THE BIOWEAPON ORIGIN OF COVID IN 3 TWEETS On June 4th 2021, Fauci was briefed by the Weapons and Counterproliferation Mission Center of the CIA - who were investigating the possibility SARS-CoV-2 was a bioweapon. They shared with him that “pangolin” coronaviruses had been transferred from a "group in Beijing" to Wuhan for experiments involving humanized mice. We should be careful not to conflate WIV with the Wuhan BSL-4 facility (even the IC aren’t consistent about this!). Fauci doesn't say it, but the “group in Beijing” is almost certainly the AMMS Institute of Microbiology and Epidemiology. The CIA also divulged to him that unknown experiments were conducted by the military in Wuhan. But you don’t need BSL-4 to study a zoonotic coronavirus, this would usually be done at BSL-2. Even SARS and MERS are only BSL-3 - which AMMS has in Beijing. Why go to Wuhan? ODNI recently released CIA official's accounts of the meeting, but some key details were redacted. According to the CIA, Fauci was very interested in the pangolins, but he told them they needed to get more detail about the experiments. Fauci’s own account of the meeting is quite disparaging of the CIA presenters. Perhaps he was covering himself in case his negligence in dismissing their concerns was exposed later? (1/3)

The loss of QTQTN motif on SARS-CoV-2 spike removes a furin landing site and weakens furin cleavage efficiency but preserves binding affinity for Heparan Sulfate Proteoglycans (HSPG). There is a tradeoff between furin cleavage and heparan sulfate binding, as coronaviruses often lose FCS efficiency in exchange for heparan sulfate binding during serial passage in cell culture, perhaps because HSPG are very abundant on cell surface while the dedicated receptors are rarer. During cell culture passage, Feline CoV and HCoV-OC43 both mutate from furin-cleavage-efficient RRSRR motif to heparan-sulfate-binding RRSRG motif. The poly-basic motif functions as heparan-sulfate-binding Cardin-Weintraub motif (XBBXBX or XBBBXXBX) if not cleaved by furin. [1] Kakeya Hideki hypothesizes that some of the Covid variants like Delta and Omicron may be lab-made as well. Maybe the Delta and Omicron variants are products of serial passage or rational design in lab. The Delta and Omicron variants are even more efficient at binding heparan sulfate due to extra positively charged residues at spike protein. Compared to Wuhan-Hu-1, Delta variant spike carries 4 extra positive residues, while Omicron variant spike carries 9 extra positive residues. At the S1/S2 juncture, Delta spike contains a XBBBXBX motif (one extra positive charge) that binds heparan sulfate even more tightly than WT FCS (XBBXBX). At S1/S2 juncture, Omicron spike is even better at binding heparan sulfate with XBXBBBXBX motif. Even RBD contains extras positive charge that may enhance binding to either heparan sulfate or ACE2. [2] References: 1. de Haan CA, Haijema BJ, Schellen P, Wichgers Schreur P, te Lintelo E, Vennema H, Rottier PJ. Cleavage of group 1 coronavirus spike proteins: how furin cleavage is traded off against heparan sulfate binding upon cell culture adaptation. J Virol. 2008 Jun;82(12):6078-83. doi: 10.1128/JVI.00074-08. Epub 2008 Apr 9. PMID: 18400867; PMCID: PMC2395124. 2. Nie C, Sahoo AK, Netz RR, Herrmann A, Ballauff M, Haag R. Charge Matters: Mutations in Omicron Variant Favor Binding to Cells. Chembiochem. 2022 Mar 18;23(6):e202100681. doi: 10.1002/cbic.202100681. Epub 2022 Feb 2. PMID: 35020256; PMCID: PMC9015620.

The loss of QTQTN motif on SARS-CoV-2 spike removes a furin landing site and weakens furin cleavage efficiency but preserves binding affinity for Heparan Sulfate Proteoglycans (HSPG). There is a tradeoff between furin cleavage and heparan sulfate binding, as coronaviruses often lose FCS efficiency in exchange for heparan sulfate binding during serial passage in cell culture, perhaps because HSPG are very abundant on cell surface while the dedicated receptors are rarer. During cell culture passage, Feline CoV and HCoV-OC43 both mutate from furin-cleavage-efficient RRSRR motif to heparan-sulfate-binding RRSRG motif. The poly-basic motif functions as heparan-sulfate-binding Cardin-Weintraub motif (XBBXBX or XBBBXXBX) if not cleaved by furin. [1] Kakeya Hideki hypothesizes that some of the Covid variants like Delta and Omicron may be lab-made as well. Maybe the Delta and Omicron variants are products of serial passage or rational design in lab. The Delta and Omicron variants are even more efficient at binding heparan sulfate due to extra positively charged residues at spike protein. Compared to Wuhan-Hu-1, Delta variant spike carries 4 extra positive residues, while Omicron variant spike carries 9 extra positive residues. At the S1/S2 juncture, Delta spike contains a XBBBXBX motif (one extra positive charge) that binds heparan sulfate even more tightly than WT FCS (XBBXBX). At S1/S2 juncture, Omicron spike is even better at binding heparan sulfate with XBXBBBXBX motif. Even RBD contains extras positive charge that may enhance binding to either heparan sulfate or ACE2. [2] References: 1. de Haan CA, Haijema BJ, Schellen P, Wichgers Schreur P, te Lintelo E, Vennema H, Rottier PJ. Cleavage of group 1 coronavirus spike proteins: how furin cleavage is traded off against heparan sulfate binding upon cell culture adaptation. J Virol. 2008 Jun;82(12):6078-83. doi: 10.1128/JVI.00074-08. Epub 2008 Apr 9. PMID: 18400867; PMCID: PMC2395124. 2. Nie C, Sahoo AK, Netz RR, Herrmann A, Ballauff M, Haag R. Charge Matters: Mutations in Omicron Variant Favor Binding to Cells. Chembiochem. 2022 Mar 18;23(6):e202100681. doi: 10.1002/cbic.202100681. Epub 2022 Feb 2. PMID: 35020256; PMCID: PMC9015620.

Here too in Serial passage there were unexpected changes in certain key sections. Note these experiments are never assessed from a Biosynthesic Forensics perspective...there are too many sensitivities at @UNSW to have these types of insinuations made...and so the best that @Globalbiosec can do is point at obvious Discrepant Epidemiology issues with these and other data sets. <>

@DagobertIX @chris_komatsu @RandPaul <<FCS insertion is CTCCTCGGCGGG. The reverse complement is 5′‑ CCCGCCGAGGAG ‑3′. GCCGAG is the NmeAIII recognition site, but only visible on the antisense strand, not the sense strand.>> @tony_vandongen noted something like this when raised originally.

You will be glad to know that I have been busy doing the research that so many scientists failed to do! I have now ironed out errors spotted by @gadboit2 and published Version 2 of "The Alanine Mutations" with timely help from our colleague @gdemaneuf

co-conspirator 1 sent Morens 2 bottles of wine: “This is the first of what I hope will be a continued series of expressions of gratitude for your advice, support, & behind-the-scenes shenanigans in my battle against your bosses boss, his boss, & the ultimate boss on the hill.”

For years, we were told the possibility of a lab leak at the Wuhan Institute of Virology was a conspiracy theory. Now Anthony Fauci's former senior adviser, David Morens, has pleaded guilty to conspiring to defraud the United States by concealing COVID origins records.

Threonine372 is conserved for spike proteins of all bat or pangolin SARS-CoV-2related coronaviruses, including pangolinCoV-MP789 (GenBank: MT121216.1), pangolinCoV-GD (GenBank: OQ297708.1 ), BANAL-20-236 (GenBank: MZ937003.2), BANAL-20-103 (GenBank: MZ937001.1), RshSTT182/200 (PDB: 7XBH), BANAL-20-52 (GenBank: MZ937000.1), RaTG13 (GenBank: MN996532.2), pangolinCoV-GX-P2V (MW532698.1), Rc-o319 (LC556375.1), Rs7896 (GenBank: OL674074.1), Rs4874 (GenBank: KY417150.1), ZC45 (GenBank: MG772933.1), RpYN06 (GenBank: MZ081381.1), RacCS203 (GenBank: MW251308.1), and RmYN02 (GenBank: ON131092.1). T372A is a human-adaptive mutation for SARS-CoV-2 only. According to Robert Garry, T372A substitution removes glycan at N370 and makes the spike protein more likely to adopt the open conformation, thus allowing the RBD to bind hACE2 receptor more efficiently. The downside is that the spike protein in open conformation becomes more sensitive to low pH. Therefore, SARS-CoV-2 prefers replication in the respiratory tract rather than the gastrointestinal tract. By BLAST search, I found Khosta-2 (GenBank: QVN46569.1) is the only bat coronavirus with alanine at this position, although it has a serine insertion upstream before position 371. The N370 of Khosta-2 spike protein is probably glycosylated just like in other bat coronaviruses.

Threonine372 is conserved for spike proteins of all bat or pangolin SARS-CoV-2related coronaviruses, including pangolinCoV-MP789 (GenBank: MT121216.1), pangolinCoV-GD (GenBank: OQ297708.1 ), BANAL-20-236 (GenBank: MZ937003.2), BANAL-20-103 (GenBank: MZ937001.1), RshSTT182/200 (PDB: 7XBH), BANAL-20-52 (GenBank: MZ937000.1), RaTG13 (GenBank: MN996532.2), pangolinCoV-GX-P2V (MW532698.1), Rc-o319 (LC556375.1), Rs7896 (GenBank: OL674074.1), Rs4874 (GenBank: KY417150.1), ZC45 (GenBank: MG772933.1), RpYN06 (GenBank: MZ081381.1), RacCS203 (GenBank: MW251308.1), and RmYN02 (GenBank: ON131092.1). T372A is a human-adaptive mutation for SARS-CoV-2 only. According to Robert Garry, T372A substitution removes glycan at N370 and makes the spike protein more likely to adopt the open conformation, thus allowing the RBD to bind hACE2 receptor more efficiently. The downside is that the spike protein in open conformation becomes more sensitive to low pH. Therefore, SARS-CoV-2 prefers replication in the respiratory tract rather than the gastrointestinal tract. By BLAST search, I found Khosta-2 (GenBank: QVN46569.1) is the only bat coronavirus with alanine at this position, although it has a serine insertion upstream before position 371. The N370 of Khosta-2 spike protein is probably glycosylated just like in other bat coronaviruses.

Not only was SARS-CoV-2 a bioweapon - there's strong evidence that variants were also designed to be immune evasive bioweapons. Evolutionary biologists are still at a loss to explain the mutations we saw - even amongst the chaos of vaccine trials etc.

In silico prediction shows SARS-CoV-2 spike protein may interact with laminin (laminin β-1 and γ-1 subunits) because of spike protein’s mimicry of laminin, though the exact docking model is unpublished. [1] Experimental data seem to match with prediction in silico. Bamberger et al. (the paper you sent me) reported that immunoprecipitation using spike protein (especially S2) could pull down laminin β-3 and laminin γ-2. [2] Yapici-Eser et al. noted that “SARS-CoV-2 mimics various proteins that increase the vulnerability of thrombosis.” [1] I think spike S2 fusion coil probably mimics long helix on laminin and may engage in coiled-coil interaction with laminin β and γ. The HMI-Pred server predicts viral-human protein interaction by identifying interface mimicry. The algorithm performs two steps: 1) structural alignment (structural superposition) of viral protein with human protein at interface; 2) verification of binding by docking analysis at interface. Sadly, Yapici-Eser et al. didn’t publish a docking model of spike-laminin interaction. Maybe the post-fusion spike S2 mimics helical coil on laminin and engages trimeric coiled-coil interaction with laminin β and γ subunits. It would be helpful if Yapici-Eser et al. publish their docking model, but they didn’t. The exact binding mode is unknown. Their paper only showed a model of spike-fibrinogen interaction—the α-helical fusion coil of spike S2 appears to engage fibrinogen beta chain. [2] Look at the docking model between spike and fibrinogen. Although an intact spike protein probably won’t engage fibrinogen because S2 fusion coil is buried, binding may occur if the spike S2 fusion coil is exposed. In other words, the furin cleavage site may be the culprit. Large amounts of spike S2 fusion coil are surface-exposed after furin cleavage (post-fusion conformation), and perhaps this phenomenon leads to excess blood coagulation. According to Charles Rixley’s post, former vaccine researcher Philip Dormitzer said poly-basic cleavage motif [FCS] shouldn’t be included in influenza vaccines. I performed a structural superposition between laminin (PDB ID: 5XAU) and postfusion spike S2 (PDB ID: 6XRA) on Pymol. As shown in the attached picture, laminin α subunit is colored green, laminin β is colored cyan, laminin γ subunit is colored magenta, and spike monomer is colored orange. The postfusion spike S2 mimics laminin β in coil shape. By the way, nsp8 and nsp9 are predicted to bind glutamate receptor NMDAR by structural mimicry. [1] Maybe this is another factor in neurological impact of COVID. References: 1. Yapici-Eser H, Koroglu YE, Oztop-Cakmak O, Keskin O, Gursoy A, Gursoy-Ozdemir Y. Neuropsychiatric Symptoms of COVID-19 Explained by SARS-CoV-2 Proteins' Mimicry of Human Protein Interactions. Front Hum Neurosci. 2021 Mar 23;15:656313. doi: 10.3389/fnhum.2021.656313. PMID: 33833673; PMCID: PMC8021734. 2. Bamberger C, Pankow S, Martínez-Bartolomé S, Diedrich J, Park R, Yates J 3rd. The Host Interactome of Spike Expands the Tropism of SARS-CoV-2. bioRxiv [Preprint]. 2021 Feb 16:2021.02.16.431318. doi: 10.1101/2021.02.16.431318. Update in: J Proteome Res. 2023 Dec 1;22(12):3742-3753. doi: 10.1021/acs.jproteome.3c00387. PMID: 33619478; PMCID: PMC7899442.

It is the further evidence of ongoing undisclosed Chimeric Spike experiments that is important. Early versions of RaTG13 from 2017 with reads 27 to 33 here demonstrate two things from a bioinformatic forensics methodology perspective; 1) there is enough variation from the earliest to the latest versions of RaTG13 to demonstrate that versions of Ra4991 or similar were under selection pressure from serial passage…not that these discrepancies simply need to be accepted as bad reads instead of evidence of dangerous biological warfare methodology. 2) these WIV experiments 2017-2018 and 2019 ongoing also involved 7896 ORF8 series data in ways where earlier Chimeric studies of this nature sought to investigate DURC Apoptosis and Immune evasion. In October 2019 these experiments were repackaged to look like Viral Evolution experiments. But the evidence of ORF8 chimera linked data is there from July 2018

@SitSilver @breakfast_dogs @tommy_cleary A Chinese-language bioweapon book written in 2011 eerily prophesied today’s situation. The book is marketed as a bioweapon introductory for teenagers. Why did the Chinese government allow such a book to be published? The book’s purpose appears to indoctrinate teenagers for biological warfare. The book is titled “Cutting-edge Weapons Technology of Keen Interest to Teenagers—Technical Knowledge for Biological Weapons,” written by Feng Wenyuan and published by LiaoHai Publishing House (ISBN: 978-7-5451-1253-5). It used to be downloadable from Amazon Kindle a couple of years ago but has been pulled off shelf. The book mentioned a few interesting points: 1) biological Hiroshima; 2) the world may be destroyed by scientists; 3) humanity will go into extinction if HIV is transmissible by air; 4) chimeric germs with virulence genes borrowed from other pathogens; 5) bioweapon can be deployed by humans or by balloons. In today’s observation, SARS-CoV-2 is not related to HIV, but it can damage the human immune system just like HIV. Below are a few translated excerpts of the book: “In Future Shock, Alvin Toffler wrote, ‘The clock is ticking; we are moving toward a biological Hiroshima.’ This statement speaks precisely to that reality.” “Prof. Yang Huanming, Secretary-General of China’s major ‘Human Genome Project,’ remarked in an interview: ‘Even a small laboratory like ours can do something like linking the HIV virus with the influenza virus—how terrifying is that! It has often been said that the world won’t be destroyed by a few lawless thugs; if it is to be destroyed, it will be by scientists.’” “Although HIV is transmitted only through sexual contact or blood, the number of people infected worldwide is already staggering; if AIDS could be spread simply by sneezing, humanity would likely have gone extinct long ago.” “Furthermore, if oncogenes or genes from the plague-causing Yersinia pestis were inserted into E. coli and allowed to replicate, it could just as easily wipe out all of humanity. There is also a peculiar type of genetic weapon known as ‘fever toxin,’ [sic. botox?] by which a mere 20 grams would suffice to kill off the entire human race.” 托夫勒在《未来的震荡》里说，“时钟滴答作响，我们正在向‘生物学的广岛’靠拢”。说的正是这样一个现实。 中国“人类基因组计划”重大项目秘书长杨焕明在接受记者采访时说，“就连我们这么小的实验室都能做这样的事，把艾滋病毒跟流感病毒连接到一起，多可怕！有人常说过，这个世界不是毁在几个不懂法的流氓手里，要毁就毁在科学家手里。” 艾滋病毒虽只通过性交合血液，尚且在世界范围有如此巨大的感染人群，如果打一个喷嚏就可以传播艾滋病，恐怕人类早就灭绝了。 再有，如果把引起鼠疫的鼠疫杆菌的基因或致癌基因移入大肠杆菌中，令其繁殖，同样可以轻松毁灭全人类。还有一种叫“热毒素”的奇特基因武器，只需20克便可致全人类于死地。 “Compared to other modern weaponry, genetic weapons—in addition to being difficult to defend against and hard to treat—offer advantages such as low cost, ease of manufacture, convenience of use, and immense lethality. They can be deployed via human means, conventional artillery, warships, aircraft, balloons, or missiles, targeting enemy front lines, rear areas, waterways, cities, and transportation hubs to rapidly spread disease.” “Introducing a ‘genetic weapon’ based on a super-virulent hemorrhagic fever pathogen into an adversary's water system could incapacitate the majority of the population in that watershed—an effect dozens of times more devastating than a nuclear weapon. The deployment of genetic weapons in future conflicts would fundamentally transform the nature of warfare: “The mode of warfare would shift. Hostile parties might employ genetic weapons prior to war to devastate enemy personnel and living environments, thereby stripping a nation or people of their combat capability and economic vitality, and leading to their subjugation without a single shot being fired.” “Military organizational structures would undergo change. Combat units would likely be slashed in number, while medical support units would likely be expanded.” 基因武器与其他现代化武器比较，除不易防御和被害后难治疗等特点以外，还有成本低、易制造、使用方便、杀伤力大等优势。基因武器可以用人工、普通火炮、军舰、飞机、气球或导弹进行施放，可以投在对方的前线、后方、江河湖泊、城市和交通要冲使疾病迅速传播。 将一种超级出血热菌的“基因武器”投入对方水系，会使水系流域的居民多数丧失生活能力，这要比核弹杀伤力大几十倍。一旦基因武器投入未来战争，将使未来战争发生巨大变化： 战争模式将发生变化。敌对双方可能在战前使用基因武器，使对方人员及生活环境遭到破坏，导致一个民族、一个国家丧失战斗力，经济衰退，在不流血中被征服。 军队的编制体制结构将发生变化。战斗部队将减少，而卫生勤务保障部队可能要增加。