FAUCI AND REMDESIVIR

Anthony Fauci has numerous patents, owned by HHS, including but not limited to 4 patents on a combination drug relevant to Remdesivir

• Government employee inventors of government owned patents personally receive royalties.
• Although the technology is owned by We The People (“HHS”), the government licenses them and hides the licenses. A decent journalist would FOIA to identify to whom they were licensed.

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• The fact that government employees receive royalties on taxpayer funded and owned intellectual property is a major conflict of interest. This is also standard with University scientists, but without the same conflict of interest.

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• Government licenses its patents to industry, including exclusive licenses. This is standard. The fact that HHS owns them reveals nothing regarding who benefits from them.

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https://www.ott.nih.gov/royalty/information-nih-inventors

https://www.ott.nih.gov/licensing.

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FPTO%2Fsearch-bool.html&r=0&f=S&l=50&TERM1=fauci&FIELD1=INNM&co1=AND&TERM2=&FIELD2=&d=PTXT

Anthony Fauci has numerous patents, owned by HHS, including but not limited to 4 patents on a combination drug relevant to Remdesivir

• Government employee inventors of government owned patents personally receive royalties.
• Although the technology is owned by We The People (“HHS”), the government licenses them and hides the licenses. A decent journalist would FOIA to identify to whom they were licensed.

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**Patents could be licensed to an intermediate company or directly to Gilead.

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**If the University model is being followed at HHS, it is not unreasonable to think Fauci has ownership in a spin out company receiving the hidden license, and then it is licensed again from there. This is common with University inventors.

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Any decent Journalist would ask Fauci if he (directly or indirectly) has ownership in or benefits from any company with licenses to the patents, which would increase direct benefit to him over the HHS royalties.

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https://www.ott.nih.gov/royalty/information-nih-inventors

https://www.ott.nih.gov/licensing.

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FPTO%2Fsearch-bool.html&r=0&f=S&l=50&TERM1=fauci&FIELD1=INNM&co1=AND&TERM2=&FIELD2=&d=PTXT

Anthony Fauci has numerous patents, owned by HHS, including but not limited to 4 patents on a combination drug relevant to Remdesivir

• Government employee inventors of government owned patents personally receive royalties.
• Although the technology is owned by We The People (“HHS”), the government licenses them and hides the licenses. A decent journalist would FOIA to identify to whom they were licensed.

https://www.ott.nih.gov/royalty/information-nih-inventors

https://www.ott.nih.gov/licensing.

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FPTO%2Fsearch-bool.html&r=0&f=S&l=50&TERM1=fauci&FIELD1=INNM&co1=AND&TERM2=&FIELD2=&d=PTXT

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Expect HHS to be filing more connected patents.

Ingredient A plus Ingredient B=claim 20

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A

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B

A=monoclonal antibody plus B=Remdesivir

Through NIAID, Fauci funded the development of Remdesivir

NIAID under Fauci funded the development Remdesivir (GS-5734) through Grants toward a joint venture of Dr. Ralph Baric at UNC Chapel Hill and Gilead.

“The partnership grant awarded to Baric…establishes a collaboration between the Gillings School and Gilead Sciences Inc...and will focus specifically on GS-5734”

https://sph.unc.edu/sph-news/gillings-researchers-receive-6m-grant-to-fight-infectious-disease/

https://sph.unc.edu/sph-news/remdesivir-developed-at-unc-chapel-hill-proves-effective-against-covid-19-in-niaid-human-clinical-trials/

https://mv-voice.com/news/2020/04/29/remdesivir-drug-trials-show-patients-are-recovering-from-covid-19

Through NIAID, Fauci has now designed, sponsored and funded the clinical trials for FDA approval of Gilead’s drug which is outrageous

• FDA approves commercial drugs through drug company sponsored trials agreed to by FDA, not NIH trials.
• Fauci sponsored and funded trials through NIAID where the endpoint was changed, has no real scientific conclusion, Gilead ended 2 company sponsored trials, and Fauci submitted NIAID data to get FDA emergency approval.
• Fauci is intentionally tanking HCQ, funding bogus “studies” while pushing Remdesivir

https://sph.unc.edu/sph-news/gillings-researchers-receive-6m-grant-to-fight-infectious-disease/

https://sph.unc.edu/sph-news/

The drug in Fauci’s patents is a combination drug including a monoclonal antibody plus a nucleoside/nucleotide reverse transcriptase inhibitor�USPTO 9,896,509 claim 20 and 21)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5551389/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6409847/

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• Gilead’s drugs GS-5734/Remdesivir is a nucleoside/nucleotide reverse transcriptase inhibitor in the HIV (RNA virus) retroviral drug class.
• It is a virtual copy of Gilead’s prior HIV drug GS-7340/Tenofovir with a couple of anticipated additions and a slight modification.
• They are both HIV drugs, but Remdesivir is being tested and marketed as a broad-based antiviral to work on any number of RNA viruses, although it has mostly failed to date.

The drug in Fauci’s patents is a combination drug including a monoclonal antibody plus a nucleoside/nucleotide reverse transcriptase inhibitor�USPTO 9,896,509 claim 20 and 21)

• Gilead’s drugs GS-5734/Remdesivir is a nucleoside/nucleotide reverse transcriptase inhibitor in the HIV (RNA virus) retroviral drug class.
• It is a virtual copy of Gilead’s prior HIV drug GS-7340/Tenofovir with a couple of anticipated additions and a slight modification.
• They are both HIV drugs, but Remdesivir is being tested and marketed as a broad-based antiviral to work on any number of RNA viruses, although it has mostly failed to date.

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• It doesn’t matter whether Gilead’s drug is used on or for HIV for the patent. It only matters that the agent is an inhibitor of entry replication of HIV. A reverse transcriptase inhibitor inhibits replication of HIV by definition.

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• HIV drug class Nucleoside Reverse Transcriptase Inhibitors (NRTIs) block reverse transcriptase (an HIV enzyme). HIV uses reverse transcriptase to convert its RNA into DNA (reverse transcription). This is what Remdesivir does.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5551389/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6409847/

Fauci is now pushing the combination of Remdesivir and a monoclonal antibody covered by his patents...but of course

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https://mv-voice.com/news/2020/04/29/remdesivir-drug-trials-show-patients-are-recovering-from-covid-19

FAUCI AND THE MONSTER VIRUS

The US government, particularly NIAID under Fauci, was the number one funder in the world of Gain of Function/Chimera Virus research

• Throughout the early 2000’s through present day, researchers studied viruses using advanced techniques manipulating natural viruses in laboratories to gain function to:

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• understand virus evolution for pandemic risk and
• to develop vaccines and therapeutic drugs

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• This is called gain of function (GoF) research and is performed in labs to manipulate viruses stored in the lab.

GoF has 3 main techniques alone or in combination to mutate a virus to gain function of virulence-pathogenicity and/or transmissibility �(more dangerous and/or more contagious)

The main GoF techniques include:

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• computer generating edits to genome code

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• cut and pasting segments from other viruses, and
• promoting mutation in animals that have been genetically modified to promote the target viral mutations needed for human effects in forced serial infections, usually in modified mice

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GoF has 3 main techniques alone or in combination to mutate a virus to gain function of virulence-pathogenicity and/or transmissibility �(more dangerous and/or more contagious)

The main GoF techniques include:

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• computer generating edits to genome code,

• cut and pasting segments from other viruses, and
• promoting mutation in animals that have been genetically modified to promote the target viral mutations needed for human effects in forced serial infections, usually in modified mice.

CUT AND PASTE

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BackY

GoF has 3 main techniques alone or in combination to mutate a virus to gain function of virulence-pathogenicity and/or transmissibility �(more dangerous and/or more contagious)

The main GoF techniques include:

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• computer generating edits to genome code,

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• cut and pasting segments from other viruses, and
• promoting mutation in animals that have been genetically modified to promote the target viral mutations needed for human effects in forced serial infections, usually in modified mice.

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• Sequential infections in genetically altered mice drives the virus to adapt and mutate toward the target of the research (e.g. ACE2).
• These are “mouse adapted” (MA) viruses.
• The mutations look more natural, generated through forced biologic processes.

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MA13

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GoF has 3 main techniques alone or in combination to mutate a virus to gain function of virulence-pathogenicity and/or transmissibility �(more dangerous and/or more contagious)

The main GoF techniques include:

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• computer generating edits to genome code

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• cut and pasting segments from other viruses, and
• promoting mutation in animals that have been genetically modified to promote the target viral mutations needed for human effects in forced serial infections, usually in modified mice

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A Chimera Virus contains parts from two or more viruses put together

• Chimera comes from mythology for a “monstrous fire-breathing hybrid creature…composed of the parts of more than one animal.”

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• “It is usually depicted as a lion, with the head of a goat protruding from its back, and a tail that might end with a snake's head.”

https://en.wikipedia.org/wiki/Chimera_(mythology)

https://en.wikipedia.org/wiki/Chimera_(virus)

Viruses captured from animals or humans are given a model number

• Captured viruses are sequenced by researchers and the sequences are stored in public virus data storage banks (unless hidden by NIH directive)

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• Not always are they made public, but often they are (thanks to NSABB some are hidden)

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• When natural lab stored or chimera viruses are further modified through animal (e.g. mouse) adaptation, they are given model number designations like MA#.

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• The 15^th mouse adaptation of a chimera from natural virus SCH014 is called chimera SCH014 MA15 with its unique genome that would not be the same as the original.

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HKU3

SARS COV-1

HKU5

SARS rSH WIV16 WIV1

An uproar in the scientific community occurred in 2012 when NIAID under Fauci funded an H5N1 Chimera making it air transmissible in lab genetically modified mammals

• Dutch researchers Fouchier et al. made a chimera virus with more animal adapted GoF mutations making a very dangerous virus air transmissible in ferrets-mammals, that had not existed on earth until this;

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• Concern and outrage ensued over the creation of this serious global pandemic risk, too risky for the planet

https://europepmc.org/article/med/22723413

“The genetically modified A/H5N1 virus acquired mutations during passage in ferrets, ultimately becoming airborne transmissible in ferrets….This work was financed through NIAID-NIH contract HHSN266200700010C.”

This was a science community freak-out that led to a “Pause”or “moratorium” on GoF until the Government assigned task force, NSABB, could figure out what to do: terminate, make rules, what?

Fauci was a key member of NSABB, and because NIAID was the primary funder of this research, this task force was to make recommendations about the research that HE mostly controlled.

“…the United States had shown how the H5N1 virus could be made contagious through the air in mammals. This provoked a wide-ranging debate about whether, and how, the work should be published, or, indeed, whether it should have been carried out in the first place….My bottom line: Fouchier started with a highly worrisome and sometimes lethal virus to humans and appears to have enhanced its transmissibility by the respiratory route. Nothing said in recent days changes these facts…And Lemon said bluntly ‘The major concern has been about acquisition of the capability for aerosol transmission of the virus to a mammal’.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3442247/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4271556/

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Virologists had a range of opinions between banning all GoF, where no benefit is worth the risk, to all GoF is good with few limits needed

• Harvard’s Dr. Lipsitch was the most vocal to ban all GoF: no benefit is worth the risk, concluding common lab accidents cause pandemic risk between 5-60% killing millions or billions of people
• Fauci was opposite, defending all GoF no matter how dangerous, except when it could not theoretically mutate in such a way in nature. Creating monsters that do not currently exist “for all infectious disease research” is acceptable, so long as one day such a monster could theoretically evolve

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https://youtu.be/BACqqgRpktA

https://youtu.be/d5fe7KEkwQM

1141 Lab Accidents caused infections 1979-2005

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After deliberation and review of public letters, NSABB ended the “moratorium” in 2017 with secrecy options added instead of a ban

• In letters to NSABB, most people and scientists wanted a full or substantial ban. Like Fauci, most gov. scientists plus UNC’s Baric (pg. 28) wanted largely unfettered GoF research but wanted to classify them confidential…do the work but hide it from publication.
• Naturally, NSABB decided to allow all GoF to continue with only extreme limits and a review process put in place for public knowledge risk mitigation.
• GoF produced under grants are reviewed and if deemed highly dangerous with great public risk for misuse or mishandling, are classified under Executive Order 13526 thus not generally avail to compare.

https://osp.od.nih.gov/wp-content/uploads/2013/06/Gain_of_Function_Deliberative_Process_Written_Public_Comments.pdf

NIAID/Fauci funded at least $90M coronoavirus GoF research at Dr. Ralph Baric’s UNC Chapel Hill lab before, DURING and after the “moratorium”

2016: “… University of North Carolina…: project title: Generating infectious clones of Bat SARS-like CoVs… These studies were initiated before the US Government Deliberative Process Research Funding Pause on Selected Gain of Function Research Involving Influenza, MERS, and SARS Viruses…and the current paper has been reviewed by the funding agency, the National Institutes of Health (NIH). Continuation of these studies has been requested and approved by the NIH…Research was supported by the National Institute of Allergy and Infectious Disease..” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4801244/

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https://taggs.hhs.gov/Detail/AwardDetail?arg_awardNum=U54AI057157&arg_ProgOfficeCode=104

https://sph.unc.edu/sph-news/baric-to-lead-10-million-nih-grant/

https://sph.unc.edu/sph-news/gillings-researchers-receive-6m-grant-to-fight-infectious-disease/

https://sph.unc.edu/sph-news/niaid-renews-5-year-grant-for-research-on-emerging-viruses/

NIAID/Fauci also funded Baric’s collaboration with Wuhan Institute of Virology & Ecohealth Alliance to make chimera and mouse adapted strains of coronaviruses (model numbers SCH014, WIV1, WIV16, and Urbani)

2015: Dr. Baric (UNC), Dr. Daszak (Ecohealth), Dr. Xing-Yi Ge (Wuhan Institute / previously worked at UNC) co-authored making chimeric and mouse adapted viruses: “Experiments with the full-length and chimeric SHC014 [lab made] viruses were initiated and performed before the GOF research funding pause and have since been reviewed and approved for continued study by the NIH.”https://www.nature.com/articles/nm.3985.pdf

2016, Baric: “We thank Dr. Zhengli-Li Shi of the Wuhan Institute of Virology for access to bat CoV sequences and plasmid of WIV1-CoV spike protein. Research was supported by the [NIAID] and the [NIA] of the NIH under Awards U19AI109761 and U19AI107810 (to R.S.B.), AI1085524 (to W.A.M.), and F32AI102561 and K99AG049092 (to V.D.M.). ..Support for the generation of the mice expressing human ACE2 was provided by NIH Grants AI076159 and AI079521 (to A.C.S.).” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4801244/

2016: Wuhan Institute work was funded by NIAID GRANT To Ecohealth Alliance:.. “This work was jointly funded by the National Natural Science Foundation of China (81290341, 31321001, and 81401672) and the National Institutes of Health (NIAID R01AI110964)” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936131/

2018: Ecohealth Alliance and Wuhan Institute of Virology NIAID GRANT “Award Number R01AI110964, and PREDICT project Grant” https://www.ecohealthalliance.org/wp-content/uploads/2018/03/Virologica-Sinica-SARSr.pdf

DURING

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DURING

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DURING

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AFTER

They used the tools to create, influence and direct mutations in the lab, especially to bind to ACE2 that is a critical function of Sars Cov-2

“The combined power of genetic engineering of mice, reverse genetic systems for CoVs, mouse-adaptation, and genetically diverse mouse populations afford the tools to develop models that reproducibly recapitulate severe respiratory disease that can be caused by hCoVs in humans… Funding was provided by [NIAID](Grant Nos. AI110700, AI089728).”

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6132729/

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Ralph Baric/UNC, Xing-Yi Ge(formerly UNC)/Wuhan Institute of Virology, Peter Daszak/Ecohealth Alliance

They used the tools to create, influence and direct mutations in the lab, especially to bind to ACE2 that is a critical function of Sars Cov-2

“The identification of WIV1-CoV and its capacity to use ACE2 [genes]... provides an opportunity to prepare for a future CoV outbreak…using reverse genetic systems to construct full-length and chimeric viruses.” Baric et al.

https://www.pnas.org/content/113/11/3048

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Ralph Baric/UNC, Xing-Yi Ge(formerly UNC)/Wuhan Institute of Virology, Peter Daszak/Ecohealth Alliance

They used the tools to create, influence and direct mutations in the lab, especially to bind to ACE2 that is a critical function of Sars Cov-2

“Additional passaging of MA15 resulted in the generation of other mouse-adapted SARS-CoV strains including MA20 (20 passages).”

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Ralph Baric/UNC, Xing-Yi Ge(formerly UNC)/Wuhan Institute of Virology, Peter Daszak/Ecohealth Alliance

They used the tools to create, influence and direct mutations in the lab, especially to bind to ACE2 that is a critical function of Sars Cov-2

“Attenuation of WIV1-MA15 was partially overcome by infecting HFH4 mice that overexpress the hACE2 receptor… indicating that mouse adaptation of the WIV1-MA15 to mACE2 could enhance disease...mouse adaptation of an infectious...clone of an HKU5-SE chimeric resulted in dramatic respiratory disease… it was more practical to replace the HKU5 spike with the mouse-adapted SARS-CoV spike.”

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https://link.springer.com/article/10.1007/s00335-018-9760-9

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Ralph Baric/UNC, Xing-Yi Ge(formerly UNC)/Wuhan Institute of Virology, Peter Daszak/Ecohealth Alliance

They used the tools to create, influence and direct mutations in the lab, especially to bind to ACE2 that is a critical function of Sars Cov-2

“Both full-length and chimeric WIV1-CoV readily replicated efficiently in human airway cultures and in vivo, suggesting capability of direct transmission to humans”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4801244/

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Ralph Baric/UNC, Xing-Yi Ge(formerly UNC)/Wuhan Institute of Virology, Peter Daszak/Ecohealth Alliance

They used the tools to create, influence and direct mutations in the lab, especially to bind to ACE2 that is a critical function of Sars Cov-2

“In a previous study in our laboratory, we demonstrated that the SARS-CoV TRN could be reprogrammed, provided the individual TRSs were replaced with matching sequences. The rewired TRN replaced the conserved 6-nt TRS with a 6-nt cassette that is not used in any other characterized CoVs, encoding a net change of 3...(ACGAAC to CCGGAU).”

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https://www.nature.com/articles/s42003-018-0175-7

Ralph Baric/UNC, Xing-Yi Ge(formerly UNC)/Wuhan Institute of Virology, Peter Daszak/Ecohealth Alliance

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They used the tools to create, influence and direct mutations in the lab, especially to bind to ACE2 that is a critical function of Sars Cov-2

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Ralph Baric/UNC, Xing-Yi Ge(formerly UNC)/Wuhan Institute of Virology, Peter Daszak/Ecohealth Alliance

Ralph Baric et. al example quotes

‘For this purpose, a second panel of derivative…viruses that contained either the MA15 nsp9 mutation or the S glycoprotein mutation alone…was constructed on an Urbani [model name] virus backbone [main part]. We also constructed ..viruses containing both the MA15 S and nsp9 [genes] (designated WT+N9/S) while maintaining the [natural] Urbani [genes] at the other four positions. In parallel, a [lab constructed] virus that contained four mouse-adapted mutant [genes] but retained the [natural] Urbani [genes] in the nsp9 and S proteins (designated MA?N9/S) was constructed“

WIV1

SCH014 Chimera

RsWIV1

Y442-Y491 for ACE2

WIV1-MA15

ORFS

Editing

Chimeras

WT+N9 or WT+S

HKU Chimeras RBDs

S Genes Backbones

Ralph Baric et. al example quotes

“we also produced WIV1-CoV chimeric virus that replaced the SARS spike with the WIV1 spike within the mouse-adapted backbone (WIV1-MA15, Fig. S1B). WIV1-MA15 incorporates the original binding and entry capabilities of WIV1-CoV, but maintains the backbone changes to mouse-adapted SARS-CoV. Importantly, WIV1-MA15 does not incorporate the Y436H mutation in spike that is required for SARS-MA15 pathogenesis.”

Chimeras

WT+N9 or WT+S

WIV1

SCH014 Chimera

RsWIV1

Y442-Y491 for ACE2

ORFS

Editing

WIV1-MA15

HKU Chimeras RBDs

S Genes Backbones

Ralph Baric et. al example quotes

“…live bat SL-CoV termed WIV1 …was demonstrated to be able to infect cells of both bat and human origin via the recognition of ACE2 receptor….Using.. reverse genetic system to generate full-length … chimeric viruses consisting of the WIV1 and SHC014 S protein in the backbone of the SARS-CoV mouse adapted strain MA15. Full-length WIV1-CoV and SHC014-CoV, as well as chimeric WIV1-MA15 and SHC014-MA15, replicated efficiently…through the binding to human ACE2 receptor.”

Chimeras

WT+N9 or WT+S

RsWIV1

Y442-Y491 for ACE2

WIV1-MA15

ORFS

Editing

WIV1

SCH014 Chimera

HKU Chimeras RBDs

S Genes Backbones

Ralph Baric et. al example quotes

Adaptation of MA15, MA20 and MA25 of chimeras for ACE2 binding… “The Y436H residues interacting with RBD sites that adapted to mACE2…The Y442L and N479K adaptations for …mACE2 …MA20 K479 can bind to both N30 and N31 of MA20 …MA25 L442 likely interacts with Q34 of mACE2. ..MA20 RBD; mouse ACE2;.. residue that changed in MA20;…interacting with RBD sites that adapted to mACE2. Adaptation of MA25 to mACE2….Y436H change [for] D38 of mACE2…with the K353H difference….Y442F adaptation…mediating a better fit between MA25 and mACE2”

Chimeras

WT+N9 or WT+S

WIV1

SCH014 Chimera

WIV1-MA15

ORFS

Editing

RsWIV1

Y442-Y491 for ACE2

HKU Chimeras RBDs

S Genes Backbones

Ralph Baric et. al example quotes

“To determine the significance of the SARS-CoV group-specific ORFs in virus replication in vitro and in mice, we systematically deleted five of the eight group-specific ORFs, ORF3a, OF3b, ORF6, ORF7a, and ORF7b…”

Chimeras

WT+N9 or WT+S

WIV1

SCH014 Chimera

RsWIV1

Y442-Y491 for ACE2

WIV1-MA15

ORFS

Editing

HKU Chimeras RBDs

S Genes Backbones

Ralph Baric et. al example quotes

“Using reverse genetics, substitution of minimal S portions was used to overcome receptor-binding issues,… synthesized HKU3 and HKU5 genomes being made viable by substituting in portions of the SARS-CoV S genes. When assembled, these chimeric viruses could infect and replicate efficiently in vitro and in vivo, demonstrating that receptor binding was a primary barrier for HKU3 and HKU5 infection of human cells … While insertion of the SARS-CoV RBD was sufficient to confer replication competency to HKU3, the entire SARS-CoV ectodomain was required for HKU5, suggesting that multiple domains of the S protein may work in concert across a CoV group…A complementary strategy was used to test the capacity of CoV S genes to mediate infection independent of their backbones.”

Chimeras

WT+N9 or WT+S

WIV1

SCH014 Chimera

RsWIV1

Y442-Y491 for ACE2

WIV1-MA15

ORFS

Editing

HKU Chimeras RBDs

S Genes Backbones

Ralph Baric et. al example quotes

“Recently utilized with SHC014-CoV and WIV1-CoV, the S genes of zoonotic CoVs were inserted into a replication-competent backbone, the mouse adapted SARS-CoV MA15. The SHC014-MA15 and WIV1-MA15 chimeras could replicate in vitro and in vivo…These initial studies justified further examinations and characterizations of full-length SHC014-CoV and WIV1-CoV and indicated that mutations in the viral backbones are also required for emergence and pathogenesis. Together, these two strategies leverage reverse genetics to create chimeric coronaviruses, bypassing the limitations of species specific culture systems…

Chimeras

WT+N9 or WT+S

WIV1

SCH014 Chimera

RsWIV1

Y442-Y491 for ACE2

WIV1-MA15

ORFS

Editing

HKU Chimeras RBDs

S Genes Backbones

Ralph Baric et. al example quotes

CLICK EACH TO SEE QUOTES

https://www.sciencedirect.com/science/article/pii/S0042682217304142

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5287300/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287583/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3255850/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5869085/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2588415/

Chimeras

WT+N9 or WT+S

WIV1

SCH014 Chimera

RsWIV1

Y442-Y491 for ACE2

WIV1-MA15

ORFS

Editing

HKU Chimeras RBDs

S Genes Backbones

Baric makes a chimera with a mutation of the spike that simulates a natural evolution event as if 2 viruses merged in a wild bat

“To test a possible route of emergence from ..Bat-SCoV to human SARS-CoV, we designed a consensus Bat-SCoV genome and replaced the Bat-SCoV Spike receptor-binding domain (RBD) with the SARS-CoV RBD (Bat-SRBD)…To test whether the RBDs of Bat-SCoV and SARS-CoV were interchangeable, we replaced the Bat-SCoV RBD (amino acid 323–505) with the SARS-CoV RBD (amino acid 319–518) …simulating a theoretical recombination event that might occur during mixed infection in vivo.” (meaning as if 2 viruses merged in a bat in a cave)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2588415/

recombination event is where virus lineage changes creating a new ancestral line

Baric patented creating S Spikes in chimeras and collaborated with Shibo Jiang who cut and pasted “furin cleavage sites”: the most critical distinguishing aspects of Sars Cov-2 from any possible natural lineage

“..There is no explanation for the origin of the furin polybasic cleavage site …, which does not exist in any of the bat or pangolin close relatives yet identified, a structure that is known to enhance pathogenicity and transmissibility in coronaviruses.

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Alternatively, the inconsistencies of the naturally-occurring argument could be resolved if one assumes that COVID-19 was bioengineered. There are two US patents related to that type of bioengineering, “Methods and Compositions for Chimeric Coronavirus Spike Proteins” and “Insertion of Furin Protease Cleavage Sites in Membrane Proteins and Uses Thereof,” patent numbers US9884895B2 and US7223390, respectively.”

https://www.wionews.com/opinions-blogs/how-us-expertise-may-have-inadvertently-contributed-to-covid-19-296512

Wuhan Institute of Virology proved Sars Like Bat Coronaviruses Could not attach to human ACE2 from the S Spike protein without RBD edits that they performed using HIV-1 Inserts…

(WIV stands for Wuhan Institute of Virology)

Published 2008 and 2010, the Wuhan researchers working with Baric made Chimeras with HIV-1 inserts to the S RBD so a bat SLCov could attach to human ACE2, which they proved otherwise could not. They took a regular Sars S protein, modified it with HIV-1 inserts to replace the bat SL-Covs S at the same RBD locations that are also found in Sars Cov-2, and ran them through human ACE2 cells to develop chimeras.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2258702/

file:///C:/Users/mann-/Downloads/bat-ace2-archivesofvirology-2010.pdf

“A 193-residue fragment (amino acids [aa] 318 to 510) in the SARS-CoV S protein was demonstrated to be the minimal receptor-binding domain (RBD) which alone was able to efficiently bind to ACE2 (1, 42a, 45)... Whether it is possible to construct an ACE2-binding SL-CoV S protein by replacing the RBD with that from SARS-CoV S proteins is also unknown. In this study, a human immunodeficiency virus (HIV)-based pseudovirus system was employed to address these issues….However, when the RBD of SL-CoV S was replaced with that from the SARS-CoV S, the hybrid S protein was able to use the huACE2. it was predicted that the S protein of SL-CoV is unlikely to use huACE2 as an entry receptor (30)...SL-CoVs discovered in bats so far are unlikely to infect humans using ACE2 as a receptor”

Wuhan Institute of Virology and the Chimera model # rWIV1-GFP-ΔX�(WIV stands for Wuhan Institute of Virology)

WUHAN INSTITUTE made a chimera of WIV1 called rsWIV1-Cov with a new Spike protein. Then they spliced in an ORFX GFP gene from the highly contagious staphylococci in between the ORF6 and ORF7 gene they had already mutated in chimera WIV. They have now made another chimera of a chimera.

https://jvi.asm.org/content/90/14/6573

https://covid19.elsevierpure.com/zh/publications/bat-severe-acute-respiratory-syndrome-like-coronavirus-wiv1-encod

Published 2015, Wuhan made the Chimera rWIV1-GFP-ΔX:

“Using this method, we also rescued an ORFX deletion mutant virus (rWIV1-ΔX) and a mutant with a GFP sequence placed in the coding region of ORFX (rWIV1-GFP-ΔX)…Construction of WIV1 mutants. To delete ORFX, the fragment F... Fragment G ...These two products were then cloned... The two fragments were inserted into the BAC along with the other fragments as described above. The rescued mutant was named as rWIV1-ΔX. To place GFP into the open reading frame of ORFX, the F fragment was amplified.... The GFP gene was amplified…The two PCR products were ligated ...and the product was inserted... The rescued mutant was named rWIV1-GFP-ΔX.”

Blah Blah Blah… they are making mutant viruses

What they published was directly or indirectly applicable to unique aspects of Sars Cov-2, and then add the secrets and unpublished

• ACE2 binding on the S Spike
• Furin Cleavage Site
• Fusing trimerization motifs
• ORFs
• Binding Sites Y436, Y436F, Y442L, Y442F, N479K K479, L442 K353H, and Nsp9
• RBD residue sites
• RGD and LDI integrin binding on the S Spike Protein (same and similar, short but relevant binding sequences as on GP120 of HIV)

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And then “washed” like an old pair of jeans, their spliced and edited changes through mouse-adaptation-washing-machines with genetically engineered mice to smooth out their chimeras and add the necessary forced biological adaptations that look randomly natural.

Fauci Patent

So many similarities to Sars Cov-2

“The spike protein of SARS-CoV-2 acquired a RGD motif known to bind integrins. This motif is absent from other coronaviruses…The integrin-binding motif is present at the surface of the spike protein, close to the ACE2 receptor-binding region…. Integrin may act as an alternative receptor for SARS-CoV-2 and could be implicated in its transmission and pathology…Integrin binding may be a promising therapeutics target, and should be tested experimentally.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7114098/

“SARS-CoV-2 Attachment to Host Cells is Possibly Mediated via RGD-Integrin Interaction…Our study revealed that SARS-CoV-2 harbors a RGD motif in its receptor binding domain (RBD) and the motif is absent in all previously known SARS-CoVs. The RGD motif plays a key role in cell-cell adhesion... The molecular docking experiment showed the RBD of spike protein binds with integrins precisely at RGD motif”

https://osf.io/chvsa

RGD & LDI on HIV

ORF’s

RGD & LDI

RBD & Y436

Sars Cov-2 & WIV1

RGD & Integrins

AKA Fauci Patent

So many similarities to Sars Cov-2

“..other integrin‐binding sites are specifically expressed in SARS‐COV‐2, and, particularly, a change from a LDV to a LDI motif is likely significant. The LDV/LDI switch in human immunodeficiency virus infection has been shown to play a key role …contributing to high viral infectivity.…. This polyprotein has RGD (KRGDK), LDI, LDV, LDG, LDS, LET, KTS, IDG homologous sequences LDV and IDA, LDA and IDS, all these serving as ligand binding sites for alpha/beta subfamilies of integrin.” https://onlinelibrary.wiley.com/doi/10.1002/jmv.25831

RGD & Integrins

RGD & LDI on HIV

ORF’s

RBD & Y436

Sars Cov-2 & WIV1

RGD & LDI

So many similarities to Sars Cov-2

RGD IN HIV: “The identification of a highly conserved functional RGD site on HIV-1 tat is the first example, to our knowledge, of a specific cell adhesion site on a retrovirally encoded regulatory protein. The identification of a cell attachment site on tat indicates that tat binds to…possibly an integrin.” https://core.ac.uk/download/pdf/7818018.pdf

LDI IN HIV: NIAID Fauci’s group published :“HIV-1 gp120 binds to integrin α4β7 [alpha/beta]... This interaction is mediated by the LDI/V tripeptide encoded in the V2-loop. “ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4966603/

Sars Cov-2: “insertions 1 and 2 in 2019-nCoV have 6-AA motifs identical to those in V4 and V5 of certain HIV-1 gp120 isolates…. Insertion 4 was found in Gag protein of HIV-1” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7033698/

RGD & Integrins

ORF’s

RGD & LDI

RBD & Y436

Sars Cov-2 & WIV1

RGD & LDI on HIV

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2258702/ : SARS LIKE BAT CORONAVIRUS CHIMERAS WITH HIVSPLICED TO CREATE RBD CHANGES FOR ACE2 BINDING

So many similarities to Sars Cov-2

“Numerous investigations have depicted that ORFs and ACE2 genes play a key role during novel coronavirus disease.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7161481/

“..What is the difference between Covid-19 and the r-WIV1 virus from 2016? In Covid-19..new ORF8 gene on Covid-19 is 57% different from previous strains and behaves the same as the ORFX gene did on rWIV1. Amazing coincidence?”

https://advocacy-consulting.com/lobbying/lobbyist/did-a-2016-wuhan-virus-become-covid-19/

RGD & Integrins

RGD & LDI on HIV

RGD & LDI

RBD & Y436

Sars Cov-2 & WIV1

ORF’s

So many similarities to Sars Cov-2

“..SARS CoV and SARS-CoV-2 share a similar genotype in RBD, including two insertions (positions 432-436 and 460-472), and [genes] 427N and 436Y. Both 427N and 436Y belong to a helix that interacts with the human ACE2 receptor.” https://www.biorxiv.org/content/10.1101/2020.02.10.942748v2.full.pdf

RGD & Integrins

RGD & LDI on HIV

ORF’s

RGD & LDI

Sars Cov-2 & WIV1

RBD & Y436

“In the current SARS-CoV-2 pandemic, ACE2 receptors can be considered ‘devils’, being the ‘entry door’ for the virus…” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167588/

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‘SARS-CoV-2 has a 10–20-fold higher affinity for ACE2 than does the 2002 SARS-CoV” https://www.frontiersin.org/articles/10.3389/fcvm.2020.00071/full#B22

So many similarities to Sars Cov-2

SARS VHH-72 is cross-reactive against WIV1-CoV and SARS-CoV-2 https://www.biorxiv.org/content/10.1101/2020.03.26.010165v1.full.pdf

RGD & Integrins

RGD & LDI on HIV

ORF’s

RGD & LDI

RBD & Y436

Sars Cov-2 & WIV1

So many similarities to Sars Cov-2

https://www.sciencedirect.com/science/article/pii/S0042682217304142

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5287300/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287583/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3255850/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5869085/

https://www.biorxiv.org/content/10.1101/2020.03.26.010165v1.full.pdf

RGD & Integrins

RGD & LDI on HIV

ORF’s

RGD & LDI

RBD & Y436

Sars Cov-2 & WIV1

CLICK EACH TO SEE QUOTES

https://www.promocell.com/news/news-announcement/study-and-fight-coronavirus-with-research-tools-from-promocell/

No one has run sequence comparisons on the most relevant NIH funded chimeras, MA strains or parts they were collaborating on

• Chimera rWIV1-GFP-ΔX
• GFP ORF
• RBD segments of published and unpublished Taxpayer owned
• MA15, MA20, MA25 versions of their chimeras
• Key features the collaborators were working on for any other chimeras
• No one has gone to Baric’s NIH funded records
• Or Wuhan NIH funded records
• NIH/NIAID quarterly reports, communications, secrete genome files

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No wonder China destroyed all the Wuhan Institute stored samples...

It is time for FOIA NIH/NIAID

What Are The Odds?

• Of all the viruses in the world, of all the places it could break out, Sars Cov-2 broke out within 200 yards of the Wuhan Institute of Virology.
• The chimera monster viruses they were making included many changes and used tools to combine, edit, cut and paste, and then biologically mutate through genetically engineered mice, all of which make the arguments that “computer software couldn’t predict this so it must be natural,” a false argument. Small changes do not mean natural. They mean smart and/or Mouse Adapted with intentionally driven mutations.
• The mutations they were making and the methods they were using to bind to ACE2, and design and test integrin related therapeutics all point to the same virus we have now.
• The chances that it is a coincidence that this virus naturally broke out from an unrelated source within 200 yards of the Wuhan Institute of Virology doing this work with these mutations, must be 1 in a quadrillion. Someone should do the math.

IT COMES FULL CIRCLE

What was the purpose of this chimera GoF research? �….Product Development

2009 BARIC: “Such knowledge could allow rapid synthesis of chimeric viruses for use in evaluating and developing effective antiviral treatments”

https://www.sciencedirect.com/science/article/pii/S0042682209005832

2016 BARIC “To achieve this goal, a new platform is required to translate metagenomics findings; the approach must generate critical diagnostic reagents, define emergence potential of novel strains, and determine efficacy of current therapeutics.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4801244/

2018 MENACHERY: ( Barics’s most common co-author) “Construction of these chimeras [viable portions from established CoVs in conjunction with zoonotic sequences] could also prove useful in vaccine and therapeutic development, as a candidate's efficacy against zoonotic strains may predict its utility against future emergent viruses.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5869085/

Fauci funded Baric to make chimeras, develop Remdesivir, and test Remdesivir and monochlonal antibodies on the chimeras they made

BARIC 2017: “Broad-spectrum antiviral GS-5734 inhibits both epidemic and zoonotic coronaviruses…We show that a nucleotide prodrug, GS-5734… can inhibit SARS-CoV and MERS-CoV replication in multiple in vitro systems…GS-5734 was also effective against bat CoVs, prepandemic bat CoVs…thus demonstrating broad-spectrum anti-CoV activity… Grants from the NIH (AI108197 and AI109761)” https://stm.sciencemag.org/content/9/396/eaal3653?ijkey=eb5f2f6bc113f481e8845411981a67643bce07e7&keytype2=tf_ipsecsha

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“Building on this premise, we developed … full-length and chimeric viruses.. Importantly, monoclonal antibody strategies against SARS were effective against WIV1-CoV spike unlike available vaccine approaches. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4801244/

Fauci Paid for the Study, Trashed HCQ, got FDA approval all without a shred of legit evidence and bypassing all FDA trials set up with Gilead

https://arxiv.org/ftp/arxiv/papers/2003/2003.00728.pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5844999/

Anthony Fauci

• It’s undeniable that he made the monster destroying us: he paid for it, he drove its development, he knew the risks
• He patented the drug (a combo product)
• He used taxpayer dollars to develop the drugs for his patent
• He trashed the competitor of the drug he needs
• He paid for the FDA approval trials with taxpayer money
• He used his position to get emergency FDA approval on behalf of a drug company without scientific justification and instead of the drug company
• He is positioning to get the combination drug moved forward that his patent describes

Someone needs to start getting answers …FOIA

ANTHONY FAUCI�“Researchers will now compare a combination of remdesivir with an anti-inflammatory drug, a monoclonal antibody, [Fauci] said.”�

Copyright 2020 © Carla Woods All Rights Reserved.

https://www.theverge.com/2020/4/3/21206011/anthony-fauci-coronavirus-pandemic-stan-fandom-hero-donald-trump-white-house-task-force