SARS-CoV-2 - mRNA Spike and viral persistence

"I AM IMMORTAL"

The cover for this article came from this artist, and it is to signify the Spike/Virus sending signals to all cells =P

As some or perhaps many of my readers are aware by now, I have been trying very hard to stop being reductive (jab bad, virus nothing, and any assessment in the middle) so today I will cover 2 different papers, both extraordinarily significant. First, the low-hanging fruit of “covid writing”, the following is rather a short letter rather than a complete paper.

Detection of recombinant Spike protein in the blood of individuals vaccinated against SARS-CoV-2: Possiblemolecularmechanisms

As a surprise to no one who kept up to date with research or has some knowledge of protein structure and behavior (this one is quite harder and rarer) the author developed a testing method and found mRNA-devired (Mutant) Spike Protein from 69 to up to 187 days, and finding Mutant Spike even in tissue (data yet to be published), meaning they found Spike on organs or skin. Some Japanese researchers found Mutant Spike in the skin of an older lady who developed an allergic reaction to the mRNA vaccine.

Some science and scientific history. Proline is one of the “weirdest” amino acids in nature because chemical structure and shape. It is a very “rigid” amino acid, and it is very resistant to proteolysis, the natural breakdown of proteins by our bodies. Given its unique features among other amino acids, since the early 2000’s Proline has been explored and eyed as a good substitute for protein engineering to make other proteins more stable.

This substitution is paramount for the function of the mRNA vaccine, because the two Proline substitutions play essential roles, to the detriment (or perhaps original design ?) of the product. (This also enables other teams and doctors to be able to distinguish where the Spike Protein came from)

• It makes the Mutant Spike rigid keeping its shape, and it doesn’t breakdown easily

• It makes it more thermostable, a problem few addressed so far because the mRNA is so foreign to the cells it literally will produce enough energy/heat to affect the protein shape and function

• The most important aspect of all, the 2 Prolines turn the Spike into an endotoxin molecular bomb

• The two Prolines also turn the Spike into an even better membrane slicer and a biofilm buster

• Circulating Spike Protein is also responsible for a significant portion of heart damage

The authors propose 3 possible mechanisms for persistent Spike production, the first being the most espoused one, genetic integration, unless a group of researchers write and design a proper paper I will stick to my primary assessment of this being unlikely at scale unless evidence to the contrary presents itself. The second proposition is the pseudo-uridine substitutions make the Spike always active, unlikely. Third, the mRNA-LNP is picked up by bacteria, and integrated and bacteria continuously produce the Spike Protein. It is abundantly clear where I stand on this (the third one).

The fact that SARS-CoV-2 behaves and often acts as a bacteriophage leads to more credence and likelihood to the third one. I still need to do research on this topic to further elaborate my observations, I’ve held the opinion for months the mRNA Spike Protein is not just interacting with biofilms, it is effectively becoming a new polymeric substance.

The unique features described above, especially in regards to Mutant Spike guarantee long-term most of what was written here in the past 12 months, and this is why I focused so much on researching and writing about Endotoxins, Endototix Tolerance, latent viruses, and more recently Human Endogenous Retroviruses (HERVs). This will play a significant, disproportional role in long-term damage and dysfunction, and halting some or most of the inflammatory and (bad) immunological pathways is paramount for long-term health. Spike persistence (or viral for that matter) will also play a significant role in what I will write in the HERV Part II.


In simple terms, a part of the people vaccinated (the more doses, the more likely) will need to stay on supplementation of certain nutrients for years, or decades until a group or novel next-next-gen AI models figure out the “off” button. The supplementation is the same, with a paramount focus on enzymes such as serrapeptase/nattokinase, antioxidation, and cellular energy (NAD), and if you can “tolerate” melatonin (addicting Vitamin C helps, a lot). A way to high dose Melatonin is taking X mg every time you wake up at night. I will make my focus on antioxidation and cellular energy abundantly clear in the HERV Part II.

Now to the other side of the coin, and ironically something I proposed in 2021 to the detriment of basically every doctor and scientist.

SARS-CoV-2 RNA Persists in the Central Nervous System of Non-Human Primates Despite Clinical Recovery

The authors used the Wuhan strain and 8 monkeys to test the hypothesis of SARS-CoV-2 persistence in the nervous system, at this point in time no consensus exists on how or why, while recent evidence points toward the virus being able to travel using the nerves.

SARS-CoV-2 invades the brain using the nerves

Spike Protein accumulation in the brain

The Spike protein and its impact in the cholinergic system

By infecting the primates and analyzing their tissues (olfactory epithelium and pyriform cortex/amygdala) in necropsy they found both ACE2 and TMPRSS2 to be downregulated in the pyriform cortex/amygdala. Second, and most significant, they found SARS-CoV-2 mRNA in recovered animals. To elucidate the persistence of SARS-CoV-2 mRNA in the brains of recovered animals the authors attempt to test which cell types in the brain and nervous system could harbor SARS-CoV-2, with pericytes being at the top of the list since they abundantly express both ACE2 and TMPRSS2.

Pericytes are cells present at intervals along the walls of capillaries (and post-capillary venules). In the CNS, they are important for blood vessel formation, maintenance of the blood–brain barrier, regulation of immune cell entry to the central nervous system (CNS) and control of brain blood flow

Using a biomarker (PDGFRβ) that is exclusively expressed in pericytes they found both SARS-CoV-2 and PDGFRβ to be co-localized, meaning SARS-CoV-2 is in the CNS of recovered animals, another group previously reported productive infection of pericyte-like cells within cortical organoids (organoids are mass of cells or tissue grow in labs to study the effects of a multitude of things in “humans”, without using humans…someone should tell Pfizer and Moderna to stop using humans). Similar findings were published as far as late 2021 using 16 older patients.

Upon further statistical analysis, they found that viral load in many tissues, or disease severity does not predict the extent to which SARS-CoV-2 mRNA invades the central nervous system. This is rather surprising, since up to this point, most of the evidence and tests done pointed out severity = viremia (virus everywhere) = virus in the brain. I will now let the authors own words conclude their significant paper.

Taken together, examination of post-mortem pyriform cortex/amygdala brain tissue of non-human primates clinically recovered from SARS-CoV-2 infection revealed two early pathophysiological mechanisms potentially underlying PASC. First, a history of SARS-CoV-2 inoculation results in the downregulation of ACE2 and TMPRSS2 mRNA in the pyriform cortex/amygdala. Second, SARS-CoV-2 mRNA are harbored in pericytes of non-human primates clinically recovered from SARS-CoV-2 infection. Additional studies are necessary to identify long-term CNS alterations induced by SARS-CoV-2, as brain tissue was collected from non-human primates only 28 days after inoculation. Therapeutic interventions targeting the downregulation of ACE2, decreased expression of TMPRSS2, and/or persistent infection of pericytes in the central nervous system may effectively mitigate the debilitating symptoms of PASC.

Before going any further, the same supplements I always suggest will also up-regulate ACE2 via different mechanisms and pathways, some of them are Metformin (Berberine via another mechanism), Nicotine, potentially Choline, and Vitamin D. Besides these, Melatonin is often the answer.

Role of Melatonin on Virus-Induced Neuropathogenesis—A Concomitant Therapeutic Strategy to Understand SARS-CoV-2 Infection

Melatonin has a wide range of neuroprotective actions by modulating the pathophysiological mechanisms and signaling pathways observed in neurodegenerative diseases [5,6]. Along with its antioxidant, immunomodulatory, anti-inflammatory, and anti-apoptotic properties, melatonin also regulates abnormal protein dynamics, mitochondrial dysfunction and altered bioenergetics [7].

The persistence of Spike Protein, especially Proline-Mutant Spike anywhere is already bad enough, the persistence of SARS-CoV-2 in the CNS is also worrisome. Both can go seemingly anywhere via different pathways and mechanisms, but the “problem” here is two-fold.

Herpes viruses love to become latent at different “spots” in the nervous system, and you have to remember, depending on which Herpes virus you choose, the global infection rate on average fluctuates between 60% to 80%. These viruses will actively cause cell death and compromise the Blood Brain Barrier, further than the virus/spike already does on their own. Spike persistence, and SARS-CoV-2 dysregulation of ACE2 (higher localized inflammation) will inevitably also lead to the production of Endogenous Retroviruses, and some HERVs share the same receptor as Endotoxin in endothelial cells, and pericytes possess a functional TLR4 receptor.

Endotoxin and the Spike Protein interaction are the primary mechanisms by which the Spike Protein induces dozens of metabolic and immunological cascades, and in many of these Galectin-3 plays an extraordinarily important role, with the unique variation that each person is unique. Addressing these primary changes and inflammatory responses limits the potential long-term damage. What we covered here will be important in the next 2 substacks, the one about misfolded proteins and one about Spike-independent interaction with ACE2, all substacks referred to here are suggested readings.

Your support enables me to do this research full time, thank you.