January 10, 2022
When I first began studying the SARS-CoV-2 virus I was initially concerned about its Spike Protein’s potential ability to induce prion disease, as the spike has homology with our Prion protein and it induces a strong Unfolded Protein response.
However, almost two years after I reached that conclusion, I believe it is only part of the story. Yes, I am still concerned that it may induce Prion Disease. But, what concerns me more is that its interactions and mimicking of the human Prion Protein may be more “effective” having a role in tumorigenesis and metastasis.
In fact, the more I look at the Spike Protein now, and with the now common knowledge that the Spike Protein mimics Trousseau Syndrome, I now believe that the Spike Protein may be a genetic “Flash Drive” capable of initiating and/or rapidly progressing cancers.
By looking at the Spike Protein’s interactome, we can see a landscape where it would seem inevitable that aggressive cancer would be initiated or an existing, perhaps even occult cancer, become hyper aggressive.
It has been determined that the Spike Protein interacts with TLR4. This is currently viewed as being involved with the onset of Sepsis in severe COVID-19. This is certainly true. However, as with much regarding this virus, nothing is ever as it initially seems. TLR4, has been the center of attention regarding its contributory role in many inflammatory diseases including sepsis shock and asthma. Notably, mounting pieces of evidence have proved that this receptor is aberrantly expressed on the tumor cells and the tumor microenvironment in a wide range of cancer types and it is highly associated with the initiation of tumorigenesis as well as tumor progression and drug resistance.
The Spike Protein also interacts with Neuropilin-1. This is also an important receptor in the development of cancer. Immunoreactivity for NRP1 was seen in vessels from normal tissues adjacent to cancer and in 98–100% of carcinomas. Tumour cell expression of NRP1 was also observed in 36% of primary lung carcinomas and 6% of primary breast carcinomas, but no colorectal adenocarcinomas.
The Spike Protein bears homology with the human Prion Protein. It has been determined that PrPC misfolding and aggregation can cause fatal neurodegenerative conditions (98). Studies in recent years show that it also plays a role in cancer. PrPC can stimulate cancer progression by promoting cancer cell proliferation, invasion/metastasis, drug resistance, and cancer stem cell development.
Another receptor that the Spike Protein interacts with. And yes, HS has important emerging roles in oncogenesis and heparin derivatives represent potential therapeutic strategies for human cancers. Here we review recent insights into HS signaling in tumor proliferation, angiogenesis, metastasis, and differentiation.
Obviously, the Spike Protein interacts with ACE2 and depletes it. It may even induce autoantibodies against it. In the case of ACE2, upregulation was associated with favorable survival in pan-cancer and in multiple individual cancer types. These results suggest that ACE2 is a potential protective factor for cancer progression.
Given these findings and the fact that the Spike Protein disrupts the endothelium, allowing it to invade virtually every organ, it may be the case that even an asymptomatic infection could induce an aggressive cancer. These words feel ominous as doctors throughout the world have been reporting marked increases in cancers. Especially aggressive cancers. The Spike Protein appears to be a "Flash Drive" with a complete set of "instructions" to induce and/or accelerate hyper-aggressive cancers.
The SARS-CoV-2 host cell receptor ACE2 correlates positively with immunotherapy response and is a potential protective factor for cancer progression
Heparan sulfate signaling in cancer
SARS coronavirus 2 interactome
The role of toll-like receptor 4 (TLR4) in cancer progression: A possible therapeutic target?
Interactions Of The Spike Protein And Heparin
Neuropilin-1 expression in cancer and development