billwilliam

I send you forth as sheep in the midst of wolves: be ye therefore wise as serpents, and harmless as doves.

[Bocquet Annelise 🔬🧬📚🚜 @AnneliseBocquet]

Thank you Kevin... 🙏🙏🙏

@GauteNilsen, all blood products (albumin, plasma, etc.) must be considered contaminated until we have systematic ultrasensitive testing for Spike and its amyloid fibrils.
Vaccinated and unvaccinated blood must be screened before any use. The problem is the SARS-CoV-2 Spike protein - whatever its origin. And the Spike protein does not necessarily float freely; it can bind and form stable complexes with the albumin present in blood donations.
https://t.co/ke9jU7L8zQ

[Gordon G. Chang @GordonGChang]

China attacked our diplomats in Guangzhou late last decade with sonic weapons, causing injuries. Our presidents did nothing in response.

[Emily Kopp @emilyakopp]

NEW docs declassified by Tulsi Gabbard and released by Rand Paul on Fauci, COVID, and the Biodefense Blob. 🧵

Why did the U.S. work with a military lab in Wuhan?

A CIA report sets the stage: Bioweapons are harder to detect than nuclear weapons. Virologists should collect intel through conferences and labs.

[The Washington Times @WashTimes]

Director of National Intelligence Tulsi Gabbard in coming days is expected to release declassified intelligence documents on the origin of the COVID-19 virus -- a disclosure that comes after years of disputed and controversial assessments on whether the pandemic originated in a Chinese laboratory or came from a wild animal. https://t.co/PvAAr5MRFh

[Rebecc@ ███████ @Rebecca21951651]

New email released --

[billwilliam @billwilliam321]

@SitSilver @atranscendedman @breakfast_dogs The Guangzhou National Lab developed an AI docking model named UniBind, which can predict binding affinity between spike protein and antibodies.
In other words, immune-evasive mutation can be deliberately designed by computation.

https://t.co/FH4tXOWC0e

[billwilliam @billwilliam321]

Notch signaling increases infection rate of SARS-CoV-2. After ligand binding and subsequent proteolysis by ADAM10/ADAM17, the liberated Notch intracellular domain (NICD) translocates into the nucleus to form transcriptional complex, which induces expression of genes including furin and miRNA-145. [1] In other words, viral activation of Notch upregulates furin and makes furin cleavage site even more efficient. Moreover, furin also cleaves immature Notch protein to mature herodimeric form for cell surface expression. [1] Notch signaling and furin form positive feedback loop.

In addition, miRNA145 inhibits ADAM17 expression level. ADAM17 mediates proteolytic cleavage and ectodomain shedding ACE2, and soluble ACE2 serves as decoy blocking viral spike protein. Activation of Notch signaling inhibits this innate antiviral mechanism. [1]

Hyperinflammation forms self-sustaining positive feedback loop. NOTCH1 can bind IL-6 promoter directly to activate its transcription, and IL-6 in turn triggers expression of NOTCH ligands such as DLL1 and DLL4 (Delta-like ligands). [1] TNF-α also upregulates expression of NOTCH1 and NOTCH4. [1]

Besides the harmful effects, Notch signaling is beneficial by aiding adaptive immune protection, immune memory generation, and antibody production. [1] Notch signaling is also helpful for tissue regeneration in the lungs after viral infection. Activation of Notch enhances proliferation of basal cells necessary for healing and regeneration of other lung cell types. [1] However, excessive Notch activation perturbs balance of cell differentiation and promotes formation of fibrosis and honeycomb-like cysts. [1]

Multiple viral factors may be involved in triggering Notch signaling. First of all, SARS-CoV-2 spike protein is known to trigger hyperinflammation by interaction with Toll-like receptors (especially TLR4). [2] TLR4 typically recognizes hydrophobic molecules such as bacterial lipopolysaccharide (LPS). Viral spike protein binding to host TLR4 produces sepsis-like inflammation, including production of IL-6 and TNF-α. This phenomenon may kick start the positive feedback loop between IL-6 and Notch.

Wang et al. found Porcine epidemic diarrhea virus (PEDV) activates Notch signaling (upregulation of mRNA levels of JAG-1, DLL4, Notch-1) primarily through ORF3. [3] ORF3 is a transmembrane ion channel that plays functions in viral replication and virulence. Perhaps ORF3 induced endoplasmic reticulum stress and subsequent Notch activation are a common feature among various coronaviruses. SARS-CoV-2 also contains ORF3a. Of note, some studies suggest SARS-CoV-2 ORF3a is a calcium ion channel, whereas SARS-CoV-1 homolog is a selective potassium channel. [4] SARS-CoV-2 ORF3a may be a more enhanced virulence factor that induces ER stress by allowing calcium ions to leak out.

Breikaa et al. suggest that 5’UTR of SARS-CoV-2 genome may interact with proteins associated with Notch2 receptor signaling. [5]

ORF7a and ORF8 are additional virulence factors that trigger hyperinflammation. They may enhance Notch signaling and positive feedback loop by upregulating IL-6. ORF8 mimics IL17a. [6]

Hypoxia from viral infection activates Notch. [5] Notch signaling also exacerbates SARS-CoV-2-associated blood coagulation. [5]

Notch activation is quite common among several different viruses such as Epstein-barr virus, influenza virus, RSV, HPV, Human T-cell leukemia virus type 1 (HTLV-1), Hepatitis C virus (HCV), HBV, HIV. [5]

Anyway, the conclusion is that Notch activation can be engineered artificially. Some mutations in the spike protein may enhance binding with TLR4. Given that the Wuhan lab and other labs have collected thousands of viral samples, they could have selected for high-virulence forms of ORF3 (high-efficiency calcium ion channel). Other virulence factors like ORF7a and ORF8 can be deliberately selected or engineered.

References:

1. Baindara P, Sarker MB, Earhart AP, Mandal SM, Schrum AG. NOTCH signaling in COVID-19: a central hub controlling genes, proteins, and cells that mediate SARS-CoV-2 entry, the inflammatory response, and lung regeneration. Front Cell Infect Microbiol. 2022 Aug 4;12:928704. doi: 10.3389/fcimb.2022.928704. PMID: 35992174; PMCID: PMC9386183.
https://t.co/jZhJ9oe7pt

2. Sahanic S, Hilbe R, Dünser C, Tymoszuk P, Löffler-Ragg J, Rieder D, Trajanoski Z, Krogsdam A, Demetz E, Yurchenko M, Fischer C, Schirmer M, Theurl M, Lener D, Hirsch J, Holfeld J, Gollmann-Tepeköylü C, Zinner CP, Tzankov A, Zhang SY, Casanova JL, Posch W, Wilflingseder D, Weiss G, Tancevski I. SARS-CoV-2 activates the TLR4/MyD88 pathway in human macrophages: A possible correlation with strong pro-inflammatory responses in severe COVID-19. Heliyon. 2023 Nov 17;9(11):e21893. doi: 10.1016/j.heliyon.2023.e21893. PMID: 38034686; PMCID: PMC10686889.
https://t.co/G5d9Rgd7GE

3. Wang Y, Yang S, Zhao Y, Tian S, Cao Q, Geng X, Yang M, Song X, Shang H, Liu S, Guo R, Li Y, Sun M, Hu M, Fan B, Li B. PEDV infection downregulates goblet cell differentiation through activating the Notch pathway. Vet Res. 2025 Aug 12;56(1):168. doi: 10.1186/s13567-025-01599-5. PMID: 40797223; PMCID: PMC12341102.
https://t.co/wdXkNXU8Ci

4. Zhang J, Ejikemeuwa A, Gerzanich V, Nasr M, Tang Q, Simard JM, Zhao RY. Understanding the Role of SARS-CoV-2 ORF3a in Viral Pathogenesis and COVID-19. Front Microbiol. 2022 Mar 9;13:854567. doi: 10.3389/fmicb.2022.854567. PMID: 35356515; PMCID: PMC8959714.
https://t.co/exRxhemTiY

5. Breikaa RM, Lilly B. The Notch Pathway: A Link Between COVID-19 Pathophysiology and Its Cardiovascular Complications. Front Cardiovasc Med. 2021 May 26;8:681948. doi: 10.3389/fcvm.2021.681948. PMID: 34124207; PMCID: PMC8187573.
https://t.co/xFZ7rWcJvd

6. Wu X, Xia T, Shin WJ, Yu KM, Jung W, Herrmann A, Foo SS, Chen W, Zhang P, Lee JS, Poo H, Comhair SAA, Jehi L, Choi YK, Ensser A, Jung JU. Viral Mimicry of Interleukin-17A by SARS-CoV-2 ORF8. mBio. 2022 Apr 26;13(2):e0040222. doi: 10.1128/mbio.00402-22. Epub 2022 Mar 28. PMID: 35343786; PMCID: PMC9040823.
https://t.co/SbeBkqMCmY

[billwilliam @billwilliam321]

Notch signaling increases infection rate of SARS-CoV-2. After ligand binding and subsequent proteolysis by ADAM10/ADAM17, the liberated Notch intracellular domain (NICD) translocates into the nucleus to form transcriptional complex, which induces expression of genes including furin and miRNA-145. [1] In other words, viral activation of Notch upregulates furin and makes furin cleavage site even more efficient. Moreover, furin also cleaves immature Notch protein to mature herodimeric form for cell surface expression. [1] Notch signaling and furin form positive feedback loop.

In addition, miRNA145 inhibits ADAM17 expression level. ADAM17 mediates proteolytic cleavage and ectodomain shedding ACE2, and soluble ACE2 serves as decoy blocking viral spike protein. Activation of Notch signaling inhibits this innate antiviral mechanism. [1]

Hyperinflammation forms self-sustaining positive feedback loop. NOTCH1 can bind IL-6 promoter directly to activate its transcription, and IL-6 in turn triggers expression of NOTCH ligands such as DLL1 and DLL4 (Delta-like ligands). [1] TNF-α also upregulates expression of NOTCH1 and NOTCH4. [1]

Besides the harmful effects, Notch signaling is beneficial by aiding adaptive immune protection, immune memory generation, and antibody production. [1] Notch signaling is also helpful for tissue regeneration in the lungs after viral infection. Activation of Notch enhances proliferation of basal cells necessary for healing and regeneration of other lung cell types. [1] However, excessive Notch activation perturbs balance of cell differentiation and promotes formation of fibrosis and honeycomb-like cysts. [1]

Multiple viral factors may be involved in triggering Notch signaling. First of all, SARS-CoV-2 spike protein is known to trigger hyperinflammation by interaction with Toll-like receptors (especially TLR4). [2] TLR4 typically recognizes hydrophobic molecules such as bacterial lipopolysaccharide (LPS). Viral spike protein binding to host TLR4 produces sepsis-like inflammation, including production of IL-6 and TNF-α. This phenomenon may kick start the positive feedback loop between IL-6 and Notch.

Wang et al. found Porcine epidemic diarrhea virus (PEDV) activates Notch signaling (upregulation of mRNA levels of JAG-1, DLL4, Notch-1) primarily through ORF3. [3] ORF3 is a transmembrane ion channel that plays functions in viral replication and virulence. Perhaps ORF3 induced endoplasmic reticulum stress and subsequent Notch activation are a common feature among various coronaviruses. SARS-CoV-2 also contains ORF3a. Of note, some studies suggest SARS-CoV-2 ORF3a is a calcium ion channel, whereas SARS-CoV-1 homolog is a selective potassium channel. [4] SARS-CoV-2 ORF3a may be a more enhanced virulence factor that induces ER stress by allowing calcium ions to leak out.

Breikaa et al. suggest that 5’UTR of SARS-CoV-2 genome may interact with proteins associated with Notch2 receptor signaling. [5]

ORF7a and ORF8 are additional virulence factors that trigger hyperinflammation. They may enhance Notch signaling and positive feedback loop by upregulating IL-6. ORF8 mimics IL17a. [6]

Hypoxia from viral infection activates Notch. [5] Notch signaling also exacerbates SARS-CoV-2-associated blood coagulation. [5]

Notch activation is quite common among several different viruses such as Epstein-barr virus, influenza virus, RSV, HPV, Human T-cell leukemia virus type 1 (HTLV-1), Hepatitis C virus (HCV), HBV, HIV. [5]

Anyway, the conclusion is that Notch activation can be engineered artificially. Some mutations in the spike protein may enhance binding with TLR4. Given that the Wuhan lab and other labs have collected thousands of viral samples, they could have selected for high-virulence forms of ORF3 (high-efficiency calcium ion channel). Other virulence factors like ORF7a and ORF8 can be deliberately selected or engineered.

References:

1. Baindara P, Sarker MB, Earhart AP, Mandal SM, Schrum AG. NOTCH signaling in COVID-19: a central hub controlling genes, proteins, and cells that mediate SARS-CoV-2 entry, the inflammatory response, and lung regeneration. Front Cell Infect Microbiol. 2022 Aug 4;12:928704. doi: 10.3389/fcimb.2022.928704. PMID: 35992174; PMCID: PMC9386183.
https://t.co/jZhJ9oe7pt

2. Sahanic S, Hilbe R, Dünser C, Tymoszuk P, Löffler-Ragg J, Rieder D, Trajanoski Z, Krogsdam A, Demetz E, Yurchenko M, Fischer C, Schirmer M, Theurl M, Lener D, Hirsch J, Holfeld J, Gollmann-Tepeköylü C, Zinner CP, Tzankov A, Zhang SY, Casanova JL, Posch W, Wilflingseder D, Weiss G, Tancevski I. SARS-CoV-2 activates the TLR4/MyD88 pathway in human macrophages: A possible correlation with strong pro-inflammatory responses in severe COVID-19. Heliyon. 2023 Nov 17;9(11):e21893. doi: 10.1016/j.heliyon.2023.e21893. PMID: 38034686; PMCID: PMC10686889.
https://t.co/G5d9Rgd7GE

3. Wang Y, Yang S, Zhao Y, Tian S, Cao Q, Geng X, Yang M, Song X, Shang H, Liu S, Guo R, Li Y, Sun M, Hu M, Fan B, Li B. PEDV infection downregulates goblet cell differentiation through activating the Notch pathway. Vet Res. 2025 Aug 12;56(1):168. doi: 10.1186/s13567-025-01599-5. PMID: 40797223; PMCID: PMC12341102.
https://t.co/wdXkNXU8Ci

4. Zhang J, Ejikemeuwa A, Gerzanich V, Nasr M, Tang Q, Simard JM, Zhao RY. Understanding the Role of SARS-CoV-2 ORF3a in Viral Pathogenesis and COVID-19. Front Microbiol. 2022 Mar 9;13:854567. doi: 10.3389/fmicb.2022.854567. PMID: 35356515; PMCID: PMC8959714.
https://t.co/exRxhemTiY

5. Breikaa RM, Lilly B. The Notch Pathway: A Link Between COVID-19 Pathophysiology and Its Cardiovascular Complications. Front Cardiovasc Med. 2021 May 26;8:681948. doi: 10.3389/fcvm.2021.681948. PMID: 34124207; PMCID: PMC8187573.
https://t.co/xFZ7rWcJvd

6. Wu X, Xia T, Shin WJ, Yu KM, Jung W, Herrmann A, Foo SS, Chen W, Zhang P, Lee JS, Poo H, Comhair SAA, Jehi L, Choi YK, Ensser A, Jung JU. Viral Mimicry of Interleukin-17A by SARS-CoV-2 ORF8. mBio. 2022 Apr 26;13(2):e0040222. doi: 10.1128/mbio.00402-22. Epub 2022 Mar 28. PMID: 35343786; PMCID: PMC9040823.
https://t.co/SbeBkqMCmY

[Emily Kopp @emilyakopp]

NEW: Tulsi Gabbard is actively working to declassify intelligence about the origins of COVID and Havana Syndrome by June 30, an ODNI official tells @DailyCaller. A CIA whistleblower recently testified that Fauci and Biden's intel chief suppressed evidence of a Wuhan lab leak.

[billwilliam @billwilliam321]

@mike71715365973 @breakfast_dogs Interesting finding.

[Secretary Marco Rubio @SecRubio]

On June 4, the world marks 37 years since the Chinese Communist Party ordered its troops to attack thousands of peaceful demonstrators in and around Tiananmen Square. Those who sacrificed to uphold their unalienable rights of free expression and peaceful assembly will be vindicated someday.

[billwilliam @billwilliam321]

@DoGoodScience A few point mutations can pop up naturally. Don’t know whether the mutations are from natural evolution or serial passage.

[billwilliam @billwilliam321]

https://t.co/KBPwpNlFib

[billwilliam @billwilliam321]

@breakfast_dogs Just a hypothesis. Not experimentally confirmed.

[billwilliam @billwilliam321]

The new Bundibugyo virus contains two interesting mutations.

N79S mutation on VP35 may create a new phosphorylation site. VP35 is homologous to phosphoprotein of other negative-sense viruses.

Y387H mutation on glycoprotein creates a tandem His-His motif, which is a more efficient substrate to cathepsin L at pH4.6 than His-Tyr motif in other Bundibugyo viruses. EBOV glycoprotein requires cathepsin cleavage at glycan cap and mucin-like domain to mediate fusion.

https://t.co/dc4x8DPhub

[billwilliam @billwilliam321]

https://t.co/D26gYF2qsg

[billwilliam @billwilliam321]

https://t.co/D26gYF2qsg

[billwilliam @billwilliam321]

@breakfast_dogs @gdemaneuf @thackerpd The illegal lab in California reportedly contained vials labeled ebola, though the samples were destroyed.

[Laura Loomer @LauraLoomer]

🚨 BREAKING: 🚨

Dr. Vincent Munster, a foreign born national virologist who works at the Rocky Mountain Laboratory under @NIH and Claude Kwe, one of his foreign born colleagues from Cameroon who also works at NIH in the same lab have officially been charged with smuggling monkeypox and other deadly pathogens (possibly Ebola) into the United States from the Democratic Republic of Congo and lying about it when confronted by Border Patrol!!!

@WhiteCoatWaste and I are totally vindicated after we broke this story several weeks ago about how NIH was covering up the fact that several foreign born virologists working at NIH under the Trump admin at Rocky Mountain Laboratory, a Biosafety Level 4 laboratory, snuck lethal pathogens into the US. They work at the same lab where an Ebola infected monkey bit an NIH researcher, and this was also covered up by @DrJBhattacharya and NIH.

According to the press release,

“On January 25, 2026, Munster and Kwe arrived at the McNamara Terminal at Detroit Metropolitan Airport with travel originating from Brazzaville, Republic of Congo, where an outbreak of monkeypox was occurring. Monkeypox is an infectious virus that can result in painful rash, enlarged lymph nodes, fevers and other ailments.

Munster and Kwe were inspected and interviewed by Customs and Border Protection (CBP) officials upon their arrival. CBP officers observed Kwe and Munster traveling with a large black plastic case. Munster and Kwe falsely told CBP officers that the black case contained diagnostics and testing equipment. But subsequent investigation by CBP and FBI agents revealed that the case actually contained 113 vials in Styrofoam coolers. As of the date of the complaint, the FBI has tested 20 of the 113 vials. Seventeen of them contained deactivated monkeypox virus, one contained the Chickenpox virus, and two contained only human DNA. 

“These NIH experts apparently broke our laws by smuggling viral pathogens on a packed commercial airplane from an outbreak in the Republic of Congo. Let that sink in,” United States Attorney Gorgon stated.

“No researchers should believe their positions, credentials, or professional status place them above the law,” said Jennifer Runyan, Special Agent in Charge of the FBI Detroit Field Office. “The allegations in this case are serious. They involve the dangerous and unlawful smuggling of deactivated Mpox virus into the United States and alleged efforts to mislead our federal agents.”

The FBI admits only 20 of the 113 vials have been tested, which means we could soon learn that other lethal pathogens from Africa were illegally smuggled into our country by foreign born virologists who are Dr. Fauci acolytes.

Additionally, as I have previously reported, Munster’s wifeEmmie de Wit still works at NIH in the same laboratory where she studies Ebola. She should not be allowed to continue working at NIH, as White Coat Waste and I exposed she was also allegedly traveling with her husband and his colleague when they were caught at the airport in Michigan smuggling viruses into the United States from an outbreak zone in the Congo.

Munster and Kwe face a maximum sentence of five years in prison. 

The investigation is being conducted by the Detroit Field Office of the Federal Bureau of Investigation, the U.S. Customs and Border Protection Detroit and the U.S. Department of Health and Human Services Office of Inspector General (HHS-OIG). 

@TimSheehyMT @JustinRGoodman @SenRickScott

Read the full press release here:

https://t.co/jmJpEBFkIr

[Rebecc@ ███████ @Rebecca21951651]

@MonaRahalkar Love the abstract:

"SARS-CoV-2 has a mosaic genome, to which different progenitors contribute."

😂🤣 🔥🔥🔥🔥🔥🔥🔥🔥🔥🔥🔥

AKA a chimera!

[D. Janković (aka Dog's Breakfast) @breakfast_dogs]

This may be the reason for the PRRAR FCS.

Diabolical if so.

RRAR had already been shown to be very good at binding Neuropilin-1.

But not as good as RPAR, so why not use that?

[billwilliam @billwilliam321]

@SitSilver @PutrinoLab @DocFlo4 @mike71715365973 @breakfast_dogs @grok But MED20 doesn't contain DEDDSEPV motif. Why does auto antibody pull down MED20 instead of myosin-16?