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In Is COVID-19 a Bioweapon, Richard M. Fleming presents a controversial theory: The SARS-CoV-2 virus was not naturally occurring, but an engineered bioweapon deliberately created through decades of research into enhancing the infectiousness and deadliness of coronaviruses, known as "gain-of-function" studies.

Fleming provides evidence of unusual genetic sequences in SARS-CoV-2, alterations like the PRRA insert, and claims the virus inflicts harm through an "InflammoThrombotic Response" that damages multiple organs beyond the respiratory system. He argues figures like Ralph Baric, Shi Zhengli-Li, and Peter Daszak played key roles in developing SARS-CoV-2 under funding from the U.S. government, risking violations of international bioweapons treaties.

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  • The PRRA sequence refers to a specific amino acid sequence (proline-arginine-arginine-alanine) found in the spike protein of SARS-CoV-2. This sequence is part of a furin cleavage site, which is a region that can be cut by the enzyme furin, facilitating the virus's entry into human cells.
  • Other coronaviruses, such as those causing the common cold, do not have the PRRA sequence, which may partly explain differences in their transmissibility and severity compared to SARS-CoV-2.
  • Transmissibility is the ability of a virus to spread from one host to another. Changes in viral proteins, like the spike protein in coronaviruses, can increase how easily a virus is transmitted.
  • Removing the PRRA sequence could enhance the safety profile of a vaccine by reducing the risk of the vaccine virus reverting to a more virulent form, which is a concern with live-attenuated vaccines.
  • The concept of deliberate engineering involves the hypothesis that certain features of a virus, like the PRRA insert, could be artificially introduced to study viral behavior or enhance certain characteristics, such as transmissibility or pathogenicity, for research purposes.

Investigations have identified a part of the SARS-CoV-2 spike protein that is similar to a portion of the HIV glycoprotein 120, potentially resulting in heightened inflammation, blood clotting, and damage to the nervous system.

The writer argues that the spike protein of SARS-CoV-2 not only contains the PRRA sequence but also possesses an extra segment, namely the gp120 observed in HIV. Fleming discusses the widespread recognition of Shi Zhengli-Li's work on altering the spike protein of coronaviruses following the SARS outbreak in 2002. She endeavored to increase the ability of SARS viruses to spread among humans. Fleming argues that the gp120 component of HIV is engineered to bind to a receptor on human cells known as the sialic acid receptor. He explains that this connection initiates a process characterized by inflammation and the formation of blood clots, similar to the processes that result in heart and blood vessel diseases. Individuals who contract COVID-19 experience more severe outcomes.

The detection of HIV genetic sequences in SARS-CoV-2 suggests that the virus may have been subject to sophisticated lab alterations rather than having evolved through natural selection.

Fleming posits that the presence of HIV gp120 and the PRRA insert in SARS-CoV-2's spike protein suggests deliberate alteration instead of a coincidental event. The author emphasizes that since 2002, the scientific community has been cognizant of the potential for HIV gp120 to cause prion-related neurodegenerative diseases, suggesting that the creators of the virus could have been aware of the neurological dangers involved with the integration of gp120 into the viral architecture. Fleming assigns responsibility to the funders and approvers of research that seeks to enhance the virulence of disease-causing agents, citing their disregard for ethical and legal obligations given the hazardous character of such research and the risk of catastrophic outcomes.

Other Perspectives

  • The claim requires rigorous scientific validation through peer-reviewed research, and until such evidence is presented, it remains a hypothesis rather than a confirmed fact.
  • Similarities between viral genetic sequences can arise due to convergent evolution, where unrelated viruses evolve similar solutions to the same problem, such as binding to host cells, without any human intervention.
  • The suggestion that the virus was created with knowledge of potential neurological dangers assumes intent without direct evidence linking the creators to such knowledge.
  • Assigning responsibility to funders and approvers without clear evidence of negligence or malicious intent could be seen as speculative and may overlook the complexity of scientific research and its governance.
  • Researchers typically undergo ethics training and must adhere to principles of responsible conduct in research.
  • The catastrophic outcomes are not a certainty but a possibility, and with proper risk management and containment protocols, the likelihood of such outcomes can be minimized.

The analysis of SARS-CoV-2's genetic makeup has revealed unusual insertions and changes uncommon in naturally occurring coronaviruses, indicating the possibility of laboratory-based modifications.

Fleming suggests that additional evidence supports the notion that the virus responsible for COVID-19 may have been artificially created, potentially in a lab setting, aside from the PRRA and HIV gp120 insertions.

Researchers have identified 18 RNA fragments in SARS-CoV-2 that are homologous to segments of HIV and other retroviruses, indicating the virus was likely created through combining genetic material from multiple sources.

Fleming scrutinizes Pradhan's discovery of four unique genetic sequences in the pathogen responsible for COVID-19. He maintains that his investigation supports the idea that SARS-CoV-2 is a derivative of SARS-CoV-1, which was originally developed for biowarfare purposes, a hypothesis initially suggested by the scientist Dr. Li Meng Yan. The author highlights research conducted by the scientist known for discovering the human immunodeficiency virus. Montagnier noted that the genetic sequence of SARS-CoV-2 bears resemblance to 18 segments commonly found in HIV or primate retroviruses. Fleming scrutinizes Montagnier's research, indicating that a portion of the SARS-CoV-2 spike protein, which is made up of a chain of 590 amino acids, bears resemblance to HIV-1. He argues that the inclusion of the PRRA insert alters the structure of the spike protein, leading to a region similar to a prion at the point of contact with human cell receptors.

Other Perspectives

  • The identified RNA fragments might be common in many viruses, not just HIV or retroviruses, which would make them less indicative of a unique or engineered origin.
  • The methodology and data used to identify these sequences must be transparent and robust to rule out the possibility of coincidental matches or errors in sequence analysis.
  • The genetic differences between SARS-CoV-1 and SARS-CoV-2 are significant, suggesting that SARS-CoV-2 evolved naturally rather than being artificially derived from SARS-CoV-1.
  • Intelligence agencies and scientific panels in multiple countries have investigated the origins of SARS-CoV-2 and have not found credible evidence to support the biowarfare hypothesis.
  • Montagnier's observations may be subject to confirmation bias, where data is interpreted in a way that fits a preconceived hypothesis, without considering all possible explanations.
  • The spike protein's primary function is to bind to the host cell receptor, and any similarities to HIV-1 may be related to this shared function rather than a unique or engineered feature.
  • The presence of the PRRA insert could be a result of natural evolutionary processes such as recombination and convergent evolution, rather than intentional manipulation.

The physiological processes, inflammatory routes, and clinical manifestations associated with COVID-19.

Fleming argues that COVID-19 is more than just a respiratory disease, as it can lead to a condition that causes clotting and can affect multiple organs via an InflammoThrombotic Response (ITR). He argues that the unique alterations in the virus's spike structure are crucial in triggering a cascade of reactions leading to inflammation, coagulation of blood, and damage to various organs.

The attachment of the spike protein from SARS-CoV-2 to the ACE2 receptor is an essential precursor to its interaction with the TMPRSS2 site, which allows the virus to penetrate and harm human cells.

Fleming emphasizes the importance of understanding the interaction between the spike protein of SARS-CoV-2 and the cells it targets in humans. He clarifies the mechanism through which the spike protein attaches itself to the ACE2 receptor present on cell membranes. The initiation of the virus's replication cycle and its entry into the cell are facilitated by the activation of the TMPRSS2 enzyme, which triggers a series of reactions leading to the division of the virus's surface protein.

Differences in the expression levels of ACE2 and TMPRSS2 across various ethnic groups might explain the unequal susceptibility and severity of COVID-19 infections observed.

Fleming emphasizes that our own chromosomes contain the genetic blueprints for TMPRSS2 and ACE2. He argues that the specific genetic codes for these receptors vary from person to person because of our distinct genetic constitution. Fleming proposes that the genetic variation among different ethnic populations, along with the varying amounts of ACE2 and TMPRSS2 present, could contribute to the unequal impact and outcomes of COVID-19 observed in these communities. Dr. Fleming highlights that people with African ancestry have a significantly increased presence of TMPRSS2, potentially contributing to their greater vulnerability to intense COVID-19 cases.

Practical Tips

  • Start a personal health journal to track any symptoms or reactions you have to medications or treatments, noting any patterns that might be related to your ethnic background. This can be a valuable tool when consulting with healthcare professionals, as it provides concrete data that can help in making more informed decisions about your health management.
  • Start a personalized nutrition and lifestyle plan based on your genetic information. Once you have your genetic data, you can work with a dietitian or a nutritionist who specializes in nutrigenomics to tailor a diet and lifestyle plan that takes into account your body's specific needs and predispositions, potentially influencing the expression of ACE2 and TMPRSS2.
  • Consider advocating for more inclusive clinical trials by participating in surveys or signing petitions that call for diverse representation in medical research. This can help ensure that future studies and treatments consider the genetic variations across different ethnic groups, potentially leading to more effective and equitable healthcare solutions.

The region of the SARS-CoV-2 spike protein with prion-like characteristics enhances the virus's ability to breach the blood-brain barrier, which could result in damage to the nervous system.

Fleming warns that the modifications involving PRRA and gp120 in the spike structure of SARS-CoV-2 lead to a segment that possesses characteristics similar to prions. Prions are misfolded proteins capable of spreading from cell to cell, causing damage. Conditions such as Alzheimer's and mad cow disease, which lead to the deterioration of the nervous system, could originate from diseases linked to prions. He explains that the organism contains a prion-like segment, which allows it to penetrate the brain's usual defense against potentially harmful substances circulating in the bloodstream.

Studies involving animal subjects suggest that the spike protein associated with SARS-CoV-2 could lead to neurological disorders characterized by inflammation, the emergence of spongiform conditions akin to mad cow disease, and the formation of atypical protein aggregates commonly linked with neurodegenerative illnesses.

Fleming cites studies that use mice with human physiological characteristics and rhesus monkeys to show that the spike protein of SARS-CoV-2 can penetrate the blood-brain barrier, causing significant harm to the nervous system. In his assertion, he highlights that studies on genetically engineered mice designed to mimic human responses revealed a disturbing mortality rate of 95% within a fortnight, not due to pulmonary complications but due to cerebral damage following exposure to the spike protein. The animals exhibited symptoms of cerebral edema and damage to their neural frameworks, which profoundly impacted the neurons within their spinal cords. Fleming describes how the virus reaches the brain by following the route connected to our sense of smell. He goes on to detail experiments on a certain primate species where researchers observed inflammatory responses and disorders resembling those seen in cattle with mad cow disease and in humans with Alzheimer's.

Other Perspectives

  • Inflammation is a broad and non-specific response that can be triggered by a variety of factors, not necessarily indicative of a direct causal relationship with the spike protein.
  • The sample size and conditions of the animal studies might not be representative of the broader population, which could limit the generalizability of the findings.
  • The formation of atypical protein aggregates in animal studies does not necessarily imply the same will occur in humans, as the underlying mechanisms can vary significantly.
  • The findings from animal studies need to be corroborated by clinical data to confirm their relevance to human health.
  • The genetic modifications made to the mice to mimic human responses could introduce variables that do not exist in natural human biology, possibly skewing the results.
  • The findings need to be replicated and validated by other independent research groups to rule out experimental errors or biases in the initial studies.
  • The olfactory route might not be the most significant route of entry for the virus into the brain, as other mechanisms could play a more prominent role in potential neurological impacts.
  • The inflammatory responses and disorders observed in primates may not directly translate to humans due to species differences in immune response and brain physiology.

COVID-19 is characterized by the InflammoThrombotic Response (ITR), which leads to inflammation, blood clotting, and multi-organ damage, stemming from the virus known as SARS-CoV-2.

The author, Fleming, asserts that COVID-19's origin extends beyond a mere viral cause. The syndrome is identified as an InflammoThrombotic Response (ITR), a concept originally suggested to connect inflammation with cardiovascular conditions. Fleming's hypothesis, formulated in 1994, sheds light on the common route underlying numerous chronic diseases associated with inflammation, including heart attacks, strokes, Alzheimer's disease, along with specific forms of cancer, all characterized by the occurrence of blood clots.

Treatments for COVID-19 that concentrate on the body's reaction to immune thrombosis, rather than solely targeting the pathogen, have markedly enhanced the recovery prospects for patients.

Fleming contends that an effective strategy must go beyond merely relying on antiviral medications or vaccines. He emphasizes that the strategy for treating COVID-19 should concentrate on the primary biological processes that drive the disease's inflammatory response, characterizing it as a state that encompasses thrombotic and inflammatory activities. He asserts that a combination of anti-inflammatory medications, antithrombotic agents, and therapies aimed at the ITR has resulted in a 99.83% cure rate for those afflicted with COVID-19.

Context

  • COVID-19 can cause a hyperactive immune response, known as a cytokine storm, which leads to severe inflammation and can damage organs.
  • Antithrombotic agents, including anticoagulants, help prevent or treat blood clots, which are a significant risk in severe COVID-19 cases.
  • The disease involves a complex interplay of viral replication, immune response, and coagulation pathways. Effective treatment strategies need to address all these aspects to mitigate severe disease progression.
  • The term "cure rate" in medical contexts typically refers to the percentage of patients who fully recover from a disease without long-term effects, but it is crucial to understand how "cure" is defined in this context and whether it includes long-term follow-up.

The book delves into the evolution of virus research and scrutinizes the development of biological arms within a historical framework and organizational connections.

Fleming suggests that there has been a longstanding effort to augment the potential of coronaviruses, similar to investigations carried out on various other viruses. He constructs a complex tale of conspiracy, claiming that the study was supported financially and logistically by a range of governments (including the US, China, Paris, Israel, and the UK), national and international entities, philanthropic groups, and academic institutions, including facilities at a university in the United States and virus research centers in Wuhan. He accuses certain organizations of intentionally misleading the public regarding the origin, traits, and related dangers of the virus that causes COVID-19.

Since the 1990s, studies that amplify coronaviruses through gain-of-function research have been spearheaded by scientists such as Ralph Baric and Shi Zhengli-Li.

Fleming compiles an array of academic papers and patent submissions, showing that the intensification of the harmfulness of coronaviruses can be linked to the 1990s, with significant input from individuals like Ralph Baric and Shi Zhengli-Li. The author charts the progression of their research, which began with basic observational studies and advanced to intricate experiments designed to deliberately modify the genetic makeup of coronaviruses, enhancing their infectiousness and transmissibility.

The study, financially supported by United States government bodies, entailed altering the genetic structure of coronaviruses to enhance their capacity to infect and cause harm to humans.

Fleming suggests that a considerable amount of the work focused on increasing the potency of coronaviruses may have been financed by different sectors of the US government, including agencies like the National Institutes of Health, the National Institute of Allergy and Infectious Diseases, and the Department of Defense. He supports his claim by explaining that these organizations have provided millions of dollars to researchers like Baric and Zhengli-Li for their work on coronaviruses. He argues that this monetary backing has enabled the development of advanced techniques to modify the genetic structure of these viruses, ultimately leading to the appearance of SARS-CoV-2.

Context

  • As part of the NIH, NIAID focuses on research to understand infectious diseases, including viruses like coronaviruses, to develop vaccines and treatments.
  • Scientists like Ralph Baric and Shi Zhengli have been prominent in coronavirus research, contributing to the understanding of how these viruses can jump from animals to humans.
  • The concept of enhancing viral potency is not new and has been part of virology research for decades. It has been used to study influenza, HIV, and other viruses to anticipate mutations and prepare for potential outbreaks.
  • The DoD funds research that can have dual-use applications, meaning it can be used for both civilian and military purposes. This includes research on infectious diseases that could impact military personnel.
  • In the U.S., research involving potentially dangerous pathogens is subject to oversight by various regulatory bodies to ensure safety and ethical standards are maintained.
  • Research on viruses often involves international collaboration, as pathogens do not respect borders. This can complicate the attribution of funding and the sharing of research outcomes.
  • While some researchers explore the possibility of laboratory involvement, the majority of the scientific community supports the natural origin theory, based on genetic analyses and epidemiological studies.

The theory posits that the creation of SARS-CoV-2 as a potential bioweapon may stem from a collaborative effort between Chinese and American researchers, pooling together their expertise and resources.

The writer accuses the American administration of deliberately funding the development of a biological weapon designed for warfare. He contends that the creation of SARS-CoV-2 was a deliberate maneuver aimed at destabilizing nations and their economic structures, circumventing the overt and chaotic destruction typically associated with conventional warfare. In his examination, Richard M. Fleming characterizes SARS-CoV-2 as a more advanced form of the biological weapon previously identified as SARS-CoV-1. He contends that there was a concerted global initiative to engineer a pathogen with the capability to swiftly proliferate and destabilize international economies, medical infrastructures, and the routine existence of individuals globally.

The Virology Institute situated in Wuhan is closely linked with research aimed at augmenting the potential of pathogens.

Fleming underscores the critical importance of the group led by Peter Daszak, known as the EcoHealth Alliance, in the development of SARS-CoV-2. He argues that Daszak, with his sustained connections to Shi Zhengli of the Wuhan Virology Lab, served as a conduit for channeling US government funds into studies aimed at increasing the transmissibility or deadliness of coronaviruses. Fleming criticizes Daszak's efforts to distance himself from allegations of intentional virus modification and to redirect attention toward the theory that the virus originated naturally from an animal source. He argues that Daszak, receiving significant funding from U.S. federal agencies, is heavily invested in promoting the theory that the virus originated naturally, because revealing his involvement, as well as that of his colleagues, in Gain-of-Function research could lead to a decrease in funding and possible legal repercussions.

Practical Tips

  • Volunteer with a nonprofit organization to gain firsthand experience with grant writing and funding processes. This will give you practical insight into how organizations seek and manage federal funding, which can be valuable knowledge if you're interested in the intersection of finance and public interest.

Other Perspectives

  • The phrase "closely linked" is vague and does not specify the nature or extent of the research, which could range from basic science to applied research, not all of which would involve enhancing pathogens.
  • Gain-of-Function research is a broad term that encompasses many types of studies, some of which aim to understand how viruses evolve and infect hosts, which can be critical for developing vaccines and therapeutics.
  • Peter Daszak and the EcoHealth Alliance have consistently stated that their work is focused on understanding the origins of viruses and preventing pandemics, not on enhancing the pathogenicity of viruses.
  • The scrutiny of Daszak might be influenced by geopolitical tensions and the politicization of the COVID-19 pandemic, which could skew the interpretation of his actions and statements.
  • Daszak's support for the natural origin theory could be a stance taken in the interest of public health, aiming to understand and prevent future zoonotic spillovers.
  • The implication that Daszak would face legal repercussions for Gain-of-Function research is speculative, as such research is not inherently illegal and is subject to strict oversight and regulation.
  • Transparency about research activities can build public trust and support for the scientific community, potentially leading to sustained or increased funding.

Fleming accuses certain agencies within the U.S. for continuing to fund research that seeks to enhance the virulence of pathogens, even though they recognize the risks associated with the deliberate unleashing of an engineered virus.

Individuals accountable for the development of SARS-CoV-2 with the intent of utilizing it as a biological weapon should be held liable for their detrimental actions towards humankind.

Fleming underscores the importance of conducting a thorough investigation into the origins and development of SARS-CoV-2, in addition to evaluating the level of financial support from the United States and other countries for the research that led to its appearance. He argues that those participating in these actions, such as researchers and policymakers, must face consequences for their transgressions against humankind, claiming that their conduct breached international agreements, moral standards, and statutes established by American national authorities.

Practical Tips

  • Volunteer with a public health advocacy group to contribute to the conversation on research funding. Even without a science background, you can support campaigns or initiatives that aim to ensure research funding is directed responsibly. Your involvement could range from helping with social media awareness to participating in community outreach programs.
  • You can deepen your understanding of virus tracking by using online genomic databases to observe the evolution of viruses. Websites like GISAID or NCBI offer public access to genomic data, where you can follow the changes in SARS-CoV-2 and other viruses over time. By comparing the genetic sequences from different time points, you can visualize how the virus may have developed and spread.
  • You can track policy changes and research developments by setting up Google Alerts for terms related to international agreements and moral standards. By doing so, you'll receive notifications about the latest news and reports, which will enable you to stay informed about any potential breaches or violations. For example, if you're interested in environmental policies, you could set up alerts for "Paris Agreement compliance" or "climate change policy violations."

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