Long COVID as Prion Disease

The disease has so far remained elusive, perhaps because it is not viral at all.

Writing this post has been the most concerning of all the posts I have written to date. We must determine if what I am seeing is certain. The evidence and logic for this hypothesis disturb me greatly.

A very interesting paper about an extremely rare form of Prion Disease caught my attention. As the readers of my Substack know, I have believed since the beginning of the Pandemic that the Spike Protein is capable of inducing Prion Disease. However, if you have been following my work, I now believe that the Spike Protein ITSELF behaves as a Prion.  

If we look closely at Long COVID, we can observe that it, also, may actually be a Prion Disease. 

First let us review an extremely rare form of Prion Disease: PrP Systemic Deposition Disease 

After our first report, the Patient 1’s cognitive function declined from 27/30 on the Mini-Mental State Examination at 34 years to 22/30 at age 36 years. In addition, her heart function decreased to 39.1% of ejection fraction at 37 years of age. Because of heart failure, impaired absorption, and hypothermia (body temperature < 35.0 ˚C), she suffered severe pneumonia and died when 37 years old (11 years after the onset). No abnormal intensities were found on magnetic resonance imaging including diffusion-weighted imaging throughout her disease course of 11 years. The clinical characteristics of patient 2, her younger brother: He began to suffer from frequent diarrhea at age 20. At age 28, he developed syncope due to orthostatic hypotension. He began to suffer from urinary retention at age 30, vomiting at age 32 and thermoanesthesia at age 34. Polymerase chain reaction RFLP analysis of PRNP with BssSI showed a 2-bp deletion (CT) in codon 178 that causes an additional variable 25 amino acids at the C-terminal, from the mutation site to the premature stop codon, in both Patient 1 and 2 (Fig. 1b).   Pathological analysis of the autopsied samples of Patient 1 Histological examination of the cerebral cortices showed severe spongiosis and neuropil degeneration. Immunohistochemical analysis with anti-prion protein (anti-PrP) showed coarse deposits in the cerebral cortex, but not in the white matter. PrP was also deposited along the small vessels of the cerebral cortex, but not in white matter, the artery, or arteriole which have muscular layer. PrP was also deposited in the spinal cord and ganglions. Remarkable PrP deposits were also found in her femoral and sural peripheral nerves. Double  PrP Systemic Depositon Disease   immunofluorescence also revealed PrP deposits in peripheral nerves. Abnormal PrP deposits were also detected in almost all other organs. In the heart, PrP accumulated in the myocardium and epicardial nerve fibers. Unlike the normal control, immunostaining for tyrosine hydroxylase revealed a marked loss of positive nerve fibers of patient 1. In the digestive tracts, PrP was deposited in the muscularis mucosa, muscularis propria, Meissner's plexus, and Auerbach's plexus, but not in the mucosa. In the urinary bladder, PrP was deposited in the muscularis propria and nerve plexus of the bladder. 

“PrP systemic deposition disease”: clinical and pathological characteristics of novel familial prion disease with 2-bp deletion in codon 178 
https://ousar.lib.okayama-u.ac.jp/files/public/5/55031/20170615132308352722/K0005478_fulltext.pdf 

Why I believe Long COVID is a Prion Disease has to do with the above in relation to the following finding. 

Among 17 patients with SARS-CoV-2 onset between February 21, 2020, and January 19, 2021, treated in 10 states/territories (Table 1), 16 had mild COVID. The one (#9) with severe COVID (1 month stay in intensive care with ventilatory support) had electrodiagnostically confirmed sensorimotor polyneuropathy ascribed to critical care illness in addition to SFN. Medical histories and comprehensive blood screening (not shown) identified none with conventional neuropathy risks nor evidence of systemic dysimmunity. Imaging of the brain or spine, if performed, was unrevealing. 

Peripheral Neuropathy Evaluations of Patients With Prolonged Long COVID 
https://nn.neurology.org/content/9/3/e1146 

And this is key. Please recall the following from the paper on PrP Systemic Deposition Disease. 

No abnormal intensities were found on magnetic resonance imaging including diffusion-weighted imaging throughout her disease course of 11 years. 

So, given the similarities between PrP Systemic Deposition Disease and Systemic Amyloidosis, I believe we must now investigate Long COVID as being a Prion Disease.