Jaineysez

Jaineysez

30-08-2022

20:42

💀 To Sp!ke or Not to Sp!ke 💀 probably-eng!neered 🦠 VS eng!neered 💉❓ That is the question. Early in 2020 scientists asked another: Is the viral Sp!ke Pr0te!n (SP) t0☠️ic? These questions are related. In 2020 @wtyl_live @Doctor_I_am_The and others >

questioned the use of the SARS-C0V-2 SP in gene therapies. We tweeted, blogged, streamed their❓s. Our speech was censored and our accounts locked. A chronology of some of the science we found: "we identified the presence of pri0n-like domains in the SRS-C0V-2 SP. >

Compared with other viruses, a striking difference was observed in the distribution of pri0n-like domains in the sp!ke pr0te!n, since SC2 was the ONLY C0R0NAVIRUS WITH A PRI0N-LIKE DOMAIN FOUND IN THE RECEPTOR-BINDING DOMAIN OF THE S1 SP!KE PR0TE!N.” -03/19/20 >

"The "SP" of S4RS-C0V-2 contains a cleavage site for the protease furin that is absent from SARS... neuropilin-1 (NRP1), which is known to bind furin-cleaved substrates, and potentiates SC2 infectivity. NRP1 is abundantly expressed in the respiratory and olfactory epithelium >

WITH HIGHEST EXPRESSION IN ENDOTHELIAL AND EPITHELIAL CELLS...the furin-cleaved S1 fragment of the sp!ke pr0te!n binds directly to cell surface NRP1." -10/20/20 #Dance10Looks3 #Turn2Stone >

The endothelium and the epithelium are 2 major organs in the body responsible for covering and protecting all the other organs, blood vessels and lymph nodes. If a pathogen infects them it can cause systemic breakdown in the body. #EverythingAllTheTime #LifeInTheFastLane >

This article explains.👇It shows the SP has a unique binding site enabling it to infect hard to reach organs like the 🧠 In effect, the SP might act as a cardi0t0xin and a neur0t0xin: "Until now...questions have remained unanswered as to why SC2 readily infects organs >

"We show here that Sp!ke Pr0te!n ALONE can damage vascular endothelial cells...manifested by impaired mitochondrial function" -12/04/20 #ICanDoBadAllByMyself >

"the trimeric Sp!ke Pr0te!n of SC2 could bind to TLR4 directly and robustly activate downstream signaling in monocytes and neutrophils…We recently found that SC2 PROVOKED AN ANTI-BACTERIAL LIKE RESPONSE and activation of TLR4 pathway at the very early stage of >

'We observed that SP potently induces inflammatory cytokines and chemokines...in human and mouse macrophages….When stimulated with extracellular Sp!ke Pr0te!n, human lung epithelial cells also produce inflammatory cytokines and chemokines.” -03/17/21 >

"the exposure of human endothelial cells to cell culture supernatant derived from SC2 Sp!ke Pr0te!n expression displayed cellular senescence markers leading to enhanced leukocyte adhesion with CORONARY BLOCKADE POTENTIAL.” -04/16/21 >

"we generated a construct that expresses membrane-localized CoV-2 Sp!ke Pr0te!n S1...in cardiomyocytes (it) caused heart dysfunction, induced hypertrophic remodeling, and elicited cardiac inflammation" -06/20/21 >

"the SP from SC2 binds to the blood coagulation factor fibrinogen and induces structurally abnormal blood clots with heightened proinflammatory activity” -10/13/21 > #TheInvisibleThread #PeopleAreStrange #TurntoStone #ClotClotBaby

"Here we show that exposure to SC2 Sp!ke promotes platelet activation, adhesion and spreading, both when present on the envelope of virions or upon expression on the plasma membrane of cells. SP!KE WAS EFFECTIVE...AS A SOLE AGONIST " -12/14/21 >

From 2020, to 2021, we had scientific results from labs around the world corroborating or reproducing other results to give an idea of the t0xi!city of the SC2 Sp!ke Pr0te!n. Reproducibility is important in science. It gives us confirmation of results and enables scientists>

to establish a working theory. They can build on this establish theory to form new hypothesis. Interesting research came from the lab of @konstantinospo7 2020. It showed toxic epitopes on the SC2 Sp!ke Pr0te!n>

He asked a prescient question >

Then statement by Professor Poulas was one of the most interesting of all the pandemic research:

His research is echoes findings of the lab of carlobrogna1 -10/2020 scroll down to the bottom of the page to see the early publications on the🦠. >

Recent findings of the Brogna lab >

Here is where we come back to the early SP papers in this🧵and Scott's question: What is the long term risk of infection vs the long term risk of the sh0ts, and was it known? No, it was not known, but, from early research papers>

We knew the SP: -had a pr!0n-like domain -was easily cleaved by furin -was efficiently bound by neuropilin-1 (NRP1) -NRP1 was highly expressed on the endothelial and epithelial organs >

(In early 2021 a🧵 "Welcome to Your Endothelium" was posted by the now defunct Janiesaysyay explaining the significance of the SP's ability to invade these organs.) If we put together the early research and Poulas' theory, about "the memory of the to☠️ification" >

the phenomenon of Post Acute Sequelae Covid #PASC or #LongCovid becomes clearer. Scientists around the world, had a working theory, based on results in labs, that the SP (from the🦠and the💉) is☠️and might be a cause of LC. >

This theory might ❓ be supported by the 2021-2022 research of the finding of the Sp!ke Pr0te!n S1 subunit in immune cells by #IncellDx and the finding of microclots, hyperactive platelets, and immune dysregulation of #TeamClots >

Further research on PASC conducted by @: VirusesImmunity and PutrinoLab also seems to support the theory that Long Covid is chronic autonomic and immune dysregulation, in some patients, the pathology is neurodegenerative (remember the early research on NLRP1) >

in some it is systemic. -08/10/22 > #ImExhausted #KeepItComingLove #ILoveLucyJobSwitching #DontBringMeDown #IGetAround #GoWhereUWannaGo #mRNA #LNPs

All of this Long Covid research must have interested the CDC, because they removed their "Fact" that the Sp!ke Pr0tein mRNA does not last long in the body. 08/2022>

Professor Poulas' theory of a t0☠️ic Sp!ke Pr0te!n acting on the endothelium and epithelium, might partially explain the sequelae of Long Covid. What did we know and what did we guess? We guessed quite a lot in 2020 and 2021 >

knowledgeable guesses, based on honest scientific research. Unfortunately for most of the public, people without a background in biology, finding out about these educated guesses was almost impossible because of rigid censorship and repression by the scientific hegemony.

One of the earliest and most interesting papers on the Sp!ke Pr0te!n came from the team of Prashant Pradhan, at the University of Delhi -01/31/30 >

A majority of the public doesn't know about this research. The Pradhan team was forced to withdraw their paper quickly, because of enormous pressure from colleagues of the NIH. Colleagues who are suspected of trying to cover up NIH-funded Gain of Function research on >

coronaviruses and Sp!ke Pr0te!ns. See the research of Charles Rixey. Pradhan's team found 4 gene sequences unique to SARS=CoV-2 in the receptor binding domain of the Sp!ke Pr0te!n. No other coronavirus had them. They compared the 4 sequences to all of the other known >

viral genomes and found: "Surprisingly, each of the 4 inserts aligned with short segments of the Human immunodeficiency Virus-1 pr0teins, HIV-1" #2 and 3 of these inserts found were on the C-terminal domain of the Sp!ke Pr0te!n S1 subunit. The 4th is at the junction of the >

S1-S2 subdomains of the Sp!ke Pr0te!n S1 subunit. The aligned sequences on HIV-1 with homology to SC2 sequences were: HIV-1's surface glyc0pr0tein gp120 and its Gag pr0tein. Why is this homology relevant to early questions about the risks of the 🦠vs the risks of the 💉? >

Pradhan tells us: "This uncanny similarity of novel inserts in the... sp!ke pr0te!n to HIV-1 gp120 and Gag is unlikely to be fortuitous...our findings suggest unconventional evolution...that warrants further investigation." >

In January 2020 we had data that indicated the SC2 Sp!ke Pr0te!n had an "uncanny" "unconventional" or engineered "evolution." I.e. that it might have a lab origin and have gained function. We knew it might have gene sequence homology with HIV-1. This homology might have >

indicated SC2 shared pathophysiological mechanisms with HIV-1 >

What mechanisms might SC2 and HIV-1 share? Pradhan: "Gag protein of HIV is involved in host membrane binding, packaging of the virus and for the formation of VIRUS-LIKE PARTICLES. Gp120 plays a crucial role in recognizing the host cell by binding to the primary receptor CD4... >

This binding induces structural rearrangements in GP120, CREATING A HIGH AFFINITY BINDING SITE FOR A CHEMOKINE CO-RECEPTOR like CXCR4 and/or CCR5." These mechanisms and others of HIV-1 are well known by AIDS researchers and physicians, and we have therapies to treat them. >

They are so well known that when renowned AIDs researcher, and former Director of Virology at Stanford University, Dr. Bruce Patterson, saw the phenomenon of Long Covid, he wondered about a possible similar pathological mechanism to AIDs. Pattterson's ground breaking AIDs >

research showed reservoirs of HIV-1 in cells caused the immune destruction in AIDs patients: "analysis of proviral DNA and viral messenger RNA in cells in the blood of HIV-1-infected patients showed that the HIV-1 genome persists in a large reservoir of latently infected cells. >

With the use of this technique it is now possible to detect single-copy DNA or low-abundance messenger RNA rapidly and reproducibly in a minor subpopulation of cells." -05/1993 > #DontLeaveMeThisWay #LookingForMisterGoodbar #TheLimbo #ImmuneSuppression

Patterson and the technology to detect viral reservoirs have come a long way since 1993. He and his team, including Dr. Ram Yogendra, are now using the science of machine learning and proteomics to detect viral reservoirs, virus like particles >

and reactivation of latent viruses causing immune dysregulation by pro-inflammatory cytokines. This science is showing that conditions like Acute and Long Covid, ME/CFS, Lyme and PANDAS can be identified by certain biomarkers. >

Dr Patterson talks about the science -1st Quarter/2021>

Patterson et al found the SC2 Sp!ke Pr0te!n S1 subunit, a VIRAL FRAGMENT, in the intermediate and non-classical monocytes of PASC patients. This causes immune dysregulation and a chronic hyperinflammatory condition and blood pathology described by Pretorious et al. >

Here he writes about the relationship between Covid and CCR5. This is the same chemokine coreceptor Pradhan's paper showed that the HIV-1 protein, Gp120, creates a binding site for. -06/28/21 >

Research came out showing a subset of Covid patients had T-cell exhaustion. This is a pathophysiology SC2 shared with #HIV. 07/15/2020 >

"in conditions of chronic infection, persistent exposure of T cells to high levels of antigen results in a severe T‐cell dysfunctional state called exhaustion. T‐cell exhaustion leads to a suboptimal immune‐mediated control of multiple viral infections including HIV." >

The team at began diagnosing and treating #LongCovid patients, showing good results using cocktails of repurposed #AIDS drugs and statins among other therapies. 09/2020 >

This article, from the Wuhan Institute of Virology shows that SC2 Sp!ke Pr0te!n uses the same mechanism via LFA-1 to infect and destroy T-cells that HIV does. Noted authors, Zheng-li Shi and Peng Zhou. -03/11/22 >

Igor Chudov explained the research here and on Twitter. Twitter suspended his account. -03/13/22 >



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