The Spike Protein and SADS: Evidence of the Brainstem Demyelination/Destruction Hypothesis

SARS induced Death in mice via dysfunction of the Medulla via the OLFACTORY NERVE

Viral antigen distribution in the brain following intranasal inoculation. Brains were harvested from mice infected intranasally with 2.4 × 104 PFU and stained for viral antigen. (A to C) Antigen distribution in the brain at 60 h (A) and 3 (B), 4 (C), and 5 (D) days p.i. (E to J) The brain stem (E, G, and I) and hypothalamus (F, H, and J) were examined for viral antigen and inflammation. (E and F) Naïve controls. (G and H) SARS-CoV-infected brains exhibited antigen exclusively in neurons with no obvious inflammation at day 6 p.i. (compare to naïve controls). (I and J) JHMV-infected brains showed less extensive neuronal infection but severe perivascular inflammation (closed arrows) and meningitis (open arrows) at day 6 p.i. Original magnifications: ×1 (A to D) and ×5 (E to J).

Why this has not previously come to light and been discussed is beyond me. As you know, I have been researching the demyelination hypothesis as the cause of the Sudden Cardiac Deaths. I have discovered that the original SARS was able to induce Neuronal Death in the Medulla (cardiorespiratory center) resulting in the death of the subject.

Perhaps the most striking and disturbing aspect of this discovery is that the mice had VERY LITTLE INFECTION in the LUNGS. And, the virus entered the brain via the OLFACTORY BULB.

Herein, we use these mice to show that virus enters the brain primarily via the olfactory bulb, and infection results in rapid, transneuronal spread to connected areas of the brain.

In fact, this destruction of the Brain Stem was the main cause of death.

This extensive neuronal infection is the main cause of death because intracranial inoculation with low doses of virus results in a uniformly lethal disease even though little infection is detected in the lungs. Death of the animal likely results from dysfunction and/or death of infected neurons, especially those located in cardiorespiratory centers in the medulla.

Interestingly, inflammation in the brain was NOT detected while this destruction was occurring.

Spread throughout the brain happens SIMULTANEOUSLY with CLEARANCE of the virus from the site of infection.

Rapid spread throughout the brain appeared to be accompanied by virus clearance at sites of initial infection and concomitant neuronal loss.

Severe Acute Respiratory Syndrome Coronavirus Infection Causes Neuronal Death in the Absence of Encephalitis in Mice Transgenic for Human ACE2
https://journals.asm.org/doi/10.1128/JVI.00737-08

Only the N Protein was tested for. We need to perform tests and studies to determine if the S Protein is also present. Of course, you know where I stand on my prediction of those results.

I will continue to research this mechanism. This is why infection that does not produce respiratory symptoms is most likely VERY DANGEROUS. Of course, direct viral antigen in the body…

I urge clinicians to perform autopsies on all those under 60 that die suddenly. We must know if the Brainstem has undergone demyelination/neuronal death.