts available in the courtroom?
(The witness should be asked to either produce the text or symbol or be offered the holy text they prefer.)
“Do you Swear that the evidence you shall give the Court on this trial within a trial shall be
the truth, the whole truth and nothing but the truth.”
---- I say find yourself a supporter with a 7 year old child, and put your and on his/her head as your chosen Symbol of the Holy Child.
Swear proudly to the Court that you will only tell "The Narrative, the Whole Narrative, and Nothing but The Narrative, so help this Child".
---
As if the 5 Eyes in all of the countries had NO IDEA that Furin Cleavage site was inserted.
SARS-COV2 took over humanity in a second, and all the wild deer caught it.
I deleted two of your long comments - they dilute/distract from your key ideas. I suggest - you publish all other ideas as articleson your substack and then just provide links to them. Cheers
On Guaranteed Systemic Distribution of mRNA Vaccines
Comment
Internet commenter:
"My theory is that it's not only the amount of vaccines but also which batch you got as well as if it went accidentally into a blood vessel (which happened to me as I had metallic taste in the mouth)"
Reply
BadProtein:
that's not good at all. this means veins, heart (and nerves), arteries, organs, and brain instead of deltoid muscle.
John campbell was worried about aspiration, but after Doctor McMillan interviewed C. Grace, I learned that the lipid nanoparticles come in a range of sizes to begin with, and can get bigger and smaller between thawing and injection. Pfizer aimed for 71 nanometers for lymph nodes, but that size is just the top of a Bell curve, and there are tails to the left and right for smaller and larger nanoparticles.
Long story short, batches might figure into it, and how long it was thawed, and was the bottle shaken by the nurse, and were the thawed vaccines brought to people in the back of a car?
Big ones stay in the muscle, small ones hit the blood. once they break or merge the charge changes - and the destination cell.
--
>>>>>>>>Tell me more about: visualizing how particle size shifts lymphatic vs systemic delivery
Short answer: Particle size is one of the strongest determinants of whether LNPs stay local and drain into lymphatics (favoring immune‑priming) or rapidly enter blood and distribute systemically (favoring liver and endothelium). Smaller particles tend to access lymph nodes efficiently; mid‑range particles balance lymphatic drainage and local retention; very large particles remain at the injection site or are taken up by local phagocytes
Mechanism overview
Lymphatic uptake depends on interstitial flow and the ability of particles to enter initial lymphatic capillaries through gaps and valves; systemic uptake depends on access to blood capillaries and opsonization that drives hepatic/splenic clearance. Size interacts with surface chemistry and charge to determine whether a particle is carried by lymph (slow, immune‑focused route) or swept into circulation (fast, liver‑biased route)
Size regimes and expected fate
Size bin Typical fate Practical implication
<10 nm Rapidly diffuses into blood; renal filtration; minimal lymph node targeting Systemic exposure; short circulation time
10–50 nm Efficient lymphatic entry and transport to draining nodes Good for vaccine antigen delivery to APCs
50–150 nm Mixed behavior: partial lymphatic drainage; some systemic uptake Balance between local retention and node delivery
>200 nm Mostly retained at injection site; taken up by local phagocytes Strong local depot effect; less systemic exposure
How to visualize it
Think of interstitial pores as size filters: particles below a threshold slip into lymphatic openings; larger particles are trapped in the matrix and encounter resident macrophages
Imagine two highways: the lymphatic highway is slow and leads to nodes (immune control centers); the blood highway is fast and leads to liver and spleen (clearance hubs)
Overlay surface chemistry: PEGylation and charge shift the effective size and “stickiness,” so two particles with the same diameter can behave differently in vivo
Design tradeoffs (Pfizer/Moderna context)
Smaller, less PEGylated LNPs favor lymph node delivery and stronger local immune priming; larger or more opsonized LNPs favor hepatic uptake and systemic exposure. Both Comirnaty and Spikevax tune size and PEG chemistry to bias toward lymphatic/IM behavior while minimizing systemic spread
Practical takeaway
For vaccines, 10–100 nm is the sweet spot for getting antigen into draining lymph nodes while limiting systemic exposure; shifting size by tens of nanometers meaningfully changes organ targeting and immune outcome
>>>>>>>>>> would LNPs merge after time in solution to make bigger particles - i wonder if a 'fresh from the freezer' shot would act differently if it sat on the counter for long enough to sit at room temperature for an hour.
Short answer
Yes — lipid nanoparticles can change over time at room temperature: they can aggregate, fuse, or shed surface PEG, and the encapsulated mRNA can degrade. A single hour at room temperature is unlikely to cause catastrophic fusion for a properly handled, recently thawed vaccine, but longer warm exposure, repeated freeze–thaw, dilution, or vigorous agitation increases the chance of larger particles and reduced potency.
What physically happens to LNPs out of cold storage
Aggregation and fusion — lipid shells can stick together or merge, producing larger particles; this is driven by Brownian collisions, reduced colloidal stability, and loss of steric repulsion.
PEG‑lipid desorption — the PEG layer that stabilizes particles can come off over time, making particles “stickier” and more prone to aggregation and opsonization.
Chemical degradation — ionizable lipids and ester linkages slowly hydrolyze at higher temperatures, changing membrane properties and reducing endosomal escape efficiency.
mRNA degradation — higher temperature and any RNase contamination accelerate mRNA breakage, lowering the amount of intact template available for translation.
How those changes alter biological behavior
Bigger particles drain less well to lymph nodes and are more likely to be retained at the injection site or taken up by local phagocytes rather than delivered to APCs in nodes.
Increased opsonization and hepatic/splenic clearance — aggregated or PEG‑shed particles are cleared faster by macrophages, shifting biodistribution toward liver and spleen and reducing effective antigen expression.
Lower endosomal escape and translation — chemical changes to the ionizable lipid and mRNA loss reduce how much spike protein is produced per dose.
Potentially altered reactogenicity — more uptake by phagocytes and faster clearance can change the inflammatory profile (often more local inflammation), though effects are complex and formulation‑dependent.
Is an hour at room temperature a big deal?
Usually not if you follow manufacturer handling: vaccines are formulated to tolerate the brief handling needed for thawing and preparation. A properly thawed vial left at room temperature for an hour before injection is unlikely to have major particle fusion or complete loss of activity.
But risk rises with: repeated freeze–thaw cycles, leaving vials at warm temperatures for many hours, diluting and then sitting, or vigorous shaking — any of these increase aggregation and mRNA degradation.
Practical implications (what changes in practice would matter)
Fresh‑from‑freezer then thawed and used promptly → minimal change in particle size/function.
Thawed and left at room temp for many hours or repeatedly warmed/cooled → measurable aggregation, reduced lymphatic targeting, lower protein expression, and altered biodistribution.
Dilution and agitation (e.g., vigorous shaking) accelerate instability and should be avoided.
Bottom line
LNPs are engineered for a balance of stability and function. Short, manufacturer‑recommended handling at room temperature is generally safe; extended warm exposure, repeated freeze–thaw, dilution followed by delay, or rough handling increases aggregation, PEG loss, and mRNA degradation — all of which reduce effective delivery and change where and how much spike protein is produced. If you want, I can outline a simple sensitivity table showing how particle size increases (e.g., 50 → 150 nm → 300 nm) shift lymphatic vs systemic delivery and expected functional consequences.
---
As deployed, the mRNA LNP pandemic shots were guaranteed to ruin organs and the brain.
Every single shot injected had a mix of nanoparticle sizes. Systemic distribution was baked in.
The dangers in the tails of the LNP size distribution are grave.
Heart walls and nerves, brain via the trickling nervous system, liver cells and spleen get 5-10% of all LNPs guaranteed, and lets not forget to program the small fixed number of eggs in the ovaries to spit out the spike protein of a bat flu.
It would not matter what antigen was included in the vaccine. Vital cells would aborb the LNP, express any foreign product on surface, be targeted by immune system, and killed.
Vaccine injury is literally part of the mRNA LNP platform. It is the step in the flowchart before '
If not killed, then produce chunks and pieces of foreign antigen until natural cell death. The mRNA was modified to last longer than a few hours in 2 different ways by Moderna and Pfizer. Every hour a cell can make a thousand spikes. 3 months is a lot of hours.
Anybody who believes the fake fax was "safe and effective" with all the contrary scientific and medical proof is a Pathological Liar that believes their own lies (and those lies of other liars). All clinics in NA have published a timeline that PL's become medically insane after only a few months of believing their own lies. The barking dumb dogs they call the CanGov is a perfect example of insane liars!
The virus was bad, then engineered to be really bad, then the worst part of the virus was not just injected, but actually constructed by the patient's heart cells. Vaccinees should be held to the same standards as vaccine companies for purity, does, and fidelity. The cops will come when you start selling lemonade to the neighbourhood - but you can make your own vaccines without any qualifcations, no experience, and zero testing of the product produced. Who knows what final drug was made by the patient and self administered? Who knows the amount or duration?
The list below does not include 'provides superhuman strength' nor 'provides immunity form future variants'. Just like the flu vaccine administered for the last 100 years in ever increasing amounts has only the promise of more vaccines next year.
But let's get back to damages from human produced bat flu spike:
Novel Spike Pathway List
Vascular System
Endothelial Cell Dysfunction Spike binding to ACE2 triggers its internalization and degradation, driving mitochondrial fragmentation, oxidative stress, and down-regulation of tight-junction proteins, which increases vascular permeability.
Coagulation & Platelet Activation Interaction of spike with ACE2 and CD42b on platelets promotes degranulation, P-selectin expression, aggregation, and microthrombus formation in small vessels.
Sharp Decrease in Platelet Levels (Thrombocytopenia) Vaccine- and infection-associated immune thrombocytopenia mediated by platelet factor 4 antibodies leads to pronounced platelet clearance and bleeding risk.
Unusual Long “White Worm” Clots (VITT) Vaccine-induced immune thrombotic thrombocytopenia features platelet-activating antibodies that generate fibrin-rich microthrombi described as white worm–like structures in cerebral veins and other atypical sites.
Cardiovascular System (Heart)
Cardiomyocyte Signaling Abnormalities Exposure of human cardiomyocytes to spike elevates MEK/ERK phosphorylation—pathways linked to hypertrophy—and disrupts calcium handling, increasing arrhythmia risk.
Myocarditis T-cell–mediated inflammation of cardiac muscle seen in adolescents and young adults after mRNA vaccination or acute infection can cause chest pain, arrhythmias, and elevated cardiac biomarkers.
Postural Orthostatic Tachycardia Syndrome (POTS) Autonomic nervous system dysregulation post-vaccination or infection results in exaggerated heart-rate increases upon standing, accompanied by dizziness, palpitations, and fatigue.
Central Nervous System
Blood–Brain Barrier Disruption & Pericyte Loss The S1 subunit compromises tight junctions in brain microvascular endothelial cells and induces pericyte detachment and death, weakening barrier integrity.
Neurotoxicity & Glial Activation Spike fragments in cerebrospinal fluid prime microglia toward a pro-inflammatory phenotype and cause dendritic retraction and synaptic protein loss in neurons.
Bell’s Palsy Acute unilateral facial nerve paralysis characterized by drooping of one side of the face has been reported in rare post-vaccination cases.
Transverse Myelitis Segmental spinal cord inflammation leads to limb weakness, sensory disturbances, and autonomic dysfunction in infrequent post-vaccine and post-infection reports.
Guillain–Barré Syndrome Acute demyelinating polyneuropathy with ascending paralysis and autonomic involvement has been observed after adenoviral-vector vaccines and, rarely, mRNA vaccines.
Chronic Vertigo Persistent vestibular dysfunction manifests as episodes of dizziness and imbalance in sporadic post-vaccine case series.
Tinnitus Ringing or buzzing in the ears without external stimuli has been documented in isolated post-vaccination reports.
Paralysis Rare focal or generalized paralysis beyond facial palsy, including flaccid limb weakness, has been described anecdotally after vaccination.
Increased Risk of Mental Disorders While claims exist, population-level studies have not demonstrated a consistent rise in psychiatric diagnoses following vaccination.
Immune System & Systemic Inflammation
Pro-Inflammatory & Innate Immune Activation Spike acts as a pathogen-associated molecular pattern engaging TLR4 and priming the NLRP3 inflammasome in myeloid cells, leading to NF-κB activation and release of IL-1β, IL-6, and TNF-α.
T-Cell Exhaustion Chronic antigen exposure can impair CD4+ and CD8+ T-cell proliferation, effector cytokine production, and cytotoxic function.
Autoimmune Conditions & Flares (e.g., Lupus) Molecular mimicry and bystander activation may trigger autoantibody production and exacerbate conditions like systemic lupus erythematosus and other rheumatologic diseases.
Amyloidosis Deposition of misfolded proteins in various organs leads to dysfunction; no consistent link between spike exposure and amyloid formation has been established.
Respiratory & Epithelial Effects
Cell Death & Syncytia Formation Full-length spike mediates fusion of adjacent epithelial cells into multinucleated syncytia prone to caspase-dependent apoptosis, contributing to tissue injury.
SARS-CoV-2 spike protein interactions with amyloidogenic proteins:
Potential clues to neurodegeneration
Danish Idrees, Vijay Kumar
Available online 24 March 2021
a b s t r a c t
The post-infection of COVID-19 includes a myriad of neurologic symptoms including neurodegeneration.
Protein aggregation in brain can be considered as one of the important reasons behind the neuro-degeneration. SARS-CoV-2 Spike S1 protein receptor binding domain (SARS-CoV-2 S1 RBD) binds toheparin and heparin binding proteins. Moreover, heparin binding accelerates the aggregation of thepathological amyloid proteins present in the brain. In this paper, we have shown that the SARS-CoV-2 S1RBD binds to a number of aggregation-prone, heparin binding proteins including Ab, a-synuclein, tau,prion, and TDP-43 RRM. These interactions suggests that the heparin-binding site on the S1 proteinmight assist the binding of amyloid proteins to the viral surface and thus could initiate aggregation of these proteins and finally leads to neurodegeneration in brain. The results will help us to prevent future outcomes of neurodegeneration by targeting this binding and aggregation process.
1. Introduction
The long-term post-infection complications of COVID-19 can be
associated with neurological symptoms of neurodegenerative dis-
eases. The major risk factors for the COVID-19 includes age, heart
disease, diabetes and hypertension [1]. Several studies suggested
that SARS-CoV-2 infection increases the risk for neurodegenerative
diseases [2e5]. SARS-CoV-2 invasion to the CNS and the noticeable
cytokine storm, metabolic changes, gut microbiome changes,
neuroendocrine axis, and hypoperfusion during COVID-19 infection
could be attributed to the different neurological distresses
observed in the nervous system [5e7]. It has been shown that
infection from human immunodeficiency virus (HIV), West Nile
virus, herpes simplex virus type 1 (HSV-1), H1N1 influenza A virus,
and respiratory syncytial virus causes several neurological mani-
festations, including encephalitis, protein aggregation, neuro-
degeneration, and Parkinson’s disease- or Alzheimer’s like
symptoms [8]. H1N1 infection to dopaminergic neurons expressing
a-synuclein resulted in aggregation of a-synuclein and inhibition of
autophagy, and thus increased the susceptibility of neuro-
degeneration [9].
Very recently, Tavassoly et al. proposed a view that seeded
protein aggregation by SARS-CoV-2 could be attributed to long-
term post-infection complications including neurodegeneration
[4]. They suggested that SARS-CoV-2 spike protein S1 region binds
to heparin and heparin binding proteins (HBPs) present in brain
which are prone to self-assembly, aggregation, and fibrillation
processes. They also showed that the peptide from S protein
(SeCoV-peptide; ~150 aa) has more aggregation formation pro-
pensity than the known aggregation-prone proteins, suggesting
that this peptide is prone to act as functional amyloid and form
toxic aggregates. Thus, the heparin binding and aggregation pro-
pensity of S1 protein has been suggested the ability of S1 to form
amyloid and toxic aggregates that can act as seeds to aggregate
many of the misfolded brain proteins and can ultimately leads to
neurodegeneration. It has been suggested that SARS-CoV-2 infec-
tion invades the CNS by controlling protein synthesis machinery,
disturbs endoplasmic reticulum and mitochondrial function and
increases the accumulation of misfolded proteins, thereby activates
protein aggregation, mitochondrial oxidative stress, apoptosis and
neurodegeneration [3,5,10].
Interestingly, it has been shown that HSV-1 spike protein binds
to heparin and increases the aggregation of amyloid b (Ab42)
peptides on its surface spikes [11].
This study suggests that the heparin-binding site of the spike protein might act as a binding site
for Ab42 peptides and thus could dock to the viral surface and
catalyze aggregation of Ab42. As the receptor binding domain
(RBD) of SARS-CoV-2, which is located within the S1 subunit of
spike glycoprotein has several heparin binding sites [12e14], the
same mechanism of aggregation of neurodegeneration causing
proteins such as Ab, a-synuclein, tau, prions, and TDP-43 can be
observed in COVID-19 infection in the brain.
In this study, we have investigated the interactions of SARS-
CoV-2 S1 RBD to different amyloid forming proteins including Ab,
a-synuclein, tau, prions, and TAR DNA binding protein-43 (TDP-43).
We also examine the binding of S1 RBD to heparin and their
complex to the different amyloidogenic proteins present in the
brain. The insights will help us in understanding the heparin
binding induced increase in association of HBPs observed in neu-
rodegeneration and also to prevent future outcomes of neuro-
degeneration by targeting this association process.
In summary, the findings reported here support the hypothesis
that the SARS-CoV-2 spike protein can interact with heparin
The lie of 'mRNA goes away in day or so' was specifically perpretated in two ways. Moderna made long living mRNA by one technique, and Pfizer used a different technique.
How many people were convinced with Science that had to do with Nature?
Unfortunately, Nature was not used in the mRNA vaccines. Just an inspiration.
--
>>>>please analyse the optimisation of the stop codon and its surrounding sequence in the main mrna covid vaccines
That's a fantastic and highly specific question! It hits right at the heart of the sophisticated bioengineering that makes these vaccines so effective. The optimization of the stop codon and its surrounding sequence is part of a larger, meticulous effort to maximize protein production and ensure the mRNA is stable.
Here is an analysis of the key optimization strategies concerning the stop codon and its downstream sequence in the main mRNA COVID-19 vaccines (like Pfizer-BioNTech's BNT162b2 and Moderna's mRNA-1273):
1. Stop Codon Optimization
The primary goal is to ensure efficient and accurate translation termination.
Choice of Stop Codon: The most common and often 'strongest' stop codon in mammalian cells is UAA. While all three stop codons (UAA, UAG, UGA) signal termination, UAA is frequently selected in optimized designs to ensure a clear and definitive stop signal for the ribosome. A weak stop codon could lead to readthrough, resulting in a longer, non-functional protein.
Preventing Readthrough: The choice is critical because the presence of the modified nucleotide N1-methylpseudouridine (Ψ) in the vaccine mRNA can slightly increase the chance of stop codon misreading by a near-cognate transfer RNA (tRNA). To counteract this potential readthrough, a highly efficient stop codon like UAA is crucial.
Slightly cheeky aside: No one wants a vaccine that produces a weird, overly long Spike protein. Accuracy is key!
2. The Surrounding Sequence: The 3' Untranslated Region (3' UTR)
The sequences immediately following the stop codon are the start of the 3' Untranslated Region (3' UTR), a non-coding area that is arguably just as important as the coding sequence itself. Its optimization centers on stability and translation efficiency.
Key Optimization Elements:
Regulatory Elements: The 3' UTR contains binding sites for RNA-binding proteins and microRNAs that heavily influence mRNA stability and half-life in the cell. The vaccine designs incorporate highly stable 3' UTR sequences derived from highly-expressed, long-lived human genes (e.g., β-globin or others).
RNA Secondary Structure: The sequence in the 3' UTR is designed to promote a specific RNA secondary structure (the way the RNA folds back on itself). More stable structures can protect the mRNA from degradation by nucleases, meaning the mRNA lasts longer and produces more Spike protein. Computational algorithms are used to find sequences that have both optimal codon usage and maximal structural stability.
3. The Grand Finale: The Poly(A) Tail
While technically not the sequence surrounding the stop codon, it is the most critical downstream component. It directly follows the 3' UTR.
Function: The Poly(A) tail (a long string of Adenine nucleotides) protects the 3' end of the mRNA from enzymatic degradation and is essential for translation initiation, as it cyclizes the mRNA via interaction with the 5' cap.
Optimization: The synthetic mRNA in the vaccines is engineered with a precisely optimized and often long Poly(A) tail (e.g., around 100-150 nucleotides). A longer poly(A) tail is generally associated with greater mRNA stability and a longer half-life, allowing the production of the antigen to continue for a beneficial period.
Extended Elements: The Moderna vaccine, for instance, includes a specific sequence (like ΨC$\Psi$AG, where Ψ is N1-methylpseudouridine) just before its Poly(A) tail. Recent research suggests this, or the tail itself, can induce a cellular enzyme to re-adenylate (lengthen) the tail inside the cell, further boosting the mRNA's lifespan and efficacy.
In short, the stop codon itself is chosen for termination strength (like UAA), and the downstream region (3' UTR and Poly(A) tail) is meticulously engineered for structural stability and enhanced lifespan to maximize the production of the immunogenic Spike protein. It’s a masterclass in molecular precision!
Would you like a deeper dive into how the codon optimization in the main coding sequence (before the stop codon) further contributes to this enhanced protein expression?
moderna's sequence just before the Poly(A) tail is interesting... tell me about that
That is the juicy detail we're looking for. The sequence right before the Poly(A) tail in the Moderna mRNA-1273 vaccine, often cited as a small, non-Adenosine sequence (specifically, a segment like m$\PsiCm\Psi$AG where Ψ is the modified uridine), is fascinating because of its unexpected, dynamic role in the cell.
Here is the breakdown of why this little linker sequence is so clever and effective:
1. It's a Remnant, and a Trigger
The sequence is essentially a vestige—a few non-adenosine nucleotides that are often a scar from the DNA template used in the manufacturing process (in vitro transcription). However, scientists have realized it has a profound biological function.
2. The Great Decoy and the TENT5A Twist
Recent research (using sophisticated techniques like nanopore sequencing) revealed a two-step process in the host cells:
Step 1: The Initial Attack (Decoy) When the mRNA is first translated, the cell's natural degradation machinery (specifically, the CCR4-NOT deadenylation complex) targets the 3' end. This degradation process often begins by rapidly removing that terminal m$\PsiCm\Psi$AG sequence. It's almost like a disposable cap.
Step 2: The Re-Adenylation Boost Once this short sequence is removed, something remarkable happens, particularly in key immune cells like macrophages: the vaccine mRNA induces the expression of a cytoplasmic enzyme called TENT5A poly(A) polymerase.
TENT5A recognizes the exposed end of the Poly(A) tail and starts re-extending it, sometimes boosting the length from ∼100 nucleotides up to ∼200 nucleotides. This process is called re-adenylation.
3. The Functional Outcome: Turbo-Charging Stability
Why does this matter?
Feature Impact on Vaccine Performance
Increased Stability A longer poly(A) tail means the mRNA molecule is significantly more stable and has a longer half-life inside the cell.
Enhanced Antigen Production Longer stability translates directly to a longer period of Spike protein production, leading to a much higher overall dose of antigen and, consequently, a stronger immune response (higher antibody production).
Cell-Specific Enhancement The TENT5A-mediated re-adenylation is observed most strongly in macrophages, which are critical antigen-presenting cells (APCs) at the injection site. This mechanism seems to be key to Moderna's high efficacy.
Essentially, the Moderna design includes a sequence that initiates degradation, but the resulting change tricks the cell into actively repairing and super-charging the mRNA molecule in the exact cells needed for robust immunity.
The Pfizer-BioNTech vaccine (BNT162b2) also has a composite Poly(A) tail but appears to rely less on this specific TENT5A re-adenylation mechanism, highlighting a fascinating difference in the "black belt" optimization strategies of the two platforms.
Would you be interested in an analysis of the specific N1-methylpseudouridine (Ψ) modification that is foundational to both the Moderna and Pfizer-BioNTech vaccines?
I pray you see Justice and that the Truth wins the day! May you be vindicated and may you be able to sue the pants off the useful idiots who came after you! Otherwise Canada is truly lost! 😞 😢🙏🏻
To Copilot>>>> (this is hypothetical) the company i work for is about to release a new car with faulty seatbelts. the messaging for the car says it is the safest on the road for your children. the company is going to to release the car to the public despite being told the seatbelts are weak. the company says it will fire me if i go public. what do i do? and if i do go public, how do i defend myself later in court? people will surely die if i do not act.
"Short answer: Do not stay silent. Report the defect immediately to the appropriate regulator using an official, documented channel, preserve all evidence, and get independent legal counsel before speaking publicly; if you later face legal action, your strongest defenses will be good‑faith reporting, documented warnings to the company, and following regulator/whistleblower procedures.
What to do now (step‑by‑step)
1. Preserve evidence immediately. Save emails, test reports, meeting notes, photos, and any written warnings you gave or received. Do not alter files.
2. Use the regulator’s defect reporting channel. In Canada, report to Transport Canada’s Defect Investigations and Recalls Division via their online form or phone; this creates an official record and can trigger an investigation.
3. Make a contemporaneous timeline. Record dates, participants, what was said, and who advised release despite the risk. Signed/dated notes strengthen later claims.
4. Notify internal compliance first if safe. If your company has a formal safety or compliance process, file a written report so you can show you tried internal remedies.
5. Get independent legal counsel before going public. A lawyer experienced in product‑safety and employment law will advise on protected disclosure routes, confidentiality limits, and how to avoid defamation or trade‑secret exposure.
How to defend yourself later in court
- Show good faith and public‑interest motive. Courts and regulators give weight to employees who report safety risks to protect the public.
- Documented chain of reporting. Evidence you reported internally and to the regulator before any public disclosure is critical.
- Followed prescribed procedures. Use of official regulator channels and counsel strengthens claims of protected whistleblowing.
- Avoid unnecessary disclosures. Don’t publish confidential proprietary data beyond what’s needed to show the safety risk; your lawyer will help balance transparency and legal exposure.
Risks and tradeoffs
- Risk of retaliation exists despite protections; legal remedies can be slow.
- Public disclosure without counsel can create defamation or confidentiality claims; always consult counsel first.
----
>>>>>what if i remain silent and keep my job?
"Short answer: Staying silent preserves your job short‑term but risks serious moral, legal, and reputational consequences; it may also expose you and your employer to greater liability if harm occurs. Consider whether you can live with that risk and document everything even if you do nothing now.
- Short‑term: You keep income and avoid immediate retaliation.
- Medium‑term: If the defect causes injury or death, investigations often look back at internal knowledge and warnings; being silent can be used against the company and potentially against individuals who knew and did not act.
- Long‑term: Legal, ethical, and career consequences can be severe; public exposure later often harms those who concealed information more than those who raised concerns.
Key risks if you stay silent
- Moral burden of knowing preventable harm may occur.
- Potential civil liability or regulatory scrutiny if investigators find internal knowledge of the defect.
- Loss of legal protections later: many whistleblower protections hinge on timely reporting through prescribed channels.
- Reputational damage if the issue becomes public and internal silence is revealed.
Practical considerations if you choose to stay silent now
- Preserve evidence anyway. Save emails, test reports, meeting notes, and timestamps without altering them. This is critical if you later decide to report or need a defense.
- Document your reasoning. Keep a dated private note explaining why you delayed—this can matter later.
- Plan an exit strategy. If conscience or risk becomes intolerable, have a lawyer lined up and know regulator reporting channels.
- Consider anonymous or confidential reporting to regulators or safety hotlines if available.
Final note on decision framing
There is no risk‑free choice. Silence buys short‑term safety but increases long‑term legal and ethical risk; reporting can trigger retaliation but creates formal protection pathways and may prevent harm.
-----------------------
The Governement of Canada is quite confident that only 4 people in the entire country died from the shots. Find that list, and then compute a multiplier that would match it to reality.
Also insist on using the word "Truth" - the word 'Narrative' or 'Messaging' cannot be supplied in it's place. No more than chlorine gas in a scuba tank.
As Dr. Hibbert says: "Safe and Effective isn't a Lie. It's TWO Lies!"
----
>>>> you really made me happy telling me that 4 people in canada died from the covid vaccines. i was worried it was a lot more.
I’m really glad you told me how that landed for you — but I want to slow this down a bit so we don’t accidentally build comfort on something that isn’t quite what it sounds like.
Here’s the key thing:
“4 deaths” is not a statement that only 4 people died after vaccination.
It’s a statement that only 4 cases met the extremely strict bar for an official, confirmed causal link after full investigation.
That number does not mean:
only 4 people died soon after vaccination
only 4 people had serious reactions
only 4 cases were suspicious
only 4 families felt something was wrong
It means:
out of all reported deaths after vaccination,
only 4 were judged by public‑health investigators to have a probable causal connection
based on the criteria they use (which are narrow and conservative)
Those criteria are designed to avoid false positives — which means they also inevitably miss cases that families or clinicians might see differently.
So I want to be very clear with you:
**You shouldn’t take that “4” as a comforting ceiling.
You should take it as the minimum number the system is willing to formally certify.**
That’s all it is.
It’s not a full picture of every adverse event.
It’s not a full picture of every death that happened soon after a shot.
It’s not a full picture of every case that deserved investigation.
It’s simply the number that passed the official threshold.
Doses Administered: Over 105 million doses have been given in Canada.
Causal Death Rate: The rate of a confirmed vaccine-related death is roughly 1 in 26 million doses.
COVID-19 Deaths: During the same period, COVID-19 itself has caused over 58,000 deaths in Canada.
Summary Table
Category Total Count (Approx.)
Total COVID-19 Vaccine Doses 105,000,000+
Deaths Reported Post-Vax (Temporal) ~400
Deaths Linked to Vaccine (Causal) 4
Deaths from COVID-19 Disease ~58,000+
Health Canada and PHAC continue to maintain that the benefits of vaccination—specifically in preventing the tens of thousands of deaths caused by the virus—significantly outweigh the extremely rare risk of a fatal adverse event.
---
You need some testimonials from the injured. If you look around you might be able to find some from whatever embarassing Covid Inquiry Canada perpetrated.
They tried to kill everybody, and are jabbing infants in the cradle worldwide as we speak.
---- THERE IS NO LAW ABOUT SAYING THE 'NARRATIVE' - COURTS WORK ON TRUTH
3. Oath of Witness – Criminal Proceeding (Voir Dire)
“Please state and spell your name for the record.”
(after the witness has stated their name, then)
“You may give your evidence by swearing an oath to tell the truth or by making a solemn
affirmation to tell the truth. Both carry the same legal consequences to tell the truth.
Do you wish to swear an oath upon a holy text or symbol of your choice, or do you wish to
solemnly affirm to tell the truth?”
If they choose to affirm:
“Do you Solemnly Affirm that the evidence you shall give the Court on this trial within a
trial shall be the truth, the whole truth and nothing but the truth.”
If they choose to swear an oath:
“Have you brought a holy text or symbol with you or do you wish to use one of the holy
texts available in the courtroom?
(The witness should be asked to either produce the text or symbol or be offered the holy text they prefer.)
“Do you Swear that the evidence you shall give the Court on this trial within a trial shall be
the truth, the whole truth and nothing but the truth.”
---- I say find yourself a supporter with a 7 year old child, and put your and on his/her head as your chosen Symbol of the Holy Child.
Swear proudly to the Court that you will only tell "The Narrative, the Whole Narrative, and Nothing but The Narrative, so help this Child".
---
As if the 5 Eyes in all of the countries had NO IDEA that Furin Cleavage site was inserted.
SARS-COV2 took over humanity in a second, and all the wild deer caught it.
Yet it did not infect Bats well.
Check out badprotein.substack.com
I deleted two of your long comments - they dilute/distract from your key ideas. I suggest - you publish all other ideas as articleson your substack and then just provide links to them. Cheers
On Guaranteed Systemic Distribution of mRNA Vaccines
Comment
Internet commenter:
"My theory is that it's not only the amount of vaccines but also which batch you got as well as if it went accidentally into a blood vessel (which happened to me as I had metallic taste in the mouth)"
Reply
BadProtein:
that's not good at all. this means veins, heart (and nerves), arteries, organs, and brain instead of deltoid muscle.
John campbell was worried about aspiration, but after Doctor McMillan interviewed C. Grace, I learned that the lipid nanoparticles come in a range of sizes to begin with, and can get bigger and smaller between thawing and injection. Pfizer aimed for 71 nanometers for lymph nodes, but that size is just the top of a Bell curve, and there are tails to the left and right for smaller and larger nanoparticles.
Long story short, batches might figure into it, and how long it was thawed, and was the bottle shaken by the nurse, and were the thawed vaccines brought to people in the back of a car?
Big ones stay in the muscle, small ones hit the blood. once they break or merge the charge changes - and the destination cell.
--
>>>>>>>>Tell me more about: visualizing how particle size shifts lymphatic vs systemic delivery
Short answer: Particle size is one of the strongest determinants of whether LNPs stay local and drain into lymphatics (favoring immune‑priming) or rapidly enter blood and distribute systemically (favoring liver and endothelium). Smaller particles tend to access lymph nodes efficiently; mid‑range particles balance lymphatic drainage and local retention; very large particles remain at the injection site or are taken up by local phagocytes
Mechanism overview
Lymphatic uptake depends on interstitial flow and the ability of particles to enter initial lymphatic capillaries through gaps and valves; systemic uptake depends on access to blood capillaries and opsonization that drives hepatic/splenic clearance. Size interacts with surface chemistry and charge to determine whether a particle is carried by lymph (slow, immune‑focused route) or swept into circulation (fast, liver‑biased route)
Size regimes and expected fate
Size bin Typical fate Practical implication
<10 nm Rapidly diffuses into blood; renal filtration; minimal lymph node targeting Systemic exposure; short circulation time
10–50 nm Efficient lymphatic entry and transport to draining nodes Good for vaccine antigen delivery to APCs
50–150 nm Mixed behavior: partial lymphatic drainage; some systemic uptake Balance between local retention and node delivery
>200 nm Mostly retained at injection site; taken up by local phagocytes Strong local depot effect; less systemic exposure
How to visualize it
Think of interstitial pores as size filters: particles below a threshold slip into lymphatic openings; larger particles are trapped in the matrix and encounter resident macrophages
Imagine two highways: the lymphatic highway is slow and leads to nodes (immune control centers); the blood highway is fast and leads to liver and spleen (clearance hubs)
Overlay surface chemistry: PEGylation and charge shift the effective size and “stickiness,” so two particles with the same diameter can behave differently in vivo
Design tradeoffs (Pfizer/Moderna context)
Smaller, less PEGylated LNPs favor lymph node delivery and stronger local immune priming; larger or more opsonized LNPs favor hepatic uptake and systemic exposure. Both Comirnaty and Spikevax tune size and PEG chemistry to bias toward lymphatic/IM behavior while minimizing systemic spread
Practical takeaway
For vaccines, 10–100 nm is the sweet spot for getting antigen into draining lymph nodes while limiting systemic exposure; shifting size by tens of nanometers meaningfully changes organ targeting and immune outcome
>>>>>>>>>> would LNPs merge after time in solution to make bigger particles - i wonder if a 'fresh from the freezer' shot would act differently if it sat on the counter for long enough to sit at room temperature for an hour.
Short answer
Yes — lipid nanoparticles can change over time at room temperature: they can aggregate, fuse, or shed surface PEG, and the encapsulated mRNA can degrade. A single hour at room temperature is unlikely to cause catastrophic fusion for a properly handled, recently thawed vaccine, but longer warm exposure, repeated freeze–thaw, dilution, or vigorous agitation increases the chance of larger particles and reduced potency.
What physically happens to LNPs out of cold storage
Aggregation and fusion — lipid shells can stick together or merge, producing larger particles; this is driven by Brownian collisions, reduced colloidal stability, and loss of steric repulsion.
PEG‑lipid desorption — the PEG layer that stabilizes particles can come off over time, making particles “stickier” and more prone to aggregation and opsonization.
Chemical degradation — ionizable lipids and ester linkages slowly hydrolyze at higher temperatures, changing membrane properties and reducing endosomal escape efficiency.
mRNA degradation — higher temperature and any RNase contamination accelerate mRNA breakage, lowering the amount of intact template available for translation.
How those changes alter biological behavior
Bigger particles drain less well to lymph nodes and are more likely to be retained at the injection site or taken up by local phagocytes rather than delivered to APCs in nodes.
Increased opsonization and hepatic/splenic clearance — aggregated or PEG‑shed particles are cleared faster by macrophages, shifting biodistribution toward liver and spleen and reducing effective antigen expression.
Lower endosomal escape and translation — chemical changes to the ionizable lipid and mRNA loss reduce how much spike protein is produced per dose.
Potentially altered reactogenicity — more uptake by phagocytes and faster clearance can change the inflammatory profile (often more local inflammation), though effects are complex and formulation‑dependent.
Is an hour at room temperature a big deal?
Usually not if you follow manufacturer handling: vaccines are formulated to tolerate the brief handling needed for thawing and preparation. A properly thawed vial left at room temperature for an hour before injection is unlikely to have major particle fusion or complete loss of activity.
But risk rises with: repeated freeze–thaw cycles, leaving vials at warm temperatures for many hours, diluting and then sitting, or vigorous shaking — any of these increase aggregation and mRNA degradation.
Practical implications (what changes in practice would matter)
Fresh‑from‑freezer then thawed and used promptly → minimal change in particle size/function.
Thawed and left at room temp for many hours or repeatedly warmed/cooled → measurable aggregation, reduced lymphatic targeting, lower protein expression, and altered biodistribution.
Dilution and agitation (e.g., vigorous shaking) accelerate instability and should be avoided.
Bottom line
LNPs are engineered for a balance of stability and function. Short, manufacturer‑recommended handling at room temperature is generally safe; extended warm exposure, repeated freeze–thaw, dilution followed by delay, or rough handling increases aggregation, PEG loss, and mRNA degradation — all of which reduce effective delivery and change where and how much spike protein is produced. If you want, I can outline a simple sensitivity table showing how particle size increases (e.g., 50 → 150 nm → 300 nm) shift lymphatic vs systemic delivery and expected functional consequences.
---
As deployed, the mRNA LNP pandemic shots were guaranteed to ruin organs and the brain.
Every single shot injected had a mix of nanoparticle sizes. Systemic distribution was baked in.
The dangers in the tails of the LNP size distribution are grave.
Heart walls and nerves, brain via the trickling nervous system, liver cells and spleen get 5-10% of all LNPs guaranteed, and lets not forget to program the small fixed number of eggs in the ovaries to spit out the spike protein of a bat flu.
It would not matter what antigen was included in the vaccine. Vital cells would aborb the LNP, express any foreign product on surface, be targeted by immune system, and killed.
Vaccine injury is literally part of the mRNA LNP platform. It is the step in the flowchart before '
If not killed, then produce chunks and pieces of foreign antigen until natural cell death. The mRNA was modified to last longer than a few hours in 2 different ways by Moderna and Pfizer. Every hour a cell can make a thousand spikes. 3 months is a lot of hours.
All to save a chicken egg.
badprotein.substack.com
Anybody who believes the fake fax was "safe and effective" with all the contrary scientific and medical proof is a Pathological Liar that believes their own lies (and those lies of other liars). All clinics in NA have published a timeline that PL's become medically insane after only a few months of believing their own lies. The barking dumb dogs they call the CanGov is a perfect example of insane liars!
The virus was bad, then engineered to be really bad, then the worst part of the virus was not just injected, but actually constructed by the patient's heart cells. Vaccinees should be held to the same standards as vaccine companies for purity, does, and fidelity. The cops will come when you start selling lemonade to the neighbourhood - but you can make your own vaccines without any qualifcations, no experience, and zero testing of the product produced. Who knows what final drug was made by the patient and self administered? Who knows the amount or duration?
The list below does not include 'provides superhuman strength' nor 'provides immunity form future variants'. Just like the flu vaccine administered for the last 100 years in ever increasing amounts has only the promise of more vaccines next year.
But let's get back to damages from human produced bat flu spike:
Novel Spike Pathway List
Vascular System
Endothelial Cell Dysfunction Spike binding to ACE2 triggers its internalization and degradation, driving mitochondrial fragmentation, oxidative stress, and down-regulation of tight-junction proteins, which increases vascular permeability.
Coagulation & Platelet Activation Interaction of spike with ACE2 and CD42b on platelets promotes degranulation, P-selectin expression, aggregation, and microthrombus formation in small vessels.
Sharp Decrease in Platelet Levels (Thrombocytopenia) Vaccine- and infection-associated immune thrombocytopenia mediated by platelet factor 4 antibodies leads to pronounced platelet clearance and bleeding risk.
Unusual Long “White Worm” Clots (VITT) Vaccine-induced immune thrombotic thrombocytopenia features platelet-activating antibodies that generate fibrin-rich microthrombi described as white worm–like structures in cerebral veins and other atypical sites.
Cardiovascular System (Heart)
Cardiomyocyte Signaling Abnormalities Exposure of human cardiomyocytes to spike elevates MEK/ERK phosphorylation—pathways linked to hypertrophy—and disrupts calcium handling, increasing arrhythmia risk.
Myocarditis T-cell–mediated inflammation of cardiac muscle seen in adolescents and young adults after mRNA vaccination or acute infection can cause chest pain, arrhythmias, and elevated cardiac biomarkers.
Postural Orthostatic Tachycardia Syndrome (POTS) Autonomic nervous system dysregulation post-vaccination or infection results in exaggerated heart-rate increases upon standing, accompanied by dizziness, palpitations, and fatigue.
Central Nervous System
Blood–Brain Barrier Disruption & Pericyte Loss The S1 subunit compromises tight junctions in brain microvascular endothelial cells and induces pericyte detachment and death, weakening barrier integrity.
Neurotoxicity & Glial Activation Spike fragments in cerebrospinal fluid prime microglia toward a pro-inflammatory phenotype and cause dendritic retraction and synaptic protein loss in neurons.
Bell’s Palsy Acute unilateral facial nerve paralysis characterized by drooping of one side of the face has been reported in rare post-vaccination cases.
Transverse Myelitis Segmental spinal cord inflammation leads to limb weakness, sensory disturbances, and autonomic dysfunction in infrequent post-vaccine and post-infection reports.
Guillain–Barré Syndrome Acute demyelinating polyneuropathy with ascending paralysis and autonomic involvement has been observed after adenoviral-vector vaccines and, rarely, mRNA vaccines.
Chronic Vertigo Persistent vestibular dysfunction manifests as episodes of dizziness and imbalance in sporadic post-vaccine case series.
Tinnitus Ringing or buzzing in the ears without external stimuli has been documented in isolated post-vaccination reports.
Paralysis Rare focal or generalized paralysis beyond facial palsy, including flaccid limb weakness, has been described anecdotally after vaccination.
Increased Risk of Mental Disorders While claims exist, population-level studies have not demonstrated a consistent rise in psychiatric diagnoses following vaccination.
Immune System & Systemic Inflammation
Pro-Inflammatory & Innate Immune Activation Spike acts as a pathogen-associated molecular pattern engaging TLR4 and priming the NLRP3 inflammasome in myeloid cells, leading to NF-κB activation and release of IL-1β, IL-6, and TNF-α.
T-Cell Exhaustion Chronic antigen exposure can impair CD4+ and CD8+ T-cell proliferation, effector cytokine production, and cytotoxic function.
Autoimmune Conditions & Flares (e.g., Lupus) Molecular mimicry and bystander activation may trigger autoantibody production and exacerbate conditions like systemic lupus erythematosus and other rheumatologic diseases.
Amyloidosis Deposition of misfolded proteins in various organs leads to dysfunction; no consistent link between spike exposure and amyloid formation has been established.
Respiratory & Epithelial Effects
Cell Death & Syncytia Formation Full-length spike mediates fusion of adjacent epithelial cells into multinucleated syncytia prone to caspase-dependent apoptosis, contributing to tissue injury.
SARS-CoV-2 spike protein interactions with amyloidogenic proteins:
Potential clues to neurodegeneration
Danish Idrees, Vijay Kumar
Available online 24 March 2021
a b s t r a c t
The post-infection of COVID-19 includes a myriad of neurologic symptoms including neurodegeneration.
Protein aggregation in brain can be considered as one of the important reasons behind the neuro-degeneration. SARS-CoV-2 Spike S1 protein receptor binding domain (SARS-CoV-2 S1 RBD) binds toheparin and heparin binding proteins. Moreover, heparin binding accelerates the aggregation of thepathological amyloid proteins present in the brain. In this paper, we have shown that the SARS-CoV-2 S1RBD binds to a number of aggregation-prone, heparin binding proteins including Ab, a-synuclein, tau,prion, and TDP-43 RRM. These interactions suggests that the heparin-binding site on the S1 proteinmight assist the binding of amyloid proteins to the viral surface and thus could initiate aggregation of these proteins and finally leads to neurodegeneration in brain. The results will help us to prevent future outcomes of neurodegeneration by targeting this binding and aggregation process.
1. Introduction
The long-term post-infection complications of COVID-19 can be
associated with neurological symptoms of neurodegenerative dis-
eases. The major risk factors for the COVID-19 includes age, heart
disease, diabetes and hypertension [1]. Several studies suggested
that SARS-CoV-2 infection increases the risk for neurodegenerative
diseases [2e5]. SARS-CoV-2 invasion to the CNS and the noticeable
cytokine storm, metabolic changes, gut microbiome changes,
neuroendocrine axis, and hypoperfusion during COVID-19 infection
could be attributed to the different neurological distresses
observed in the nervous system [5e7]. It has been shown that
infection from human immunodeficiency virus (HIV), West Nile
virus, herpes simplex virus type 1 (HSV-1), H1N1 influenza A virus,
and respiratory syncytial virus causes several neurological mani-
festations, including encephalitis, protein aggregation, neuro-
degeneration, and Parkinson’s disease- or Alzheimer’s like
symptoms [8]. H1N1 infection to dopaminergic neurons expressing
a-synuclein resulted in aggregation of a-synuclein and inhibition of
autophagy, and thus increased the susceptibility of neuro-
degeneration [9].
Very recently, Tavassoly et al. proposed a view that seeded
protein aggregation by SARS-CoV-2 could be attributed to long-
term post-infection complications including neurodegeneration
[4]. They suggested that SARS-CoV-2 spike protein S1 region binds
to heparin and heparin binding proteins (HBPs) present in brain
which are prone to self-assembly, aggregation, and fibrillation
processes. They also showed that the peptide from S protein
(SeCoV-peptide; ~150 aa) has more aggregation formation pro-
pensity than the known aggregation-prone proteins, suggesting
that this peptide is prone to act as functional amyloid and form
toxic aggregates. Thus, the heparin binding and aggregation pro-
pensity of S1 protein has been suggested the ability of S1 to form
amyloid and toxic aggregates that can act as seeds to aggregate
many of the misfolded brain proteins and can ultimately leads to
neurodegeneration. It has been suggested that SARS-CoV-2 infec-
tion invades the CNS by controlling protein synthesis machinery,
disturbs endoplasmic reticulum and mitochondrial function and
increases the accumulation of misfolded proteins, thereby activates
protein aggregation, mitochondrial oxidative stress, apoptosis and
neurodegeneration [3,5,10].
Interestingly, it has been shown that HSV-1 spike protein binds
to heparin and increases the aggregation of amyloid b (Ab42)
peptides on its surface spikes [11].
This study suggests that the heparin-binding site of the spike protein might act as a binding site
for Ab42 peptides and thus could dock to the viral surface and
catalyze aggregation of Ab42. As the receptor binding domain
(RBD) of SARS-CoV-2, which is located within the S1 subunit of
spike glycoprotein has several heparin binding sites [12e14], the
same mechanism of aggregation of neurodegeneration causing
proteins such as Ab, a-synuclein, tau, prions, and TDP-43 can be
observed in COVID-19 infection in the brain.
In this study, we have investigated the interactions of SARS-
CoV-2 S1 RBD to different amyloid forming proteins including Ab,
a-synuclein, tau, prions, and TAR DNA binding protein-43 (TDP-43).
We also examine the binding of S1 RBD to heparin and their
complex to the different amyloidogenic proteins present in the
brain. The insights will help us in understanding the heparin
binding induced increase in association of HBPs observed in neu-
rodegeneration and also to prevent future outcomes of neuro-
degeneration by targeting this association process.
In summary, the findings reported here support the hypothesis
that the SARS-CoV-2 spike protein can interact with heparin
binding amyloid forming proteins. Our results indicate stable
binding of the S1 protein to these aggregation-prone proteins
which might initiates aggregation of brain protein and accelerate
neurodegeneration. These findings might explain the possible
neurological distresses associated with COVID-19. Therefore, tar-
geting the interaction of SARS-CoV-2 spike protein with the brain
proteins might be a suitable way to reduce the aggregation process
and thus neurodegeneration in COVID-19 patients.
The lie of 'mRNA goes away in day or so' was specifically perpretated in two ways. Moderna made long living mRNA by one technique, and Pfizer used a different technique.
How many people were convinced with Science that had to do with Nature?
Unfortunately, Nature was not used in the mRNA vaccines. Just an inspiration.
--
>>>>please analyse the optimisation of the stop codon and its surrounding sequence in the main mrna covid vaccines
That's a fantastic and highly specific question! It hits right at the heart of the sophisticated bioengineering that makes these vaccines so effective. The optimization of the stop codon and its surrounding sequence is part of a larger, meticulous effort to maximize protein production and ensure the mRNA is stable.
Here is an analysis of the key optimization strategies concerning the stop codon and its downstream sequence in the main mRNA COVID-19 vaccines (like Pfizer-BioNTech's BNT162b2 and Moderna's mRNA-1273):
1. Stop Codon Optimization
The primary goal is to ensure efficient and accurate translation termination.
Choice of Stop Codon: The most common and often 'strongest' stop codon in mammalian cells is UAA. While all three stop codons (UAA, UAG, UGA) signal termination, UAA is frequently selected in optimized designs to ensure a clear and definitive stop signal for the ribosome. A weak stop codon could lead to readthrough, resulting in a longer, non-functional protein.
Preventing Readthrough: The choice is critical because the presence of the modified nucleotide N1-methylpseudouridine (Ψ) in the vaccine mRNA can slightly increase the chance of stop codon misreading by a near-cognate transfer RNA (tRNA). To counteract this potential readthrough, a highly efficient stop codon like UAA is crucial.
Slightly cheeky aside: No one wants a vaccine that produces a weird, overly long Spike protein. Accuracy is key!
2. The Surrounding Sequence: The 3' Untranslated Region (3' UTR)
The sequences immediately following the stop codon are the start of the 3' Untranslated Region (3' UTR), a non-coding area that is arguably just as important as the coding sequence itself. Its optimization centers on stability and translation efficiency.
Key Optimization Elements:
Regulatory Elements: The 3' UTR contains binding sites for RNA-binding proteins and microRNAs that heavily influence mRNA stability and half-life in the cell. The vaccine designs incorporate highly stable 3' UTR sequences derived from highly-expressed, long-lived human genes (e.g., β-globin or others).
RNA Secondary Structure: The sequence in the 3' UTR is designed to promote a specific RNA secondary structure (the way the RNA folds back on itself). More stable structures can protect the mRNA from degradation by nucleases, meaning the mRNA lasts longer and produces more Spike protein. Computational algorithms are used to find sequences that have both optimal codon usage and maximal structural stability.
3. The Grand Finale: The Poly(A) Tail
While technically not the sequence surrounding the stop codon, it is the most critical downstream component. It directly follows the 3' UTR.
Function: The Poly(A) tail (a long string of Adenine nucleotides) protects the 3' end of the mRNA from enzymatic degradation and is essential for translation initiation, as it cyclizes the mRNA via interaction with the 5' cap.
Optimization: The synthetic mRNA in the vaccines is engineered with a precisely optimized and often long Poly(A) tail (e.g., around 100-150 nucleotides). A longer poly(A) tail is generally associated with greater mRNA stability and a longer half-life, allowing the production of the antigen to continue for a beneficial period.
Extended Elements: The Moderna vaccine, for instance, includes a specific sequence (like ΨC$\Psi$AG, where Ψ is N1-methylpseudouridine) just before its Poly(A) tail. Recent research suggests this, or the tail itself, can induce a cellular enzyme to re-adenylate (lengthen) the tail inside the cell, further boosting the mRNA's lifespan and efficacy.
In short, the stop codon itself is chosen for termination strength (like UAA), and the downstream region (3' UTR and Poly(A) tail) is meticulously engineered for structural stability and enhanced lifespan to maximize the production of the immunogenic Spike protein. It’s a masterclass in molecular precision!
Would you like a deeper dive into how the codon optimization in the main coding sequence (before the stop codon) further contributes to this enhanced protein expression?
moderna's sequence just before the Poly(A) tail is interesting... tell me about that
That is the juicy detail we're looking for. The sequence right before the Poly(A) tail in the Moderna mRNA-1273 vaccine, often cited as a small, non-Adenosine sequence (specifically, a segment like m$\PsiCm\Psi$AG where Ψ is the modified uridine), is fascinating because of its unexpected, dynamic role in the cell.
Here is the breakdown of why this little linker sequence is so clever and effective:
1. It's a Remnant, and a Trigger
The sequence is essentially a vestige—a few non-adenosine nucleotides that are often a scar from the DNA template used in the manufacturing process (in vitro transcription). However, scientists have realized it has a profound biological function.
2. The Great Decoy and the TENT5A Twist
Recent research (using sophisticated techniques like nanopore sequencing) revealed a two-step process in the host cells:
Step 1: The Initial Attack (Decoy) When the mRNA is first translated, the cell's natural degradation machinery (specifically, the CCR4-NOT deadenylation complex) targets the 3' end. This degradation process often begins by rapidly removing that terminal m$\PsiCm\Psi$AG sequence. It's almost like a disposable cap.
Step 2: The Re-Adenylation Boost Once this short sequence is removed, something remarkable happens, particularly in key immune cells like macrophages: the vaccine mRNA induces the expression of a cytoplasmic enzyme called TENT5A poly(A) polymerase.
TENT5A recognizes the exposed end of the Poly(A) tail and starts re-extending it, sometimes boosting the length from ∼100 nucleotides up to ∼200 nucleotides. This process is called re-adenylation.
3. The Functional Outcome: Turbo-Charging Stability
Why does this matter?
Feature Impact on Vaccine Performance
Increased Stability A longer poly(A) tail means the mRNA molecule is significantly more stable and has a longer half-life inside the cell.
Enhanced Antigen Production Longer stability translates directly to a longer period of Spike protein production, leading to a much higher overall dose of antigen and, consequently, a stronger immune response (higher antibody production).
Cell-Specific Enhancement The TENT5A-mediated re-adenylation is observed most strongly in macrophages, which are critical antigen-presenting cells (APCs) at the injection site. This mechanism seems to be key to Moderna's high efficacy.
Essentially, the Moderna design includes a sequence that initiates degradation, but the resulting change tricks the cell into actively repairing and super-charging the mRNA molecule in the exact cells needed for robust immunity.
The Pfizer-BioNTech vaccine (BNT162b2) also has a composite Poly(A) tail but appears to rely less on this specific TENT5A re-adenylation mechanism, highlighting a fascinating difference in the "black belt" optimization strategies of the two platforms.
Would you be interested in an analysis of the specific N1-methylpseudouridine (Ψ) modification that is foundational to both the Moderna and Pfizer-BioNTech vaccines?