Bill Gates has issued dire warnings that COVID-19 will not be the last pandemic disease to affect the world.  Given how prescient Gates has been previously in his warnings about imminent epidemics, we have decided to take this warning very seriously, anticipating COVID-20 could begin to impact the United States as early as September 2020.

Our previous research has documented that Dr. Anthony Fauci’s name appears as “inventor” on 2 U.S. patents and 2 U.S. patent applications for Glycoprotein 120, more simply known as GP120, a key component of the current COVID-19 that combines a HIV-1 attack on the human immune system with SARS-CoV-1, the pathogen from the original SARS (“Severe Acute Respiratory Syndrome”) that created an international pandemic in 2002-2003.  The pathogen in COVID-19 is named SARS-CoV-2 in medical scientific literature.

We are going to proceed on the presumption that COVID-20 will also draw on existing Fauci patents and patent applications to create SARS-CoV-3, an even more lethal virus with the potential to kill the same day the virus infects.  We stress that we have no evidence that this working hypothesis is reality, but we are confident the thought experiment will demonstrate the type of COVID-19 re-engineering that could cause death the same day a person is infected, even if that person is an adult with a healthy immune system.

In addition to the patents Fauci applied for in 2015-2016, a series of earlier patents relates his work on HIV-1 antiviral research that date from 2004-2009, dealing with the CD4 receptor.  Consider the following four patents and patent applications:

  • Publication Number: 20090285815, patent application filed March 21, 2008. Immunoconjugates Comprising CD4 and Immunoglobin Molecules for the Treatment of HIV Infection.
  • Patent Number: 7368114, granted May 6, 2008. “Fusion Protein Including of CD4”
  • Publication Number: 20040265306, patent application filed July 27, 2004. “Efficient Inhibition of HIV-1 Viral Entry Through a Novel Fusion Protein Including of CD4.”

The relevant point is that medical scientists have established that HIV binds to a CD4 receptor to enter a host cell.  “Interactions between the viral envelope gp120 [Glycoprotein 120, see previous article on Fauci patents] and the cell surface receptor CD4 are responsible for the entry of human immunodeficiency virus type 1 (HIV-1) into host cells in the vast majority of cases,” write S. Bour, R. Geleziunas, and M.A. Wainberg in an article entitled “The human immunodeficiency virus type 1 (HIV-1) into host cells in the vast majority of cases,” published in the American Society of Microbiology journal Microbiology Reviews, in March 1995.  The article’s abstract continues: “HIV-1 replication is commonly followed by the disappearance or receptor downmodulation of cell surfaces CD4.”

ACE-2 has been shown to be the receptor for SARS-CoV-2, the pathogen in COVID-19.  If COVID-19 is re-engineered to add the fusion proteins to allow COVID-20 to add CD4-fusion proteins to the GP120 already spliced into the SARS virus chassis upon which COVID-19 was engineered, the second generation combination HIV-1 plus SARS structure of COVID-20 could use the cell entry door of the CD4 receptor to penetrate host cells quickly to launch an attack on the autoimmune system that could quickly leave the human victim susceptible to a rapid development of the last stage cytokine storm syndrome.

Jin H, Hong C, Chen S, et al. in an article entitled “Consensus for prevention and management of coronavirus disease 2019 (COVID-19) for neurologists,” accepted March 31, 2020 for publication by Stroke & Vascular Neurology {2020;0. doi:10.1136/ svn-2020-000382] notes the following:

SARS-CoV-2 spike protein and HIV gp120 protein are both recognition proteins on the membrane surface, but their pathogenic mechanisms are quite different. The spike protein enables SARS-CoV-2 to identify ACE2 receptors in the mucosal epithelium and invade. However, the gp120 protein in HIV allows HIV to recognize the CD4 receptor and invade CD4+ T cells.2 There is currently no evidence indicating that SARS-CoV-2 is capable of invading T cells, any cells that express CD4 or any cells that do not express ACE2. SARS-CoV-2 does not invade cells that are not prone to infection by other known coronaviruses.

Re-engineering COVID-19 with the polypeptides needed to allow the COVID-20 to gain entry to host cells through the CD4 receptor (possibly in addition to the ACE2 receptor) could boost significantly disabling the autoimmune system to the point where even healthy adults with strong immune systems may be susceptible to infection that leads to rapid virus colonization and propagation in the pulmonary system, the prime target of COVID-19.

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 has already mutated.  In the next few months, the spread of initial COVID-20 cases could reach the level where this “mutation” has been scientifically sequenced to reveal the re-engineered mechanism needed to allow COVID-20 to enter host cells through the CD4 receptor in a manner that COVID-19 was not engineered to accomplish.