Infection/transfection with Spike Protein of SARS-CoV-2 replaces liver as amyloid source

June 2, 2022

Refining previously discussed pathogenic mechanisms of SARS-CoV-2.

In 2010 a very important article was published in the journal Blood:

Fibrinogen amyloidosis: the clot thickens!

The article states that:

Fibrinogen amyloidosis (AFib), discovered more than 15 years ago, is amyloid deposition occurring due to the presence of a variant of fibrinogen, which is produced exclusively by the liver.

It also reveals that:

They conclude that AFib is not solely nephropathic, but is a more systemic disease with a diverse and complex phenotype… Stangou et al suggest that direct amyloid deposition in vascular walls may be the first step in a disease process that leads to IMPARIED ENDOTHELIAL FUNCTION, and that nephrotic syndrome with hyperlipidemia and hypertension may then facilitate atheroma formation.

What is important here is that whereas the liver creates an aberrant, misfolded, undegraded amyloid fibril producing protein which is deposited in Fibrinogen Amyloidosis, THE EXACT SAME EFFECT IS GENERATED BY THE SPIKE PROTEIN OF SARS-CoV-2 DUE TO ITS INTERACTION WITH NEUTROPHIL ELASTASE.

As professor Per Hammarstrom discovered:

When the spike protein is cut up, it produces the exact piece of protein which, according to the researchers’ analysis, is most likely to produce amyloid. This enzyme is released in large quantities from one type of white blood cells, neutrophils, which are released early on during infections such as COVID-19. When the researchers mixed pure spike protein with this enzyme, called neutrophil elastase, unusual fibrils were produced.

We have never seen such perfect, but scary, fibrils as these ones from the amyloid-producing SARS-CoV-2 spike protein and pieces thereof. The fibrils starting from the full-sized spike protein branched out like limbs on a body. Amyloids don’t usually branch out like that. We believe that it is due to the characteristics of the spike protein.

It is due to this property that it perfectly mimics Fibrinogen Amyloidosis. In the words of Sofie Nystrom: “Our experiment shows that if fibrin is formed in the presence of spike amyloid, the plasmin can not totally remove the fibrin clots.” And there you have the exact same effect as the misfolded fibrinogen protein in Fibrinogen Amyloidosis.

Is the combination of Fibrinogen, the Spike Protein of SARS-CoV-2 and Neutrophil Elastase the basis for the pathology of Severe COVID and Long COVID?