Pli Selon Pli: The Slow, Inexorable Replacement of Our DNA with Spike Protein – and it Could Be Hereditary

Like a dot matrix printer, is each “pass” of the Spike Protein slowly corrupting our DNA into nonsense?

Coronavirus infection in human cells enhanced retrotransposon expression. (A) Bar graphs show that after 24-h MERS-CoV/SARS-CoV/SARS-CoV-2 infection in Calu-3/MRC5/A549 cells, expression of TE was generally increased. (B) Heatmap indicates upregulation of several LTR, LINE, and SINE elements induced by MERS-CoV/SARS-CoV/SARS-CoV-2 infection. Only top 5 upregulated transposable element (TE) subfamilies are shown. (C) Ratio of LINE1 upregulation was not determined by evolutionary age of LINE1 elements. Evolutionary age was calculated based on a substitution rate of 0.17%/million years. Mya, million years ago. (D) Bar graphs depict expression of genes encoding enzymes controlling DNA methylation status before and after MERS-CoV/SARS-CoV/SARS-CoV-2 infection in Calu-3/MRC5/A549 cells. (E) Bar graphs show that 24 h or 60 h post SARS-CoV-2 infection in human intestinal organoid, expression of TE was generally increased. (F) Bar graph indicates percentage of reads mapped to SARS-CoV-2 genome to total mapped reads in transcriptome of human intestinal organoids infected with SARS-CoV-2. 

Three and a half years ago I wrote a post: SARS AND RETROTRANSPOSONS: DIABETES, SCHIZOPHRENIA, DEMENTIA, CANCER, OBESITY. After studying what SARS-CoV-2 and its Spike Protein were doing, it occurred to me that the very same conditions occur in those with dysfunctioning retrotransposons.  

SARS-CoV-2 MAY OR MAY NOT WRITE ITSELF INTO YOUR DNA, BUT IT IS ALMOST CERTAINLY CUTTING/PASTING YOUR GENES, WRITING THEM BACK "WRONG" INTO YOUR DNA. LINE-1 ELEMENTS MUST BE TESTED IN ALL THOSE WITH COVID. 

Retrotransposons (also called Class I transposable elements or transposons via RNA intermediates) are a type of genetic component that copy and paste themselves into different genomic locations (transposon) by converting RNA back into DNA through the process reverse transcription using an RNA transposition Retrotransposons can be further subdivided into two subclasses: those with Long-Terminal Repeats (LTR) and those without (non-LTR). LTR elements, also known as endogenous retroviruses (ERVs), comprise ~8 % of the human genome. LTR ) elements are thought to be inactive in the human lineage. That is, until SARS-CoV-2 activates them. This is why the HERV-K protein has never before been seen circulating in the body.  

Type 2 Diabetes, Schizophrenia and Dementia patients all have dysfunctioning Retrotransposons. As has been previously believed, SARS-CoV-2 accelerates pathogenic processes.  

SARS AND RETROTRANSPOSONS: DIABETES, SCHIZOPHRENIA, DEMENTIA, CANCER, OBESITY 
https://wmcresearch.org/sars-and-retrotransposons-diabetes-schizophrenia-dementia-cancer-obesity/ 

The logic being, if your body has developed dysfunctioning retrotransposons, what happens if you introduce an agent which FORCES dysfunctioning retrotransposons – or USES them? 

And I saw the possibility of the virus writing itself into our DNA. As it turns out, this is, unfortunately, the case. What disturbs me the most is that this appears to be a trait of ALL the “sus” coronaviruses in circulation (see above graphic). Is this, perhaps, why they were targeted for “study?” 

As the creators of the above graphic write: 

Based on above analysis, we propose our hypothesis that coronavirus infection may increase retrotransposon expression through modulating TET activity to reduce global DNA methylation. Increased retrotransposon RNA may further form chimeric transcripts with coronavirus RNA, and integrate viral genomic fragments into human genome. Moreover, enforced retrotransposon expression may be harmful and probably long-term inherited. 

Exogenous Coronavirus Interacts With Endogenous Retrotransposon in Human Cells 
https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2021.609160/full 

Another point I made early on was my observation that the Spike Protein and the Prion Protein are, in some respects, synonymous. They both share similar domains. This will become relevant in the next quote.

Prion-like Domains in Spike Protein of SARS-CoV-2 Differ across Its Variants and Enable Changes in Affinity to ACE2 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8878784/ 

Stephanie Seneff, et al. brilliantly demonstrated how the Spike Protein is a retrotranscription-inducer – just like the GaG protein of HIV. They also underscore the finding that the transfected Spike retrotranscribes within hours. 

A follow-on preprint human study involved individuals who experienced PASC-like symptoms post-vaccination for COVID-19. CD16+ monocytes were isolated from six of these patients, and it was confirmed that they, too, contained both S1 and S2 sequences, as well as several mutant S1 peptides [69]. It was proposed that the continual release of spike protein fragments from these monocytes could sustain the PASC symptoms. It is conceivable that these monocytes have reverse-transcribed the mRNA into DNA, likely stored in plasmids [70]. It has been shown experimentally that human cells expressing the retrotransposon long interspersed nuclear element-1 (LINE-1) are able to reverse-transcribe the spike protein mRNA into DNA within six hours of exposure through transfection [71]. 

The Gag polyprotein, present in all retroviruses, is an essential nucleic-acid-binding protein that coordinates many aspects of virion assembly as an important step towards reverse transcription and integration into the host DNA [72]. A paper published in 2020 with the provocative title: "Prion protein PrP nucleic acid binding and mobilization implicates retroelements as the replicative component of transmissible spongiform encephalopathy," proposed that PrP is a nucleic-acid-binding antimicrobial protein that, like retroviral Gag proteins, can trigger reverse transcription by binding to LINE-1 retroelement-derived RNA. Furthermore, they claimed that PrPSC's cytotoxicity is dependent upon its ability to facilitate LINE-1 retrotransposition activity [73]. This leads to DNA double-strand breaks and cellular damage, but, as well, it can be inferred that PrPSC, and, by analogy, the spike protein itself, which is also an RNA-binding protein, may facilitate the retrotranscription of spike protein mRNA into DNA, mediated by LINE-1. While LINE-1 is inactive in most cells, neurons, like cancer cells and immune cells, actively express LINE-1, especially in association with neurodegenerative diseases [74,75]. 

A Potential Role of the Spike Protein in Neurodegenerative Diseases: A Narrative Review 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9922164/ 

Ultimately, what am I saying here?  

Our genome is BIG. THREE BILLION BASE PAIRS. 

Yet, no matter how much money you have, if you play Blackjack, the house’s one percent advantage will eventually bankrupt you. And that’s the point. If, over and over again, we are exposed to the Spike Protein, our genome gets ever so slowly overwritten. Diabolical. If this is intentional (and it almost certainly is) it is so very difficult to prove – until it is too late. The same way a dot matrix printer slowly overwrites a clean piece of paper with each pass before the picture becomes legible. 

Thank you for your continued support. I will keep working on therapeutics to mitigate the damage. As I have maintained from the start, everything Spike is about access. Deny access, avoid damage. That being said, I will leave the final word of this post to the great genius and researcher, Stephanie Seneff: 

The potential implications of all of this are sobering. 

A Potential Role of the Spike Protein in Neurodegenerative Diseases: A Narrative Review 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9922164/