Transdifferentiation: The Spike's Cellular Shell Game?

A hypothetical explanation for heterogeneous pathologies

Those who have been following my work for the past several years may recall a comment I made that the Spike Protein turns the “Rembrandt” of our cells into a “Jackson Pollack.” The more I understand the pathology of the Spike Protein the more I begin to understand how it can cause such heterogeneous pathologies. It’s not just SPED. I believe it is also transcriptional. It is CELLULAR IDENTITY THEFT. It “tells” a cell to become something it shouldn’t be. This can explain its “Whack-A-Mole” appearance. Aggressive cancers, de novo diabetes, sudden cardiac death, idiopathic pulmonary fibrosis. Such a wide panoply of disease, yet one origin.

I am working on this. So, let’s look at some evidence.

Two recent reports denoted the potential of SARS-CoV-2 to directly infect β-cells and the possible fate of β-cells under COVID-19. Both the SARS-CoV-2 nucleocapsid protein (NP) and spike protein (SP) were detected in β-cells at 2 or 6 days post infection (dpi) when healthy human islets were infected with SARS-CoV-2 ex vivo. Pretreatment of human islets with EG00229, an NRP1 antagonist, decreased the NP-positive β-cells after infection with SARS-CoV-2 at 2 dpi, suggesting that SARS-CoV-2 requires NRP1 to enter β-cells. Pathological analysis showed the existence of SARS-CoV-2 NP and spike mRNA in insulin-positive β-cells from 4 out of 7 subjects with COVID-19.

Pancreatic β-cell fate in subjects with COVID-19
https://onlinelibrary.wiley.com/doi/10.1111/jdi.13671

The engagement of human angiotensin-converting enzyme 2 (hACE2) and SARS-CoV-2 spike protein facilitate virus spread. Thus far, ACE2 and TMPRSS2 expression is correlated with the epithelial-mesenchymal transition (EMT) gene signature in lung cancer. However, the mechanism for SARS-CoV-2-induced EMT has not been thoroughly explored. Here, we showed that SARS-CoV-2 induces EMT phenotypic change and stemness in breast cancer cell model and subsequently identified Snail as a modulator for this regulation. The in-depth analysis identifies the spike protein (S), but not envelope (E), nucleocapsid (N), or membrane protein (M), of SARS-CoV-2 induces EMT marker changes.

Epithelial-mesenchymal transition induced by SARS-CoV-2 required transcriptional upregulation of Snail
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8167694/

In conclusion, our results suggest that conversion of B cells to macrophage-like cells, similar to a pathophysiological response, could be mediated by a devastating viral ligand, in particular spike protein of SARS virus, or in combination with severe local hypoxia, which is a condition often observed in afflicted lungs of SARS patients.

SARS spike protein induces phenotypic conversion of human B cells to macrophage-like cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7112600/

We need more research, and it can explain the (I believe) brainstem-related sudden cardiac deaths.

Afferent and efferent cardiac neurotransmission via the cardiac nerves intricately modulates nearly all physiological functions of the heart (chronotropy, dromotropy, lusitropy, and inotropy). Afferent information from the heart is transmitted to higher levels of the nervous system for processing (intrinsic cardiac nervous system, extracardiac-intrathoracic ganglia, spinal cord, brain stem, and higher centers), which ultimately results in efferent cardiomotor neural impulses (via the sympathetic and parasympathetic nerves). This system forms interacting feedback loops that provide physiological stability for maintaining normal rhythm and life-sustaining circulation. This system also ensures that there is fine-tuned regulation of sympathetic–parasympathetic balance in the heart under normal and stressed states in the short (beat to beat), intermediate (minutes to hours), and long term (days to years). This important neurovisceral/autonomic nervous system also plays a major role in the pathophysiology and progression of heart disease, including heart failure and arrhythmias leading to sudden cardiac death. Transdifferentiation of neurons in heart failure, functional denervation, cardiac and extracardiac neural remodeling has also been identified and characterized during the progression of disease.

Cardiac Innervation and Sudden Cardiac Death
https://www.ahajournals.org/doi/epub/10.1161/CIRCRESAHA.116.304679

Sadly, I report another 30yo dying unexpectedly in his sleep.

‘Deepest sadness’: Crypto founder Tiantian Kullander dies ‘unexpectedly in his sleep’ at 30
https://www.news.com.au/finance/business/deepest-sadness-crypto-founder-tiantian-kullander-dies-unexpectedly-in-his-sleep-at-30/news-story/60ecb8f7e50a4f9c2333b986b0fa0f20

As always, I welcome all feedback and opinions. Is the Endothelium just the cueball in this systemic cascade landing “personal” diseases in individual’s pockets?