Could the Spike Protein on its own be as the decapitated snake head: still capable of delivering a deadly bite?
Brilliant--and terrifying. Thank you for continuing to shine light with these excellent questions in such a potentially fruitful direction. I am truly wishing and hoping that our leaders and medical experts will sit up and take interest in these questions you're asking.
This is getting fascinating ... and dangerous, by the day.
Thank you for making it easier for all of us!
Every time I read an update like this I ask if China knows this and what the scientist that defected early on would say about this? I think the answers would be yes and yes it was designed to do this.
Hey. Maybe. I am fairly convinced the spike protein possesses mutagenic qualities. First off we have seen reverse transcription being possible in the Lund university liver cell study. We also see post vaccine long haul syndrome being uncannily similar to long-covid. You should see Dr Bruce Pattersons cytokine mapping. And those conditions are again similar to CFS/M.E and Gulf war syndrome, or even chronic Lyme disease. My guess is mitochondrial gene expression is changed or altered. But this has a significant effect on various systems as cells perform their functions poorly without reliable energy systems. Correct me if I am wrong.
I think I can answer some of your questions, I’ve spent the last several months analyzing data from the only study with public sequencing data after vaccination (DOI:10.1038/s41586-021-03791-x). It’s hard to overemphasize the similarities between vaccination against COVID-19 and infection with HIV-1. Both HIV-1 and SARS-CoV-2 specifically infect T cells via CXCR4 and CD4, platelets via CLEC1B and macrophages via CCR5 (and potentially LRP1). Viral RNA from both HIV-1 and SARS-CoV-2/COVID-19 vaccines induces production of mRNA editing enzymes APOBEC3A in monocytes and APOBEC3G in T cells. However, while the expression of APOBEC3G after HIV-1 infection is protective (the enzyme is defeated by the virus after some weeks), it was recently demonstrated that APOBEC3-mediated edits to SARS-CoV-2 strongly promote viral replication, propagation and persistence (DOI:10.1101/2021.12.18.473309). The first vaccine dose induces a 3-fold increase in APOBEC3G across all cell types while the second vaccine dose induces a 6-fold increase in APOBEC3A. In 5 of 6 participants the second dose induced novel monocytes (“Cluster 8 cells”) that expressed CD14 (a marker for classical monocytes), CD1C (a marker for dendritic cells) and programmed cell death 1 ligand 1 (CD274), in addition to extremely high levels of APOBEC3A and high levels of APOBEC3G (more than was detected in T cells).
Another mystery is that after the second vaccine dose a small subset of T cells started expressing genes that are normally exclusive to erythrocytes, including hemoglobin subunits (HBB, HBA1, HBA2, HBG2, HBD, HBM) and ALAS2 which participates in heme biosynthesis. These genes were expressed by some cells identified as CD4 T cells in 6 of 6 participants on Day 42 post-vaccination (the last sample day of the study). I initially assumed that this was because the T cells had formed aggregates with platelets and erythrocytes—similar to those found in HIV-1 patients—but I’m not so sure that this is the case anymore. Reverse transcription and integration of both SARS-CoV-2 and mRNA from vaccines was shown to be possible in vitro dependent on LINE-1. After integration of HIV-1, transcription of the integrated provirus is exclusively mediated by cyclin-T1 (CCNT1) which activates elongation of viral RNA by RNA polymerase II after an interaction with HIV-1 Vif. Vif also binds CCNT2 but this interaction is not believed to activate elongation. Since CCNT1 and CCNT2 are involved in cell cycle regulation, they generally control transcription of different proteins from the same protein families with opposite functions. During my investigation into the COVID-19 vaccines I identified 19 genes that were correlated with hemoglobin subunit beta (HBB). 17 of these genes (89%) were either CCNT2 target genes or had family members that were CCNT2 target genes. Unfortunately CCNT1 target genes aren’t listed in the ENCODE database.
Genes correlated with HBB that are also CCNT2 target genes: HBA1, ALAS2, KLF15, WDR31, GPC1, FEZ1, EMP2, EREG, RBAKDN
Genes correlated with HBB, with CCNT2 target genes from the same family: CHRNA1 (CHRNA5), HIST1H2BM (HIST1H2BA, C, D, F–H, J–L, N, O), ADPRHL2 (ADPHRL1), TREML2 (TREML1), NT5C1A (NT5C1B), OTUD6A (OTUD6B), SLC8A1 (SLC8A2), SLC24A5 (SLC24A2)
Genes correlated with HBB, with no relationship to CCNT2: PF4V1, TFEC
In my opinion it is too big of a coincidence that almost all genes correlated with hemoglobin after vaccination have some kind of relationship with the transcription factor that is required for replication of integrated virus. I think it’s plausible that the hemoglobin mRNA detected in T cells is not a result of aggregation with erythrocytes, but rather that it was transcribed by the T cells themselves during the transcription of integrated spike protein mediated by CCNT1.
It has been debated for a while whether the integrated spike protein could be transcribed much later on (like HIV-1), and unfortunately data was recently published online (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE200274) providing a pretty strong indication that this is actually the case. Macrophages from 6 vaccinated (1–3 weeks after dose 2) and unvaccinated subjects were purified and stimulated in vitro with either bacterial lipopolysaccharides (LPS) or recombinant S. This is exactly the same experiment that is normally performed to distinguish latently infected T cells from uninfected T cells. Latently infected T cells begin transcribing integrated HIV-1 after stimulation with LPS while uninfected T cells do not. Since the investigators in the macrophage experiment did not test for expression of S, I believe it is valid to use APOBEC3A as a proxy for expression of S. It has been demonstrated that APOBEC3A is directly induced by S mRNA from the vaccines. APOBEC3A is expressed by cells after exposure to viral DNA and RNA, and as such it should not be expressed after exposure to bacterial LPS. The data shows that macrophages from 5 of 6 vaccinated, but 0 of 6 unvaccinated subjects started expressing APOBEC3A after exposure to LPS, and the difference was significant (p < 0.01 using t test).
Therefore, I believe that macrophages/CD14 monocytes, likely also CD4 T cells and platelets, and potentially even CD8 T cells and classical dendritic cells may act as latent reservoirs of spike protein. Transcription of spike protein probably requires immune cell activation and therefore it may only be transcribed during other bacterial or viral infections, like HIV-1.
I’m new to Substack and I’m still not really sure how to include links in comments, but if you’re interested I can provide more references and figures to support my claims.
As this was a new term for me, a definition for the lazy:
An infection first recognised by secondary manifestations—e.g., increased neutrophils in the circulation or fever of unknown origin—often caused by a bacterial infection in an obscure site—e.g., a subphrenic or other intra-abdominal region
"Has the Spike Protein of SARS-CoV-2 naturally evolved to have perhaps the most profound amyloidogenic capabilities of any human virus to date"
Nah. Lots of viruses have that capability. HIV also causes amyloid to accumulate. More recent research shows HIV has a protein attached that causes amyloid to accumulate leading to neurodegenerative disorder called HAND:
HIV Regulation of Beta-Amyloid Production
However the accumulation of beta-amyloid is far less in older patients under drug therapy yet they still have HAND suggesting the beta amyloid isn't what drives the neurodegeneration:
Brain and liver pathology, amyloid deposition, and interferon responses among older HIV-positive patients in the late HAART era
"Does this mean that Long COVID is due to the presence of undegraded Spike Protein causing systemic amyloidosis, in particular, microvascular deposition?"
No because long covid isn't a real thing, or at least that is what recent papers are coming out with. A recent study (closed the browser, pubmed it if you want it) found, when compared against a control, that the long covid group were generally less healthy (obesity etc) and had higher anxiety issues about their health. As in other studies, they couldn't find any immune or physical reason for the non-specific symptoms like "no energy" and "feeling lousy". Another earlier study I remember found the majority of people with long covid actually had no N antibodies meaning they never actually had the disease, but all had the belief that they did. "Long covid" with over 250 non-specific symptoms with no physical cause is looking to be the new fibromyalgia, a type of hypochondria that has always been with us.
Bruce Patterson has done a lot of work on the S1 and S2 segments of spike infecting monocytes, still measurable 15 months post-vax.
I am sure others have asked this question but it would be great if you wrote an article about what could be done to break down these new amyloid. Maybe we don't know yet but any info that is available would be invaluable. Thank you.
here is the musical :)
I believe it's capable of more destruction after being cleaved.
At the beginning of the pandemic I saw a video from some scientific conference in which a Chinese scientist spoke on the research being done on Corona virus. (She has since disappeared from the planet.). She was showing videos and explaining how they had grafted parts of at least 8 viruses into the Corona virus. She specifically mentioned using part of the HIV virus that helps invade the cell membrane.
Tell me again this isn’t deliberate Proteine poisoning. From a bioweapon.
Interesting - but I’m not sure how Long Covid could wax and wane if that’s the case. What is the rationale for that, if you don’t mind?