At the Nexus of Cachexia and Amyloidosis

The Persistence of Spike Protein May NOT be Due to Viral Reservoir

July 1, 2022

A paper was published on June 14 proving what I have long hypothesized – that the Spike Protein is persistent and circulating in Long COVID. The paper states:

Strikingly, we detect SARS-CoV-2 spike antigen in a majority of PASC patients up to 12 months post-diagnosis, suggesting the presence of an active persistent SARS-CoV-2 viral reservoir.

Persistent circulating SARS-CoV-2 spike is associated with post-acute COVID-19 sequelae

What I believe we must consider here is that there MAY BE NO VIRAL RESERVOIR! If the Spike Protein is not cleared (and is it ever actually completely cleared? Is it propagating, prion-like, traveling via extracellular vesicles?) it may be self-propagating, providing its own eternal and ever-expanding “reservoir” within the body.

This may answer the long-standing question as to why people are exhibiting symptoms long after the virus itself has been cleared. We know for a fact that the Spike Protein has amyloidogenic properties, as the now famous paper from Sweden proved.

Amyloidogenesis of SARS-CoV-2 Spike Protein

Therefore, I believe it is highly likely that the Spike Protein is itself behaving as an amyloid. If so, then there would not need to be any “viral reservoir” as it would be performing as follows:

In a remarkable variety of diseases, specific proteins have been found to misfold and aggregate into seeds that structurally corrupt like proteins, causing them to aggregate and form pathogenic assemblies ranging from small oligomers to large masses of amyloid. Proteinaceous seeds can therefore serve as self-propagating agents for the instigation and progression of disease.

Self-propagation of pathogenic protein aggregates in neurodegenerative diseases

So, what is the result of this ever-present invasive protein? CACHEXIA AND AMYLOIDOSIS


The paper published June 14 shows that not only was the Spike Protein abundantly present in those with Long COVID, but cytokine levels were also staggeringly high. Extreme elevation of IL-6, TNF-a (among others) was observed.


The presence of the Spike Protein has been proven to induce potent inflammatory cytokines:

We observed that spike (S) protein potently induced inflammatory cytokines and chemokines, including IL-6, IL-1β, TNFα, CXCL1, CXCL2, and CCL2, but not IFNs in human and mouse macrophages.

SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway

What MUST BE UNDERSTOOD is that it is PRECISELY these cytokines, that when persistently elevated, induce Cachexia. This was proven by a group of researchers at Zhongshan Hospital of Fudan University.

Chronic inflammation, mediated by cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), has been reported to promote cancer cachexia. we conclude that chronic inflammation (especially that mediated by IL-6) might promote cancer cachexia by regulating WAT lipolysis in early-stage cachexia and browning in late-stage cachexia.

Interleukin-6 induces fat loss in cancer cachexia by promoting white adipose tissue lipolysis and browning

Biomarkers of cancer cachexia



The second process induced by the Spike Protein present in the oldest old is Amyloidosis.

The Spike Protein has been proven to have VERY STRONG binding affinity to ALL human Amyloid proteins.


It is therefore concluded that:

Stable binding of the S1 protein to these aggregation-prone proteins which might initiates aggregation of brain protein and accelerate neurodegeneration.

SARS-CoV-2 spike protein interactions with amyloidogenic proteins: Potential clues to neurodegeneration

I reference again the Swedish paper above, to illustrate that not only is this mechanism how the Spike Protein induces Amyloidosis, but also how it PROPAGATES ITSELF WITHOUT THE PRESENCE OF THE VIRUS.

I wrote posts last year pointing towards this effect. Specifically, ones describing Long COVID as Cancer Metabolism Syndrome, Cancer Without Tumors and Lethal Cancer Phenotype without Primary Tumor.




There are several questions:

How do we mitigate the presence and potential self-propagating abilities of the Spike Protein?

Does repeated exposure to the Spike Protein, either via infection or vaccination induce and/or accelerate these processes?

How to ensure the world medical and research communities address and investigate these conclusions?