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Coronavirus, as a pathogen model, was identified in 1965 and seen as modifiable for various purposes. In 1966, it was used in a transatlantic biological experiment. By 1967, human trials began, inoculating people with modified versions. The common cold was turned into a chimera in the 1970s. By 1990, coronavirus was an industrial problem for dog and pig breeders, leading to Pfizer's first spike protein vaccine patent. However, from 1990 to 2018, research indicated coronavirus mutated too quickly for vaccines to be effective. In 2002, the University of North Carolina Chapel Hill patented an "infectious replication defective" clone of coronavirus, funded by NIAID's Anthony Fauci, preceding SARS 1.0. SARS is engineered, not naturally occurring like the common cold.

Many viruses use a 2-step authentication process to enter cells, involving binding to a receptor and spike protein cleavage. Virologists have been adding furin cleavage sites to viruses since 1992, increasing their virulence. SARS-CoV-2, which likely originated from nature, contains unique furin cleavage site codons not typical in coronaviruses. This suggests a low probability of natural origin.

In 1965, coronavirus was identified as a pathogen that could be modified for various purposes. The first human manipulation experiment took place in 1966, followed by transatlantic data sharing in 1967. In the 1970s, coronavirus was modified in animals like pigs and dogs. By 1990, it was discovered that coronavirus caused gastrointestinal issues in dogs and pigs, leading to Pfizer filing the first spike protein vaccine patent. The spike protein was not a new problem, as it was known since 1990. Vaccines for coronavirus have been ineffective due to its ability to mutate quickly, as stated in numerous independent scientific publications. In 2002, the University of North Carolina Chapel Hill patented an infectious replication defective clone of coronavirus, funded by Anthony Fauci. This suggests that SARS was engineered and not a naturally occurring phenomenon.

We isolated coronaviruses from animals in the past to understand their threat to other species by culturing them on different cell types. This process, known as gain of function, involves enriching mutants that can infect new species. The speaker emphasizes that mass vaccination in humans is a significant gain of function experiment, leading to virus evolution. This real-world experiment involves constant virus changes due to human-to-human transmission under vaccine pressure.

In 1965, coronavirus was identified as a pathogen that could be modified for various purposes. The first transatlantic coronavirus experiment took place in 1966, followed by human trials in 1967. In the 1970s, coronavirus was manipulated in animals, and by 1990, it was recognized as a problem for dogs and pigs. Pfizer filed the first spike protein vaccine patent in 1990. It was known since then that coronavirus mutates too quickly for vaccines to be effective. In 2002, the University of North Carolina Chapel Hill patented an infectious replication defective clone of coronavirus, funded by Anthony Fauci. SARS 1.0 was engineered and not a naturally occurring phenomenon.

Ralph Barrick from the University of North Carolina discusses synthetic genomics of SARS. He explains the structure and genome organization of the SARS coronavirus and its various proteins. Barrick then discusses the use of synthetic genomics as a platform to control emerging infectious diseases, particularly focusing on SARS. He explains the process of synthesizing a portfolio of spike glycoprotein genes to capture the heterogeneity of the virus. Barrick also discusses the use of synthetic deoptimization schemes to attenuate SARS pathogenesis and the rewiring of SARS coronavirus transcription circuits to further attenuate viral pathogenesis. He concludes by highlighting the potential of synthetic genomics and universal attenuation schemes for developing rapid response platforms and vaccines against emerging coronaviruses.

Coronavirus was isolated in 1965 as one of the first infectious replicatable viral models, associated with the common cold. In 1966, the very first COV coronavirus model was used as a transatlantic biological experiment in human manipulation. In 1967, the first human trials on inoculating people with modified coronavirus were conducted. Between 1975 and 1977, we started modifying coronavirus by putting it into different animals, pigs and dogs. By 1990, Pfizer's first spike protein vaccine patent for coronavirus was filed. From 1990 to 02/2018, every publication on coronavirus vaccines concluded that coronavirus escapes the vaccine impulse because it mutates too quickly. In 02/2002, UNC Chapel Hill patented ‘an infectious replication defective clone of coronavirus’ funded by NIAID's Anthony Fauci from 1999 to 02/2002. That work allegedly preceded SARS-1; SARS is the research developed by humans weaponizing a life system model to attack human beings, patented in 02/2002.

The transcript argues that deflating the parasitic system is necessary because oversized states and corporations cause decay, corruption, and injustice, harming the people, workers, creators, and those harmed by elite interests. It cites examples such as Tanks for Kidney’s RT Documentary, Organ Harvesting, Black Market Transplants, and Crimes Against Humanity. It presents a quantified claim: extrapolating estimates for 2022 to 2023 plus half of 2024 yields total excess deaths of thirty-six million since the Covid Vax rollout, and adding nine million from Covid “killing protocols” in 2020 brings the total to forty-five million for four and a half years of Covid killing protocols. It describes SARS-CoV-2, the virus and vaccine bioweapons, as part of a narrative that depopulation and genocide are not taboo due to mass propaganda, corrupted science, lack of truthful science, and censorship in mainstream media and on tech platforms. It asserts that elites and many people still think SARS-CoV-2 is naturally evolved, but truthful science allegedly proves beyond doubt that SARS-CoV-2 was designed and made by humans in a bio lab. The transcript claims the genetic code of SARS-CoV-2 contains several lab-made inserts, such as PRRA and HIVGP120, which are described as too large and too numerous and only appearing in other natural viruses that are genetically very different from SARS-CoV-2, making natural mutation or recombination quasi zero. It also references a substantial trail of documents and testimonies years before and after the release of SARS-CoV-2 about these genetic codes, the existing biochemical technology to insert them, financing of the research, scientific documents, and patents. It then asserts that GenTech Covid vaccines cause human cells to produce, for months up to years, huge amounts of the toxic spike protein of SARS-CoV-2 in all organs and tissues, much greater than the mucosal infection from the virus itself in healthy unvaccinated people, which supposedly causes mild illness. The claim continues that these GenTech Covid vaccines are, in fact, bioweapons and much worse than the virus itself. It adds that not only the produced toxic spike protein but also other components and contaminations of these vaccines cause serious health damage. The source cited for these claims is Source2mia.org, with a request to like and follow.

Speaker 0: I read the sequence and it's high-resolution. Speaker 1: It may seem low at first, but it's understandable. Speaker 0: This is written in a loop. Speaker 1: This is the genetic sequence of the spike protein. The issue is that the model RNA has a sequence that surprised me. We need to design it a bit. It contains part of the sequence SB4T, which is necessary for gene expression. The problem is that it is found in a virus that has negative effects. Also, there is another problem with this sequence. The DNA that has been transferred so far becomes more susceptible to mutation. It's a problematic point. Speaker 1: So, this SB4T sequence is also included in the promoter of this SB method, which allows it to migrate to the nucleus. Speaker 0: This is quite famous. Speaker 1: Yes, it is. The issue is that it has no relation to the process of synthesizing the messenger RNA. Speaker 0: Why did they keep the promoter sequence in the SB4T that has nothing to do with the camera's perspective in the messenger RNA synthesis process?

We created coronaviruses by assembling a synthetic bat genome with the SARS clone. The genome was split into 5 kilobyte pieces with unique restriction sites to allow directional assembly. Initially, the virus couldn't replicate due to an entry defect, so we replaced the receptor binding domain with one from the human epidemic strain. This modification resulted in a virus that replicated efficiently. The growth curve data supported this success.

The symposium revolves around the science and safety implications of Replicating/Replicon vaccines and broader RNA vaccine platforms, with a sequence of expert presentations and reactions from the panel. -荒川博 presents the central premise that Replicon vaccines (replicating or self-amplifying RNA vaccines) raise unique safety and biosafety concerns beyond traditional mRNA vaccines. He frames the discussion around the idea that these vaccines “increase and mutate” within the host, potentially evolving in ways that could affect humans and populations. He references specific real-world events and case observations, including severe vascular events and tissue damage in some vaccine recipients, as motivation to scrutinize this technology carefully. -荒川 emphasizes that Replicon vaccines differ from conventional mRNA vaccines by embedding replicative machinery so that the RNA self-amplifies inside cells. He explains that, unlike ordinary mRNA vaccines, replication can produce more copies of the RNA and additional viral proteins, potentially leading to unexpected immune and biological consequences. He notes that the Alpha virus replicase used in some designs is designed to enable replication and increased antigen production, but that high mutation and recombination potential could yield variants or new properties. -藤本、藤田（参加者は複数） and others discuss the science of replication in viruses, highlighting the Central Dogma nuances. They describe that normally DNA → RNA → protein is the standard flow, but some viruses (RNA viruses and certain retroviruses) can reverse or bypass parts of this flow (RNA to DNA in retroviruses; RNA to RNA replication in some RNA viruses). This provides a conceptual basis for why replicating vaccines could, in principle, generate abnormal replication dynamics or new variants. -コロナウイルスRNAワクチンの議論では、Repliconの増殖と変異率の高さ、組換えの可能性、体内拡散の可能性を挙げて、「増えると変わる」性質が人の体内でどう影響するかが核心テーマとして挙げられます。アルファウイルス由来のレプリカーゼを使う場合、修復機能が不完全なRNAの増殖過程で、予想外の抗原変異を引き起こすリスクがあるとの指摘が出てきます。 -リスクの具体例として、ウイルスの殻（エンベロープ）とエクソソームを介した分布、自己拡散型ワクチンによる体内の遺伝子素材の取り込み、さらには他の人へ感染・伝播するアウトブレークの可能性、という仮説的懸念が提示されます。レプリコンワクチンは「空の遺伝子を抗原遺伝子に置き換えた陰性空間を持つウイルス」という説明が繰り返され、組換え・遺伝子交換・逆転など、従来のDNA・RNA動態の外に出る事象が起こり得ると議論されます。 -一部のスピーカーは、日本での試験・臨床・規制の動きを取り上げ、FDA/国内基準値を超えるDNA混入、SV40プロモーター混入の報告など、製品レベルでの懸念を指摘します。ケビン・マッカーシー氏の分析紹介では、日本市場で使われているファイザー社のコロナワクチンにDNA混入の痕跡があったこと、SV40プロモーター混入の可能性が指摘され、脂質ナノ粒子を通じた細胞内へのDNA／エクソンの取り込みリスクが懸念事項として挙げられます。これにより、RNAワクチンのフォーマットが終わるのではなく、プラットフォーム自体が拡大・進化する過程で新たなリスクを生む可能性を示唆します。 -IGG4関連疾患の急増とコロナワクチンの関連を例示する報告を紹介。IGG-4抗体が高値となり、多様な臓器炎症を引き起こす病態が観察され、ウイルス感染・ワクチン接種と免疫抑制・過剰免疫の連携が臨床で見られるケースの存在が議論されました。これにより、免疫の過剰反応・異常免疫を招く可能性があるとの懸念が示唆されました。 -ウイルス学・免疫学の専門家は、Repliconワクチンの「増殖・変異・組換えの三拍子」が、長期的・広範な公衆衛生影響をもたらし得る点を強調します。従来のウイルスワクチンの枠組みを超え、自己拡散・他者伝播・遺伝子汚染の可能性を定量的に評価する必要があると主張します。 -議論は、Repliconの潜在的リスクと実利を天秤にかけるもので、現時点で「安全」と断定できないという結論に至る場面が多くありました。実臨床での結果を長期観察で検証し、エビデンスに基づく判断を求める声が複数の speaker から出ました。 -最後に、メディア・一般市民への啓蒙の喚起と、透明性の高い情報提供、そして次世代ワクチン開発の安全性を担保するための厳格な規制・評価の重要性が強調されました。現状の科学的理解には限界があり、今後も公衆衛生への影響を見据えた厳密な検証が不可欠であるとの結論が共有されました。 overall, the event centers on the scientific basis, potential risks, and regulatory considerations of Replicon vaccines, contrasted with traditional mRNA vaccines, with emphasis on mutation, recombination, potential horizontal spread, DNA contamination concerns, immune dysregulation (including IGG4-associated phenomena), and the need for rigorous, transparent evaluation before broad deployment.

The spike protein on the surface of the coronavirus is crucial for its structure and interaction with our cells. To trigger a strong antibody response, Keith replicates the spike protein in the lab. He uses a small piece of HIV protein as a clamp to lock the spike protein into its original shape. This ensures that the spike protein maintains its structure and effectiveness.

Ralph Barrick from the University of North Carolina discusses synthetic genomics of SARS in this video. He explains the structure and genome organization of the SARS coronavirus and its various proteins. Barrick also discusses the use of synthetic genomics as a platform to control emerging infectious diseases and develop vaccines. He presents the results of experiments involving the synthesis of different SARS virus strains and their ability to infect human airway cells. Barrick also discusses the use of deoptimized codons to attenuate SARS pathogenesis and the rewiring of SARS coronavirus transcription circuits to further attenuate viral pathogenesis. He concludes by highlighting the potential of synthetic genomics and universal attenuation schemes to rapidly produce candidate live virus vaccines for emerging pathogens.

Scientists sequence the virus and compare it to known pathogens like SARS. They discovered similar coronaviruses in bats and focused on the spike protein that attaches to cells. Chinese researchers created pseudoparticles with spike proteins from these viruses to test their binding to human cells. Each step of this process helps determine if the virus can become pathogenic in humans. Manipulating the spike protein in the lab is crucial for understanding the zoonotic risk. By obtaining the sequence, scientists can predict the virus's behavior more accurately.

The spike protein of the coronavirus plays a crucial role in triggering a strong antibody response. To study it in the lab, Keith uses a small fragment of HIV as a clamp to lock the spike protein into its original shape. This helps maintain the structure of the virus on its surface.

The speaker discusses the Furin cleavage site found on the surface of the virus and its spike proteins. They explain that two enzymes, Furin and TMPRSS2, play a role in cutting the spike protein. The speaker mentions that the Spike protein is abundantly expressed in the respiratory tract, which is relevant to the virus's impact on the respiratory system. They also highlight the presence of a unique insert called PRRA in the virus, which is not found in similar viruses. The speaker questions the origin of this insert and mentions a patent from Moderna that includes a similar sequence. They find this odd and intriguing.

In 1965, coronavirus was identified as a pathogen that could be modified for various purposes. The first transatlantic coronavirus experiment took place in 1966, followed by human trials in 1967. The common cold was turned into a chimera in the 1970s, and by 1990, Pfizer filed the first spike protein vaccine patent for coronavirus. It was known since 1990 that coronavirus mutates too quickly for vaccines to be effective. In 2002, the University of North Carolina patented an infectious replication defective clone of coronavirus, funded by Anthony Fauci. This preceded SARS 1.0, suggesting it was not a naturally occurring phenomenon. SARS was engineered as a weapon against humans.

The speaker explains that the spike protein on the coronavirus is crucial for its structure and interaction with our cells. To trigger a protective antibody response, Keith replicates the spike protein in the lab and locks it into the same shape using a clamp-like protein. Surprisingly, this clamp-like protein is a small fragment of HIV.

Researchers have discovered various coronaviruses in bats, including ones similar to SARS. They focused on the spike protein, which attaches to cells, and conducted experiments in China. By inserting spike proteins from these viruses into pseudoparticles, they tested their ability to bind to human cells. This process allowed them to understand the potential pathogenicity of the virus in humans.

In 1965, coronavirus was identified as a pathogen that could be modified for various purposes. In 1966, the first transatlantic biological experiment using a coronavirus model was conducted. In 1967, human trials were conducted on modified coronavirus. In 1990, Pfizer filed the first patent for a spike protein vaccine for coronavirus. It was found that coronavirus mutates too quickly for vaccines to be effective. In 2002, the University of North Carolina Chapel Hill patented an infectious replication defective clone of coronavirus. The CDC filed a patent on SARS coronavirus isolated from humans in 2003. The RT PCR test for coronavirus was identified as a bioterrorism threat in 2002. Gain of function research on coronavirus was exempted from a moratorium in 2014. In 2016, a journal article stated that SARS coronavirus was poised for human emergence. In 2019, Moderna modified patent applications to include the term "accidental or intentional release of a respiratory pathogen." The goal was to create a universal vaccine template. The intent was to use coronavirus to achieve this. The speaker concludes by calling for an end to gain of function research and corporate patronage of science without assuming product liability.

The panel discusses replication (replicon) vaccines and their potential dangers, focusing on how they differ from conventional messenger RNA (mRNA) vaccines and what new risks might emerge as this technology develops. Key points and concerns raised - Replicon vaccines concept and fundamental differences - Replicon vaccines use replication-capable genetic material, so the embedded genetic information not only makes antigen proteins but also multiplies inside the cell. They are described as having both constitutive function (the ability to make proteins) and, crucially, the capacity to replicate, which distinguishes them from traditional, non-replicating mRNA vaccines. - It is explained that replication introduces additional mutation and recombination opportunities, because the RNA genome is copied more than once, and the process can produce variants that differ from the original design. - Central dogma exceptions and viral biology - The speakers explain that while the central dogma (DNA → RNA → protein) generally governs biology, some viruses violate this, with RNA viruses that replicate via RNA-dependent replication and even some reverse-transcribing retroviruses that convert RNA to DNA and integrate into genomes. This context is used to frame why replicon vaccines could behave unpredictably. - Potential risks of replication and spread - A core concern is that the replicon approach might allow the vaccine genome to spread beyond the initial target cells, potentially reaching other cells and tissues, or even spreading to other people via exosomes or other means. Exosomes can transport DNA, RNA, and proteins between cells; thus, the replicon genome could in theory be disseminated. - The possibility of homologous or heterologous recombination between replicon genomes and wild-type viruses could yield new variants. The panel emphasizes the difficulty of controlling such recombination in a living system. - Specific material and design considerations - The use of viral components like spike protein genes in replicon vaccines raises concerns about how these proteins might mutate or recombine during replication, potentially altering antigen presentation or safety. - A concern is raised about the lack of repair mechanisms in RNA replication (as opposed to DNA replication), which could make error rates higher and lead to unpredictable changes. - The panel notes that current replicon vaccine designs (including those using alphavirus backbones) inherently carry high mutation and recombination risk, and that the replicating systems may encounter unpredictable evolutionary dynamics inside the human body. - Safety signals and clinical anecdotes - The speakers cite cases of adverse events temporally associated with vaccines, including vascular inflammation and thrombosis, stroke-like events, and myocarditis, to illustrate that immune responses to vaccines can be complex and occasionally severe. They emphasize that such observations do not establish causality, but argue they warrant careful scrutiny. - There are references to cases of acute vascular and neural complications following repeated vaccination, and to broader immune dysregulation phenomena, including IGG4-related disease and immune dysregulation syndromes that can involve multiple organs. - One example concerns a patient who developed sudden limb problems after the third dose, requiring surgery; another describes myocardial involvement after multiple doses and subsequent inflammatory sequelae. - DNA contamination and analytical findings - Kevin McKernan’s analysis of certain Japanese CoronaVac vaccines is cited: both DNA contamination and the presence of SV40 promoter elements were detected in some vaccine lots, with DNA amounts exceeding some regulatory benchmarks in at least one case. The concern is that DNA contamination, or the presence of promoter sequences, could influence integration or expression in unintended ways. - It is noted that vaccines using lipid nanoparticles can potentially deliver nucleic acids into cells; in the presence of exons or promoter sequences, there could be unintended cellular uptake and expression. - Implications for public health and policy - The panel underscores the need for caution, thorough investigation, and long-term observation of any replication-based vaccine platform before broad deployment. There is a call to evaluate risks, monitor long-term outcomes, and consider the possibility that replication-competent constructs could drive unforeseen evolutionary dynamics within hosts or communities. - There is contention about how information is communicated to the public, with particular emphasis on avoiding misinformation while ensuring that scientific uncertainties are transparently discussed. - Broader scientific context and forward-looking stance - The speakers discuss how the field’s approach to gene-based vaccines is evolving rapidly, and they stress that the compatibility of replicon systems with human biology is not yet fully understood. - They frame their discussion as not merely about current vaccines but about the trajectory of vaccine platforms: if replication-based or self-dispersing systems prove too risky or unpredictable, the prudent path might be to favor conventional, non-replicating strategies until safety, efficacy, and containment of unintended spread are more firmly established. Closing and takeaways - The session closes with emphasis on careful evaluation of replicon vaccines, awareness that viral genetics can behave differently in humans than in theory, and a call for continued discussion, independent verification, and transparent communication as the technology develops. - Throughout, speakers acknowledge the complexity of immune responses to vaccines, the potential for unexpected adverse events, and the importance of safeguarding public health while advancing vaccine science.

In the lab, it's easy to manipulate spike proteins, which play a significant role in the zoonotic risk of coronaviruses. By obtaining the sequence and constructing the protein, we collaborated with Ralph Barrick at UNC to insert it into another virus. This allows us to conduct experiments and enhance our ability to predict outcomes based on specific sequences.

We focus on viral families that have transmitted from animals to humans. When we find a virus that resembles a known dangerous pathogen, like SARS, we examine its spike protein, which attaches to cells. Chinese researchers create pseudo particles with these spike proteins to test if they bind to human cells. This process helps us identify viruses that could potentially be harmful to humans. By narrowing down the field and reducing costs, we end up with a small number of viruses that appear to be dangerous. We then investigate if people living in the same region as the animals carrying these viruses have developed antibodies.