Universal Cellular Destruction: Lessons from The Spike Protein and Taste Buds: How the Destruction of Taste Buds May Be Mirrored in Cardiomyocytes and Mirrored Systemically

The denervation of taste buds by the Spike Protein may be mirrored by denervation in cardiomyocytes and in the brain, contributing to Sudden Cardiac Death and cognitive issues.

Taste Bud and Sensory Fiber Architecture Are Disrupted in Postacute Sequelae of Coronavirus Disease 2019 That Can Resolve Spontaneously

Like so many aspects of COVID and Spike Protein pathology, the loss of taste associated with the disease is glossed over by the public as a minor inconvenience that, under most circumstances, returns. This, of course, is the fault of the three letter agencies, academia and the media that promulgate their narratives.

What is NOT told to the public is that this loss of taste is nothing short of COMPLETE DESTRUCTION OF THE TASTE BUDS AND THEIR NERVES BY THE SPIKE PROTEIN. Let us review an article from July of this year discussing long term taste dysfunction in SARS-C0V-2.

In 9 of the 16 (56%) patients, we did not find any taste buds on visit 1 in the fungiform papillae we biopsied. In 7 of the 16 (44%) patients, where taste buds were present, their numbers were decreased, with approximately half of the fungiform papillae containing one taste bud instead of the more typical one to three per healthy fungiform papilla.

Now. This in and of itself is alarming. What makes it even more so is that in 100% of those with taste deficits, THE SPIKE PROTEIN WAS FOUND IN THE FUNGIFORM PAPILLAE!

By contrast, we found evidence of the virus in the epithelial layer (basal and suprabasal cell layers) and lamina propria of fungiform papillae from all individuals who were experiencing taste deficits from 6 to 63 weeks after testing PCR+. We show fungiform papillae sections from two patients: a 52-year-old female at 63 weeks and a 45-year-old female at 40 weeks after testing PCR+, whose epithelial cells contained SARS-CoV-2 spike and nucleocapsid proteins.

What I find even more interesting, is that the neurites were also disrupted by the presence of the Spike Protein.

Neurites in taste buds are characterized by their expression of neurofilament heavy. We observed disruption of neurites in the lamina propria as well as their absence within misshapen taste buds from fungiform papillae of patients.

Long-Term Dysfunction of Taste Papillae in SARS-CoV-2
https://evidence.nejm.org/doi/full/10.1056/EVIDoa2300046#f3

The reason I am writing this post today is that this MECHANISM is TRANSPOSABLE. It is not just taste buds and their neurites that are subject to this kind of annihilation. It is theoretically all cells that the Spike Protein comes into contact with. And there is evidence. Let us look at cardiomyocytes.

Myocardial damage can occur due to multiple reasons including decrease in oxygen levels due to ARDS, the formation of thrombi as has been observed in COVID-19 patients, and direct injury of cardiomyocytes by viral infection and the inflammatory state of the COVID-19 patients.

Physiology of cardiomyocyte injury in COVID-19
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7668750/

What, after all is a classic heart attack but an arterial blockage causing damage to heart muscle? Indeed, the Spike Protein damages heart muscle. It is, in essence, causing a real-time, spreading “heart attack.” And, it is also most likely destroying the conduction myofibers in the heart, just like neurites in the tongue. This then causes Sudden Cardiac Death.

Remodeling of injured sympathetic nerves on the heart after myocardial infarction (MI) contributes to adverse outcomes such as sudden arrhythmic death, yet the underlying structural mechanisms are poorly understood. We sought to examine microstructural changes on the heart after MI and to directly link these changes with electrical dysfunction. We developed a high-resolution pipeline for anatomically precise alignment of electrical maps with structural myofiber and nerve-fiber maps created by customized computer vision algorithms. Using this integrative approach in a mouse model, we identified distinct structure-function correlates to objectively delineate the infarct border zone, a known source of arrhythmias after MI. During tyramine-induced sympathetic nerve activation, we demonstrated regional patterns of altered electrical conduction aligned directly with altered neuroeffector junction distribution, pointing to potential neural substrates for cardiac arrhythmia.

High-resolution structure-function mapping of intact hearts reveals altered sympathetic control of infarct border zones
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8855798/

The Spike Protein is The Destroyer of Worlds.

Here is the 30,000 ft. problem: Whatever the Spike Protein may access, it can and will destroy.

Thank you for your readership and support. I will continue. And finding answers is just as important, if not more so, as ever.