Is COVID-19 a Bioweapon?: A Scientific and Forensic investigation

CHAPTER 1

What Is Gain-of-Function Research?

Beginning in 2019, most of us became familiar with a new virus. This virus was called SARS-CoV-2 (which can cause the disease called COVID-19). For most people, this virus infected either the lungs or gastrointestinal (GI) track and resolved—or at least we thought so—but as the virus spread around the world a new sense of fear and panic engulfed the world. Amid the chaos, hospital systems became overwhelmed, people began to die from the associated InflammoThrombotic Response (ITR) precipitated by this viral infection, people and societies shut down and broke down, and economies went into a free fall. People surrendered personal freedoms in exchange for perceived security. Families and nations became sharply divided, while governments implemented executive orders replacing elected officials with administratively appointed doctrine equivalent to the Enabling Act¹ of 1933.

My involvement with SARS-CoV-2 began in January 2020. In reality, it began more than a quarter of a century before when I introduced the Inflammation and Heart Disease theory at the sixty-seventh American Heart Association Scientific Sessions in November 1994. This theory was reexplained the following year at a variety of scientific conferences around the world, eventually being published in a cardiology textbook in 1999.² Also beginning in 1999, following my discovery of misinformation promulgated by nuclear imaging isotope companies, I began development of the first quantitative method for imaging the body and measuring regional blood flow and metabolism changes. This test not only provided for reductions in the amount of nuclear imaging isotopes given to patients but made it possible to accurately, consistently, and reproducibly measure these differences in the body, allowing for differentiation of changes going on in the body—changes that would become necessary to measure this virus and its response to treatments. By 2017, I had fully developed and patented the Fleming Method for Tissue and Vascular Differentiation and Metabolism (FMTVDM).³

During January 2020, I began my work with SARS-CoV-2 by investigating what drugs—based upon published research on other viruses—might have a beneficial treatment effect on this virus, including attacking the ability of the virus to infect cells and reproduce itself, as well as stopping or at least reducing the inflammation and blood clotting (InflammoThrombotic Response) caused by the immune response to the virus in people with comorbidities.⁴

Like others, I soon realized we had entered a new era in human history, when the healthy were being quarantined and tested, medications were being denied to those who were infected or hospitalized, ventilators were being used incorrectly⁵ for the level of inflammation present in the lungs, and vaccines were being touted as the only possible solution to the virus.

Like many of you, I began to ask questions, and the answers I found lead to more questions about the ultimate motives of the people involved. For patients becoming infected and those being hospitalized, we had turned the practice of medicine and honest scientific investigation over to the government and those funded by the government, just as the German Medical Association and scientists of the day had turned it over to Adolf Hitler.⁶ Germany would later apologize for the action, but it would be too little, too late.⁷

Despite the Nuremberg Code of 1947 and the International Covenant on Civil and Political Rights (ICCPR) treaty being implemented in an effort to prevent such atrocities being committed by people upon people ever again, we find ourselves in the same situation today—unethical experiments⁸ conducted by those in power upon those not in power. When the government⁹ is involved in experimentation on its citizens, it must use a combination of fear and hope to effectively control the people and manipulate them into submission. What follows is the information about those in power and their experimentation using viruses to infect and harm people using Gain-of-Function.

THE STORY OF GAIN-OF-FUNCTION

As mentioned in the foreword, around 1999, the US Department of Health and Human Services (HHS) began funding research looking at infectious diseases. This research included looking at how such infections might become more infective. One of the original proposed premises behind this type of research, known as Gain-of-Function, was to better understand how something like a coronavirus might mutate over time. If such mutations were to occur, such investigation might allow physicians and scientists an opportunity to stay ahead of such infections. However, what began as observation soon became something altogether different. Instead of asking questions about what might happen naturally, this research become one of intentionally making those changes occur, not in small incremental steps as might occur naturally, but in larger steps that would most likely take centuries to occur—if at all.

In April 2000 while working at the Carolina Vaccine Institute at the University of North Carolina, Ralph S. Baric had already successfully used reverse genetics¹⁰ to generate a chimeric¹¹ (Gain-of-Function) coronavirus. He not only published¹² this research funded by the NIH (grant numbers AI23946, GM63228, and AI26603) but also received a patent¹³ for it in 2003:

This approach facilitates the reconstruction of genomes and chromosomes in Vitro for reintroduction into a living host, and allows the Selected mutagenesis and genetic manipulation of Sequences in Vitro prior to reassembly into a full length genome molecule for reintroduction into the same or different host. (United States Patent No. US006593111B2)

In 2002 following the SARS-CoV-1 outbreak in China, Dr. Shi Zhengli, a.k.a. Shi Zhengli-Li, and colleagues at the Wuhan Institute of Virology (WIV) began investigating how SARS-CoV-1 was transmitted.¹⁴ In particular, Zhengli was interested in how SARS-CoV-1 could be transmitted from person to person. To do this, she developed chimeric (Gain-of-Function) coronaviruses using human immunodeficiency virus-based pseudovirus¹⁵ systems with the cell lines of people, civet cats, and horseshoe bats.

In March 2004, HHS announced that it was going to create the National Science Advisory Board for Biosecurity (NSABB) to be managed by the National Institutes of Health (NIH). A press release¹⁶ issued by then Secretary of HHS Thompson states the following:

Our nation has been a world leader in life sciences research because of our emphasis on the importance of the free flow of scientific inquiry. Yet, sadly, the very same tools developed to better the health and condition of humankind can also be used for its destruction. [Emphasis added.]

In 2005, Baric published a paper—omitting unpublished research (p. 21 in Baric’s paper)—declaring he could alter the genome of coronaviruses, noting the “alteration of any part of the coronavirus genome.”¹⁷

In 2006, using chimeric (Gain-of-Function) research, Chinese scientists reported their ability to combine parts of four different viruses into a single viral genome.¹⁸ This report raises a few serious questions in my mind.

First, why were these researchers combining parts of four dangerous viruses—specifically, hepatitis C virus (HCV), human immunodeficiency virus -1 (HIV-1), SARS-CoV-1 (identified as SARS-CoV-1 and not SARSCoV), and SARS-CoV-2?

Second, if as we’ve been told, SARS-CoV-2 didn’t appear until 2019 and there were no identified naturally occurring SARS-CoV-2 reported between this 2006 publication and 2019, then doesn’t this at least in part suggest that SARS-CoV-2 is not naturally occurring but man-made?

Third, if the answer to question number two is that the virus is man-made, going as far back as 2006, then doesn’t this add credence to those who have cautioned that SARS-CoV-1 was a bioweapon and SARS-CoV-2 is an upgraded version of that bioweapon?

Finally, looking at the much-talked-about number of cycles used for polymerase chain reaction (PCR) verification of the presence of these viruses, and taking into consideration what Kary Mullis recommended for cutoffs for PCR cycles when he submitted and received his patent for PCR (see chapter 2), why were the cycles used for detection of SARS-CoV-2 set so high by the FDA?¹⁹

By 2007, the US government must have had sufficient questions about the potential for a pandemic—sufficient at least for the government to fund research to address their questions. In that year, research funded by a National Science Foundation (NSF) award IIS-0513650 and the European Commission (contract 001907) was published, addressing the critical need to shut down international travel for containment purposes should an emerging disease raise concerns about global spread—that is, a pandemic.²⁰

The questions are, why wasn’t this Dr. Anthony S. Fauci’s recommendation to President Trump when pandemic concerns were first raised, and why did it fall to a politician to make the right decision when there was published scientific research paid for by the US government to answer the question about shutting down international travel?

Concerns from the scientific community about Gain-of-Function research began to be front-page news around 2011 when Gain-of-Function H5N1 lethal Asian Influenza Virus (a.k.a. bird flu) was released from labs in the Netherlands and the University of Wisconsin.²¹ The National Institute of Allergy and Infectious Diseases (NIAID) supported the H5N1 influenza transmissible studies conducted by Dr. Yoshihiro Kawaoka at the University of Wisconsin and Dr. Ron Fouchier at Erasmus Medical Center in the Netherlands.

The Centers for Disease Control and Prevention (CDC) has admitted²² that the CDC also has been involved in Gain-of-Function research with the “highly pathogenic avian influenza A (H5N1) virus.”²³ This H5N1 research included reverse genetics and the Laboratory of Infectious Diseases, NIAID.²⁴ Genetic reassortment used in this research is the mixing of genetic material of a species into new combinations.

On April 26, 2012, Dr. Fauci testified before the Committee on Homeland Security and Governmental Affairs of the United States Senate on “Dual Use Research of Concern: Balancing Benefits and Risks” as the director for the NIAID, National Institutes of Health, US Department of Health and Human Services. He was called to address the concerns regarding the NIAID-supported H5N1 influenza transmissible studies conducted by Dr. Yoshihiro Kawaoka²⁵ at the University of Wisconsin and Dr. Ron Fouchier at Erasmus Medical Center in the Netherlands and the lethal threat posed by this Gain-of-Function research.

Dr. Fauci established early in his presentation that NIAID was involved in such Dual Use Research of Drs. Kawaoka and Fouchier, stating the H5N1 influenza transmissibility studies were “NIAID-supported.” Dual Use Research is the term used when it is understood that such research might be intended for benefit but might also be easily misapplied to do harm.

Regarding such research, there are very specific questions²⁶ researchers were asked, including the following:

Can the research be reasonably anticipated to produce one or more of the seven experimental effects/categories listed below?

1. Will an intermediate or final product of your research make a vaccine less effective or ineffective? Yes/No

2. Will the final or intermediate product of your research confer resistance to antibiotics or antivirals in ways that are inherently different than those published previously? Yes/No

3. Will your work enhance the virulence of a pathogen or render a nonpathogen virulent? Yes/No

4. Will the results of your work increase the transmissibility of any pathogen? Yes/No

5. Will your research result in alteration of the host range of a pathogen? Yes/No

6. Will your research result in a product or intermediate that that may prevent or interfere with diagnosis of infection or disease? Yes/No

7. Does your research enable “weaponization” of an agent or toxin? Yes/No

8. Even though your research did not involve any of the aforementioned seven criteria, and recognizing that your work product or results of your research could conceivably be misused, is there the potential for your results/product to be readily utilized to cause public harm? Yes/No

• If the answer is no, no further action is required, but the PI [principle investigator] should conduct an ongoing assessment to be sure this continues to be the case and must file an annual report of that assessment.

• If one or more of the seven experimental effects/ categories listed above can potentially occur, the Institutional Biosafety Committee (IBC) working with the Pl assesses if the criteria defining DURC (Dual Use Research of Concern) would potentially be met. Again if the answer is no, no further action is required, but the PI should conduct an ongoing assessment to be sure this continues to be the case and must file an annual report of that assessment.

• If the criteria defining DURC would potentially be met, the IBC working with the PI must develop and implement a risk management plan based on the risk assessment. The conduct and/or communication of the research findings must adhere to the risk management plan with ongoing oversight by the IBC with respect to DURC and in consultation with the Intramural Research’s Dual Use Committee as appropriate.

Given the specificity of these questions and the admission by Dr. Fauci acknowledging such NIAID funding—along with other federal agencies— for such Gain-of-Function research, it is hard to understand how such Dual Use Gain-of-Function research could repeatedly receive funding.

Since the development of a Gain-of-Function bioweapon is a direct violation of the Biological Weapons Convention (BWC) treaty, it is easy to understand why Senator Dr. Rand Paul and Senator John Kennedy have been so interested in questioning Dr. Fauci about the Gain-of-Function research money he has been responsible for providing to Peter Daszak. Should it be determined that a criminal investigation is required and a special prosecutor be needed, Professor David A. Clements of the University of New Mexico School of Law has offered to fill that role.

The result of this 2012 investigation into Gain-of-Function research resulted in a voluntary moratorium that lasted almost one year and ended in January 2013.²⁷

In 2014, Baric and Chinese researchers published a paper demonstrating differences between spike proteins that can infect bats and those capable of infecting people.²⁸ This research was funded by NIH grants RO1AI089728 and R21AI109094.

In October 2014, only a year after lifting the voluntary moratorium, the Obama Administration placed a ban on Gain-of-Function research²⁹ after it was discovered that the CDC had accidentally exposed workers to Anthrax and unwittingly shipped out samples of influenza virus contaminated with the deadly H5N1 virus. Meanwhile, the NIH found vials of smallpox in a storeroom: that for fifty years had been unaccounted for.

Finally, in 2015, Zhengli and Baric both announced they had “reengineered” (i.e., Gain-of-Function) the spike protein of coronaviruses so they could infect human cells:

reengineered HKU4 spike, aiming to build its capacity to mediate viral entry into human cells. To this end, we introduced two single mutations. . . . Mutations in these motifs in coronavirus spikes have demonstrated dramatic effects on viral entry into human cells. [Emphasis added.]³⁰

This research was paid for by NIH grants RO1AI089728 and RO1AI110700. Following the publication, Shi Zhengli-Li and Ralph S. Baric announced to the world, as reported by scientific journalist Matt Ridley, that they were capable of making more virulent, pathogenic viruses.³¹

Recommendations for the oversight of Gain-of-Function research were made on April 7, 2016, and approved on March 15, 2016, by the National Science Advisory Board for Biosecurity (NSABB). Included in that report on the list of ex officio members is Dr. Anthony S. Fauci (on page 102).³² Also noted in that report was Speaker/Commenter Ralph Baric, PhD (on page 68).

The Gain-of-Function ban was lifted in December 2017.³³

By 2019, the November 14, 2018, research presentation made by Zhengli at the Shanghai Jiao Tong University, entitled “Studies on Bat Coronavirus and Its Cross-Specific Infection,” was deleted from the university website.

During the summer of 2019, the Wuhan Institute of Virology genetic databank records, including its viral genomes and research, were wiped— months before the recognition of the emergence of SARS-CoV-2. On December 31, 2019, the Wuhan Municipal Health Commission report briefing on what would later be identified as SARS-CoV-2 was also deleted.³⁴

Final Thoughts on Gain-of-Function

Research scientists are a particular type of people; I know because I am one. We are driven by an insatiable desire to learn, understand, or find answers to questions we have. Sometimes those questions appear to be of no interest to others, but over the course of time, all knowledge adds together. This addition of knowledge can either be used for good purposes or for not-so-good purposes. Gain-of-Function research is one such area of research where the outcomes can be used for good or evil, depending upon the motives of those involved.

While most people believe that SARS-CoV-2 first appeared in 2019, evidence shows the virus responsible for the InflammoThrombotic disease known as COVID-19 was being manipulated two provinces from Wuhan in 2006, and the work continued forward.³⁵ Those initial genetic sequences are shown in the appendix. But as you are about to see, the research into Gain-of-Function of this and other biological agents is occurring not merely in China but also around the world—including, I would argue, unfortunately, in the United States of America—and it is being funded by our federal agencies from taxpayer dollars.

As President Eisenhower said in his farewell address (see chapter 3), we need look no further than our own backyard.

CHAPTER 2

Peter Daszak of EcoHealth, Ralph S. Baric, and Shi Zhengli-Li

When research scientists receive grants—particularly from the federal government—they are expected to demonstrate that the money has been used for the purposes for which it was intended. As a result, scientists and physicians are expected to publish the results of that research. These publications leave an indelible mark on history.

Research careers are built upon proving that the work a scientist has completed has advanced the quest for knowledge, and scientists share that information with colleagues—all to advance the sciences.

The founding fathers recognized the importance of such work and granted a US constitutional right to individuals who advance science sufficiently as to produce a new invention deemed useful to humanity. The power to grant patents to inventors falls under the legislative branch of the federal government, also known as Congress. These patents therefore provide an indelible record of what has transpired and by whom.

For these reasons, we will now look at just some of the publication and patent record evidence that SARS-CoV-2, in addition to other viruses, is the result of Gain-of-Function research, with a record in published research, patents, and, as we will see in this and the next chapter, funding.

To promote the Progress of Science and useful Arts, by securing for limited Times to Authors and Inventors the exclusive Right to their respective Writings and Discoveries

—US Constitution, Article I, Section 8, § 8.

1974: The First Known Manmade Altered Virus

To the best of my knowledge, the first¹ reported genetically altered (Gain-of-Function) virus was the Qß phage in 1974.² This Gain-of-Function research—like many of the projects that followed these investigators—was paid for by Federal NIH Research Project (ROI) grants.

1985: Baric’s Early Work with Recombination of Coronaviruses

To the best of my knowledge, Ralph Baric began working with coronaviruses found in mice back in the mid-1980s. In 1985, while at the University of California, Los Angeles (UCLA), he and colleagues at the University of Texas Health Science Center at Houston (UTHSCH) conducted research on recombinant viruses, including coronaviruses.³ This research was paid for by a variety of grants, including the National Science Foundation (PCM-4507) and US Public Health research grant (AI 19244). US Public Health is a division of the US Department of Health and Human Services (HHS).

1987: Patent granted to Dr. Kary B. Mullis for Polymerase Chain Reaction (PCR)

Patent number 4,683,195 was granted to Mullis and others for “a process for detecting the presence or absence of at least one specific nucleic acid sequence in a sample containing a nucleic acid or mixture of nucleic acids.”

A clear review of this patent shows that Mullis did not exceed fifteen to twenty cycles⁴ of PCR for the identification of genetic material.

1994: Fleming Introduces the Inflammation and Heart Disease Theory

In 1994 at the American Heart Association meetings, I first presented my Theory on Inflammation and Heart Disease. I would repeat my presentation in 1995, and, by 1999, my theory would become part of a cardiology textbook.⁵ The schematic of this theory is shown in the appendix. The theory, which explains the inflammation and thrombotic chronic diseases,⁶ would later go on to be discussed on 20/20⁷ and other programs. I published the role of many factors—including bacteria and viruses—involved in producing both inflammation and blood clotting, a process I have since referred to as InflammoThrombotic Response (ITR). It is this ITR that is responsible for COVID-19 and the deaths resulting from individuals not treated for the ITR.⁸

2000: Making DNA from RNA—Reverse Transcription: Lessons Learned from HIV

In early 2000, we know that researchers in Spain, whose work was communicated by Paul Ahlquist from the University of Wisconsin, showed how combining complementary DNA (cDNA) with nuclear expression of RNA allowed the researchers to develop a synthetic virus.⁹ Complementary DNA is a single-stranded DNA molecule that is chemically made from single-stranded RNA. To do this requires an enzyme called reverse transcriptase (RT). RT makes it possible for the cDNA to be made from the RNA. During the engineering of this infectious cDNA virus, the spike protein of the virus was replaced with the spike protein genes from another virus. The result was a chimeric (Gain-of-Function) virus that infected the gastrointestinal system of pigs. The researchers concluded this could now be used for dogs, cats, and people:

This cDNA may also be the basis for a tissue-specific expression system that may be used in four species—human, porcine, canine, and feline—by replacing the S gene included in the cDNA with that of the coronavirus infecting the target species. It is anticipated that by this procedure either fully infectious viruses or at least partially competent isolates able to express foreign genes will be generated, both being of practical interest.¹⁰

2000: Making an Infective Transmissible Virus

Following funding from NIH (Grant AI 239476), Baric and others “enhanced” a transmissible gastroenteritis virus (TGEV):

The availability of TGEV infectious constructs will obviously benefit studies of all aspects of TGEV biology and pathogenesis, including analysis of the coronavirus replicase and the somewhat controversial transcription processes which govern expression of the subgenome-length mRNAs (17, 40, 42, 43).¹¹

The infection produced by the synthetically (human) made cDNA was indistinguishable from the infectious wild-type virus, as noted by Baric:

These data indicate that viruses derived from the infectious cDNA construct had phenotypes indistinguishable from those of wild-type TGEV in swine cells. [Emphasis added.]¹²

From this research it is clear that Baric and others foresaw the potential to further manipulate/engineer DNA:

Our approach, however, may provide a means to address the function of large blocks of DNA, like pathogenesis islands, or to directly engineer chromosomes that contain large gene cassettes of interest (12).

2001: Others Demonstrate the Ability to Generate Coronaviruses Using Recombinant (Genetic) Engineering

In 2001, a group of German researchers showed that they too could produce an infectious coronavirus using a vaccinia virus.¹³ (Vaccina is a linear double-stranded DNA virus. It is the source of the modern smallpox vaccine.) These researchers not only showed that they could produce an infectious coronavirus but also that they could recover it in MRC-5 cells (a type of cells that allow researchers recovery).¹⁴

To make a recombinant organism, the gene of interest must first be isolated and removed using restriction enzymes.¹⁵ These enzymes work like “molecular scissors” to cut the DNA on both sides of the gene of interest. The DNA fragment is then ligated (joined) into the DNA of a vector.

The researchers noted the benefit of this reverse-genetics approach:

Classical approach can now be complemented by a reverse-genetic approach. Moreover, the system we describe also facilitates, in principle, the analysis of coronavirus replication, independent of the virus life-cycle and without the requirement for receptor mediated infection. Thus, it can be put to great advantage in the analysis of the virus-host cell interaction in the context of virus replication, transcription, assembly and release.

Secondly, the system we describe will complement existing methods of producing recombinant coronaviruses (Masters, 1999; Almazán et al., 2000; Yount et al., 2000) and significantly advance the analysis of coronavirus pathogenesis. With the systems now available, it should be possible to generate rapidly a large collection of genetically modified coronaviruses; for example, intra- and interspecific chimeric viruses, viruses with gene inactivations or deletions and viruses with attenuating modifications or supplementary functions. The phenotypes associated with these modifications, at least those that are not lethal, can then be tested in animal models of infection. In particular, this should provide important insights into the relationship between coronavirus infection and the immune response.

Finally, the results we present should also encourage the development of coronavirus vectors for the expression of heterologous proteins. In the long term, we believe that the expression of multiple subgenomic mRNAs in coronavirus infected cells could form the basis of a vector system that allows the expression of multiple transcriptional units, each encoding a heterologous protein. These features and the autonomy of coronavirus RNA replication could then be exploited in the development of a new class of RNA vaccine vectors. (Bredenbeek & Rice, 1992; Mandl et al., 1998)¹⁶ [Emphasis added.]

As you read through the previous paragraphs, I would recommend you pay particular attention to the words I have emphasized. They provide an interesting insight to what we have seen since 2019.

2001: Baric and Colleagues Apply for a Patent to Manipulate Genes

By May 2001, Baric and Yount filed a patent designed to allow them to control and profit from genetic manipulation of plants, animals, bacteria, and viruses—including coronaviruses. The patent was granted on July 15, 2003. This patent included research supported by US taxpayer funding.¹⁷

2003: Making a Coronavirus

In 2003, Baric and others published research¹⁸ funded by NIH grants AI23946, GM63228, and AI26603, showing they could “rescue” SARSCoV Urbani viruses by using reverse genetics.¹⁹ By taking segments of cDNA and overlapping them, they could fully clone SARS viruses. These clones were then shown to be able to infect VeroE6 cells.²⁰

When the N (the nucleocapsid) transcripts were included, greater infection occurred. When cells were not infected by this coronavirus (control cells)—no antibody staining to the virus is seen.

This same research showed that cysteine proteinase inhibitors could prevent cells from being infected. It also indicated that researchers could manipulate the genes of the virus, according to the researchers:

The current data indicate that the cysteine proteinase inhibitor E64-d may inhibit SARS virus replication at any time during infection. . . . The availability of a full-length cDNA of the SARS genome should allow for genetic manipulation of the replicase gene providing new insights into the role of specific proteolytic cleavages and replicase proteins during viral replication.²¹

The first part of this conclusion to their research clearly demonstrated an interest in further genetic manipulation of the virus. The later part is critical to understanding the ability to treat SARS-CoV-2. The targeting of this transmembrane protease serine 2 by clindamycin is one of the reasons why I chose to include this in the treatment of patients infected with SARSCoV-2, and those experiencing the InflammoThrombotic Response (ITR) known as COVID-19.²²

Not only does the nucleocapsid (N) structural protein of SARS viruses appear to play a significant role in increasing infectivity, but also, for SARSCoV-2, it has been shown to insert (reverse transcribe) its genetic sequence into the human DNA—once again funded by NIH grants (1U19AI131135-01, 5R01MH104610-21). This reverse transcription (RT) has since been shown to occur in all but three of the twenty-three pairs of human chromosomes.²³

2006: Chimeric (Gain-of-Function) cDNA made from HCV, HIV-1, SARS-CoV-1, and SARS-CoV-2

In 2006, Chinese researchers spliced four target cDNA segments together to form a single 1,200-nucleotide-long RNA sequence.²⁴ This chimeric (Gain-of-Function) sequence included combining hepatitis C virus (HCV), human immunodeficiency virus – 1 (HIV-1), SARS-CoV-1, and SARSCoV-2. This genetic sequence is shown in the appendix. This research was funded by the Fujian²⁵ government (Grant number 2003Y004).

2007: SARS-CoV (SARS-CoV-1) Genome²⁶ Patent Assigned to US Department of Health & Human Services

In May 2007, a patent was granted for isolation of human SARS-CoV-1.²⁷ The assignee—the party that would profit financially from the patent—was the US Department of Health and Human Services (HHS). This isolation not only genetically identified the virus but also established the polymerase chain reaction (PCR) test to find SARS-CoV-1. In April 2020, the FDA issued an umbrella Emergency Use Authorization (EUA) for PCR testing of SARS-CoV-2.²⁸

2007: Research Shows Insertions Placed in Spike Proteins Makes It Possible for SARS-CoV to Infect Human Cells

Research published by Dr. Zhengli and researchers at the Australian Animal Health Laboratory looked at SARS-like coronaviruses (SL-CoVs) found in horseshoe bats and SARS-associated coronavirus (SARS-CoV).²⁹ While they found a significant amount of similar genetic material, they also discovered that SL-CoVs could not bind to human ACE2 receptors. Zhengli and the other scientists discovered that the SL-CoV spike protein was unable to use ACE2 receptors to infect human cells. However, if they inserted amino acids not naturally found in these viruses, at the N-terminal domain through Gain-of-Function (chimeric) manipulation, they discovered they could produce viruses able to infect human cells.

2010: Shi Zhengli-Li Conducts Chimeric Experiments Showing SARS-CoV Spike Protein Unable to Bind to ACE2 Human Cell Receptors

In 2010, Shi Zhengli conducted chimeric research on SARS-CoV-1 (then called SARS-CoV), including combining HIV-pseudovirus to look at the binding capacity of this virus with human ACE2 receptors.³⁰ Their work specifically included altering (through mutagenesis) the spike proteins to determine how to increase the spike protein binding to the ACE2 receptor.

The research showed no proline-arginine-arginine-alanine (PRRA)³¹ insert critical to the binding of the SARS-CoV-2 to ACE2 receptors on human cells. As noted in this published research (jointly done by Dr. Zhengli at the Wuhan Institute of Virology, researchers in Australia, and the University of Minnesota Medical School), not only is the spike protein from horseshoe bats unable to bind to ACE2 receptors, but also these differences along with differences in civets³² highlight a critical missing piece to the zoonotic theory of the original of SARS-CoV-2:

However, although the genetically related SARS-like coronavirus (SL-CoV) has been identified in horseshoe bats of the genus Rhinolophus [5, 8, 12, 18], its spike protein was not able to use the human ACE2 (hACE2) protein as a receptor. Close examination of the crystal structure of human SARS-CoV RBD complexed with hACE2 suggests that truncations in the receptor-binding motif (RBM) region of SL-CoV spike protein abolish its hACE2-binding ability [7, 10], and hence the SL-CoV found recently in horseshoe bats is unlikely to be the direct ancestor of human SARS-CoV.

Also, it has been shown that the human SARS-CoV spike protein and its closely related civet SARS-CoV spike protein were not able to use a horseshoe bat (R. pearsoni) ACE2 as a receptor [13], highlighting a critical missing link in the bat-to-civet/human transmission chain of SARSCoV. [Emphasis added.]

2013: SARS-CoV Associated with Lethal Blood Clotting in the Lungs

Baric and people working with him discovered in 2013 that SARSCoV—in research funded by NIAID, NIH, the National Center for Advancing Translational Sciences (NIH/NCATS), and HHS (grants HHSN272200800060C; 5UL1RR024140)—had four critical genes that were expressed following SARS-CoV infections:

The results of these studies demonstrate that a fine balance exists between host coagulation and fibrinolysin pathways regulating pathological disease outcomes, including diffuse alveolar damage and acute lung injury, following infection with highly pathogenic respiratory viruses, such as SARS-CoV.³³

They went on to show that this was critical to infection and lung damage:

The urokinase pathway had a significant effect on both lung pathology and overall SARS-CoV pathogenesis.

As the lung tissue slides from the research showed, the larger the viral load (greater infection), the greater the damage to the lungs with fibrin (blood clotting).³⁴

2014: Baric Applies for an International Patent to Alter the Spike Protein of Coronaviruses

In March 2014, Professor Baric applied for an international patent for the Methods and Compositions for Chimeric (Gain-of-Function) Coronavirus Spike Proteins. As noted in the next figure, this invention (patent) was made with the support of NIH Grant U54AI057157, which further demonstrated that the US federal government was funding Gain-of-Function research of the coronavirus spike protein.

August 2014: Baric Uncovers TMPRSS2³⁵ Link to Infectivity of MERS

In August 2014, while investigating Middle East Respiratory Syndrome coronavirus (MERS-CoV or MERS), Baric and other researchers from Shanghai University and the University of Minnesota compared MERS with two closely related coronaviruses known as HKU4 and HKU5. Despite some similarities, Baric and others showed that the spike proteins of HKU4 and HKU5³⁶ do not attach to and infect human cells. However, MERS spike protein specifically attaches to a cellular receptor found in humans known as dipeptidyl peptidase 4 (DPP4).³⁷

DPP4 is also known as adenosine deaminase complexing protein 2 or cluster of differentiation 26 (CD26). Stimulating DPP4 results in an immune response and the release of inflammatory cytokines.³⁸ Like the ACE2 receptor gene, DPP4 is also found on the X-chromosome, further explaining some of the differences between men and women in SARSCoV-2 infections.³⁹

The failure of MERS to bind to ACE2 receptors was confirmed by Chinese researchers in 2020.⁴⁰ That leads us to information provided by Dr. Li Meng Yan, namely that SARS-CoV-1⁴¹ was a genetically modified (Gain-of-Function) virus that was also a bioweapon developed by the Chinese Communist Party (CCP), with SARS-CoV-2 being the upgraded version of this bioweapon.⁴²

2015: Baric and Zhengli-Li Combine the Backbone of One Virus and the Spike Protein of Another

In June of 2015, both Shi Zhengli-Li and Ralph S. Baric—who had received funding from Peter Daszak of EcoHealth Alliance, along with NIH funding (reviewed and approved)—announced they had used reverse genetics⁴³ to generate a chimeric (formed from parts of various animals) virus:

Using the SARS-CoV reverse genetics system, we generated and characterized a chimeric virus expressing the spike of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone.⁴⁴

And according to Baric:

This virus is highly pathogenic, and treatments developed against the original SARS virus in 2002 and the ZMapp drugs used to fight Ebola fail to neutralize and control this particular virus.⁴⁵

While the original publication acknowledged funding for this research from NIH, NIAID⁴⁶ and the National Natural Science Foundation of China, and researchers from the Wuhan Institute of Virology, the University of North Carolina, and the University of Texas Medical Branch, the original publication by Baric and others failed to disclose the funding they received from Peter Daszak’s EcoHealth Alliance, the United States Agency for International Development (USAID), and the US Central Intelligence Agency (CIA). On November 20, 2015, this omission was corrected and Nature Medicine posted a corrigendum⁴⁷ (correction with additional information) showing that the funding for this research came from USAID and the CIA:

In the version of this article initially published online, the authors omitted to acknowledge a funding source, USAID-EPT-PREDICT funding from EcoHealth Alliance, to Z.-L.S. The error has been corrected for the print, PDF and HTML versions of this article.⁴⁸

The supplementary⁴⁹ material to this research published by Zhengli-Li and Baric shows that the spike protein of the SHC014-CoV (SL-COV)⁵⁰ virus that infects horseshoe bats was combined with the backbone of SARS-CoV mouse adapted (MA15) backbone. In addition to combining the spike protein from one virus with the backbone of another virus, Baric and Zhengli-Li inserted (changed) four nucleotides in Open Reading Frame 1a (ORD1a) and Open Reading Frame 1b (ORF1b) of the viral genome.

These nucleotide changes are shown in the following figure.⁵¹ These insertions change the replication proteins required to make this chimeric (Gain-of-Function) virus. A fifth nucleotide change is found at position 26428 in the Envelope Protein,⁵² a change found to be important for the SARS-CoV-2 virus to cross the blood-brain barrier, after which the virus can infect and damage the brain.

The research—as noted in the next figure—was funded by the NIAID, NIH, USAID, and EcoHealth Alliance. It specifically states that this Gain-of-Function (GOF) research was reviewed and approved by the NIH and shows funding for both Baric (R.S.B.) and Zhengli-Li Shi (Z.-L.S.).

In the abstract of this published research, Zhengli-Li and Baric specifically state they have produced a Gain-of-Function (chimeric) virus:

Using the SARS-CoV reverse genetics system, we generated and characterized a chimeric virus expressing the spike of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone.⁵³

Zhengli and Baric then go on to state:

Additionally, in vivo experiments demonstrate replication of the chimeric virus in mouse lung with notable pathogenesis. Evaluation of available SARS-based immune-therapeutic and prophylactic modalities revealed poor efficacy; both monoclonal antibody and vaccine approaches failed to neutralize and protect from infection with CoVs using the novel spike protein. On the basis of these findings, we synthetically re-derived an infectious full-length SHC014 recombinant virus and demonstrate robust viral replication both in vitro and in vivo.

In the end, the authors (Baric and Zhengli-Li) concluded they had built a more pathogenic virus:

Thus, relative to the Urbani spike–MA15 CoV, SHC014-MA15 shows a gain in pathogenesis (Fig. 1). On the basis of these findings, scientific review panels may deem similar studies building chimeric viruses based on circulating strains too risky to pursue, as increased pathogenicity in mammalian models cannot be excluded. Coupled with restrictions on mouse-adapted strains and the development of monoclonal antibodies using escape mutants, research into CoV emergence and therapeutic efficacy may be severely limited moving forward. Together, these data and restrictions represent a crossroads of GOF research concerns; the potential to prepare for and mitigate future outbreaks must be weighed against the risk of creating more dangerous pathogens.⁵⁴ [Emphasis added.]

Their chimeric (Gain-of-Function) virus was able “to replicate in human airway cultures, cause pathogenesis . . . and escape current therapeutics.” In the end, the researchers appeared to be more concerned about what limitations this might pose on future research they wanted to do than the potential harm they might do to mankind.

Many people over the years have decided they knew what was best for humanity. Bill Gates has commented on more than one occasion that the use of clustered regularly interspaced short palindromic repeats (CRISPR) technology would make it possible to “eliminate undesirable genes” and “potentially swap in preferable alternatives”⁵⁵—a concept held by others in history, including Dr. Joseph Mengele:

Like all doctors in 1930s Germany, Mengele came under Hitler’s concept of German medicine that departed from the traditional caregiving role, Marwell explains. The physician’s first responsibility was to the nation, not individual patients. As part of the Führer’s weltanschauung, doctors were “biological soldiers,” committed to ensuring Germany’s glorious destiny by “cleansing” the population of “inferior” genetic material.⁵⁶

This perspective seems to permeate today’s society.

September 2015: Zhengli and Baric Reengineer (Gain-of-Function) the HKU4 Spike Protein of MERS to Increase Infectivity in Humans

While simultaneously introducing the spike protein of SHC014 into the backbone of MA15 CoV and adding in five nucleotide Gain-of-Function substitutions, Zhengli and Baric were working to make Gain-of-Function changes in the spike protein of HKU4, also known as Tylonycteris bat coronavirus HKU4.⁵⁷ As already discussed, HKU4 does not infect human cells. By the end of this research, Baric and Zhengli had taken a virus that could not infect human cells and turned it into a virus that could and did:

To evaluate the potential genetic changes required for HKU4 to infect human cells, we reengineered HKU4 spike, aiming to build its capacity to mediate viral entry into human cells. To this end, we introduced two single mutations, S746R and N762A, into HKU4 spike. . . . Moreover, mutations in these motifs in coronavirus spikes have demonstrated dramatic effects on viral entry into human cells.

Baric and Zhengli continued:

HKU4 pseudoviruses bearing either the reengineered hPPC motif or the reengineered hECP motif were able to enter human cells, whereas HKU4 pseudoviruses bearing both of the reengineered human protease motifs entered human cells. . . . The two mutations adaptive to human cellular proteases transformed MERS-CoV spike from completely lacking to fully possessing the capacity to mediate viral entry into human cells .⁵⁸ [Emphasis added.]

This Gain-of-Function research turning a noninfectious coronavirus into an infective one and was paid for by NIH Grants RO1AI089728 and RO1AI110700.

Despite this evidence and the money funneled to Peter Daszak at EcoHealth Alliance, Peter Daszak led an intentional and knowing effort, along with other scientists, to divert attention from the lab origins of SARSCoV-2 and Gain-of-Function research. This effort went so far as to recruit other scientists in the world to join with him in March 2020⁵⁹ to denounce a laboratory origin—insisting that the scientific community support Daszak and others in a zoonotic⁶⁰ origin of this bioweapon. Daszak concluded their “statement” by stating, “We declare no competing interests.”

When the World Health Organization (WHO) sent a team of “experts” to the Wuhan Institute of Virology (WIV) in January 2021, Peter Daszak, who was the only American on the team and headed it, convinced the remainder of the team that the missing WIV data was “irrelevant.”⁶¹

In an effort to demonstrate my disapproval and to protest the ever-deteriorating objectivity of our scientific journals, I resigned from Lancet as an external clinical reviewer in 2020 after almost two decades.

One cannot help but be struck by the significant amount of information in the published literature showing the source of funding for these Gain-of-Function research projects and those involved in conducting the experiments. One also cannot remain incognizant of the Gain-of-Function research carried out on the spike protein of coronaviruses and SARS-CoV-2 and the efforts to retroactively attempt to cover the source of that funding.⁶²

CHAPTER 3

The Paper Trail of the US Funding for Gain-of-Function Research

In President Dwight D. Eisenhower’s farewell speech to the nation, he warned of a great threat to the United States posed by the military-industrial complex:

In the councils of government we must guard against the acquisition of unwarranted influence . . . by the military-industrial complex. The potential for the disastrous rise of misplaced power exists and will persist.

We must never let the weight of this combination endanger our liberties or democratic processes. We should take nothing for granted.

We must be alert to the equal and opposite danger that public policy could, itself, become the captive of a scientific-technological elite.¹

If you do not think the United States federal government has a track record of conducting unauthorized, nonconsenting research upon its citizens and military, then you have not been looking at the record. It has a record of atrocities² and of hiding the truth.³

By October 2014 the US government had issued a policy statement regarding Gain-of-Function research, including the following restrictions:

“New [US government] funding will not be released for gain-of-function research projects that may be reasonably anticipated to confer attributes to influenza, MERS, or SARS viruses such that the virus would have enhanced pathogenicity and/or transmissibility in mammals via the respiratory route. The research funding pause would not apply to characterization or testing of naturally occurring influenza, MERS, and SARS viruses, unless the tests are reasonably anticipated to increase transmissibility and/or pathogenicity.⁴

However, in a footnote to the policy statement, the federal government also decided that this moratorium on Gain-of-Function did not apply if the federal government considered the research was “urgent” for “public health or national security.”⁵ That’s an interesting statement, given the Department of Defense (DoD) was funding Gain-of-Funding research—including providing funding and a policy advisor to Peter Daszak at EcoHealth:

An exception from the research pause may be obtained if the head of the USG [US government] funding agency determines that the research is urgently necessary to protect the public health or national security.

In the previous chapter, we looked at some of the published Gain-of-Function research carried out by Ralph S. Baric and Shi Zhengli-Li. In those papers, we were able to put together the publication paper trail showing how these and other researchers affiliated with Baric, Zhengli, and Peter Daszak of EcoHealth meticulously worked on changing coronaviruses to make them more infective and harmful to humans.

These and other researchers received funding from a variety of US federal agencies, including the Department of Defense, Health and Human Services, National Science Foundation, US Agency for International Development, Homeland Security, Department of Commerce, Department of Agriculture, and Department of the Interior, in addition to receiving funding from the Helmsley, Rockefeller, and Gates Foundations—all intertwined with Jeffrey Epstein, as seen in the published papers and grants shown in this book.

In this chapter, we are going to lay to rest any question regarding the funding of these individuals for Gain-of-Function research by the US federal government. What follows is some of that money trail beginning with a report published on the UCLA Department of Epidemiology School of Public Health website in February 2002, entitled War on Health:

Diseases arising from camp life, social disruption and unhygienic field hospitals have killed far more soldiers than has battle.

That is the cheerful implication of the otherwise ominous fact that President Bush’s budget asks Congress to more than quadruple spending—from $1.4 billion to $5.9 billion—on bioterrorism. Last week Defense Secretary Donald Rumsfeld was unspecific in saying “it is likely” terrorist attacks “will grow vastly more deadly” than those of Sept. 11. But budgets often make government’s thinking clear, and the bioterrorism money may imply Rumsfeld’s meaning.

Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, says this infusion of money will accelerate our understanding of the biology and pathogenesis of microbes that can be used in attacks, and the biology of the microbes’ hosts—human beings and their immune systems. One result should be more effective vaccines with less toxicity. [Emphasis added.]⁶

From this report, it is clear that the US federal government, including Donald Rumsfeld and Anthony Fauci, have decided to spend massive amounts of money on bioterrorism:

SOME OF THE MONEY FROM THE DEPARTMENT OF DEFENSE (DOD)⁷

As you look through the following information you will notice that EcoHealth received more than the $19.7 million shown in the previous graphic. This represents only half of the $38,949,941 it actually received from the Department of Defense. The funding goes way beyond merely working on Gain-of-Function for SARS-CoV-2. This funding pays for work on a number of other viruses, raising serious concerns about new pandemics resulting from Gain-of-Function research.

As you look through most of these documents, the source and purpose of the funding, the award identification number, and the amount, you will notice a frequent recurring type of program funding—weapons of mass destruction.

Nothing speaks more clearly about this research and violation of the Biological Weapons Convention (BWC) treaty than the use of terms like weapons of mass destruction, and nothing says biological weapon more than funding from the Department of Defense (DOD)—which doesn’t work with the Girl Scouts.

You will see that this funding is not just for coronaviruses but also for a number of other potentially dangerous viruses. As the government track record clearly demonstrates, the research and Gain-of-Function manipulation have involved more than one type of virus. Because of the harm caused by SARS-CoV-2, the release of other virulent viruses like H5N1— the highly pathogenic Asian avian influenza virus—the Gain-of-Function research discussed in chapter 1, and the smallpox and anthrax fiascos, we need to view the following Gain-of-Function research funding with a new-found perspective.

What new pandemic now awaits humanity given this Gain-of-Function funding by the US federal government—and other governments, corporations, and individuals—including SARS-CoV-2 and other viruses, bacteria, and biologic pathogenic agents?