Coup de Grâce
By Jerome R. Corsi, PhD
In the first article, we referenced the list of patents Fauci has been awarded as well as applied for, arguing that important components of the HIV-1 virus attacking the immune system show up in patents naming Fauci as one of the inventors.
In that first article, we noted that a glycoprotein found in the HIV-1 virus, identified as Glycoprotein 120, or simply as GP120, has also been found to be a key component of the spikes in the current COVID-19 to produce this new disease virus that appears to combine a HIV-1 attack on the human immune system, with SARS CoV-1, the pathogen from the original SARS (“Severe Acute Respiratory System”) that created an international pandemic in 2002-2003.
In the second article, we documented that Fauci’s name also appears on patents involving the C4 receptor. HIV-1 binds to healthy cells through the CD4 receptor while COVID-19 enters healthy cells through the ACE2 receptor, producing SARS-CoV-2 pathogen. We hypothesized that by re-engineering COVID-19 to allow the SARS-CoV-2 pathogen through the CD4 receptors, COVID-20 would have a new SARS-CoV-3 pathogen that would enter the body faster, producing a virulent attack on the immune system to accompany the SARS attack on the lungs that would follow.
Here we hypothesize COVID-20 re-engineering will be complete when a third element from HIV-1 research leading to patents bearing Fauci’s name will be added: namely an attack involving the mechanism whereby integrin α4β7 is incorporated into the envelope of HIV-1 virions that becomes functionally active as it binds with MAdCAM-1 allowing the HIV-1 pathogen enters the body through the high endothelial venules in the intestinal mucosa.
Put simply, COVID-20 will boost the virulence of the HIV-1 attack component of COVID-20 by introducing a swift and effective attack on the immune system through the intestines, effectively knocking out the body’s immune system to permit the SARS pathogen to colonize more rapidly in its move to propagate within the lungs.
In addition to the patents Fauci applied for and/or received as discussed in previous articles, please consider the following:
– Patent Number: 9896509, granted February 20, 2008. “Use of antagonists of the interaction between HIV GP120 and α4β7 integrin.”
A key article was published in Science Immunology, May 12, 2017, Vol. 2, Issue 11, entitled “Virion incorporation of integrin α4β7 facilitates HIV-1 infection and intestinal homing,” authored by a group of scientists led by Dr. Christina Guzzo, Viral Pathogenesis Section, Laboratory of Immunology (LIR), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD.
The abstract of that article began with this sentence: “The intestinal mucosa is a key anatomical site for HIV-1 replication and CD4 T-cell depletion. “
The abstract continued:
Here, we show that integrin α4β7 is efficiently incorporated into the envelope of HIV-1 virions. Incorporated α4β7 is functionally active as it binds MAdCAM-1, promoting HIV-1 capture by and infection of MAdCAM-expressing cells, which in turn mediate trans-infection of bystander cells. Functional α4β7 is present in circulating virions from HIV-infected patients and SIV-infected macaques, with peak levels during the early stages of infection. In vivo homing experiments documented selective and specific uptake of α4β7+ HIV-1 virions by high endothelial venules in the intestinal mucosa.
The introduction began with the following:
Although human immunodeficiency virus type-1 (HIV-1) establishes a life-long infection that progresses to overt disease over the course of several years or even decades, the early events of virus-host interaction are critical in determining the pace of disease progression. A key anatomical site for virus replication and pathogenesis during primary HIV-1 infection is the gut-associated lymphoid tissue, which is believed to provide the largest reservoir in the body of CD4+ T lymphocytes, the primary target cells for HIV-1 replication
Accordingly, the principal gut-homing integrin, α4β7, has been identified as an additional cellular receptor for HIV-1 and is emerging as a critical molecule in the pathogenesis of HIV-1 disease. Expression of α4β7 on T cells promotes their trafficking to the gut via interaction with MAdCAM-1, which is expressed at high levels on high endothelial venules (HEV) in the intestinal Peyer’s patches, lamina propria and mesenteric lymph nodes, as well as on follicular dendritic cells (DCs) in the gut mucosa. Intestinal DCs play a critical role in the recruitment and retention of T cells into the gut compartment through the production of retinoic acid (RA), a vitamin A metabolite that induces α4β7 expression, thereby imprinting a gut-homing phenotype on these cells.
While there is no way to know at this point whether or not this hypothetical reengineering of COVID-20 has occurred, we suspect the first news may have been signaled in reports that COVID-19 is rapidly mutating. If COVID-20 has been created and already released, we anticipate the newly re-engineered virus could hit the United States as early as September 2020, some four months hence from the drafting of this article.
If COVID-20 were to be re-engineered in the fashion described in these three articles, we believe COVID-20 would be faster acting and more lethal that COVID-19, with the ability to infect and cause mortality among even younger adults with relatively healthy immune systems. Those experiencing comorbidity conditions and the elderly would be particularly vulnerable. We can even imagine that some of those with weaker immune systems could be infected and die within a relatively short period of time. With the immune system impaired by the HIV-1 attack, the SARS-like pulmonary attack could colonize and propagate in the lungs with significantly reduced resistance.