December 19, 2021

When Joseph Tritto wrote his work early in the pandemic about COVID-19, Cina COVID-19, he quoted an UK virologist who wished to remain anonymous. This virologist stated that, once infected with COVID-19, the virus would never let its victim go, even if it didn’t kill upon initial infection.

That statement, which I had read elsewhere in February of 2020, has been one of the forces driving my search for what SARS-CoV-2 actually is.

First and foremost. BEFORE SARS THERE WERE NO KNOWN BAT CORONAVIRUSES THAT USED ACE2 FOR CELLULAR ENTRY. None. Not one. None of them used ACE2. Not for entering a single cell.

Secondly, bat viruses which have previously spilled over to human populations have been incredibly VIRULENT. But not SARS or SARS-CoV-2. Nothing like Nipah or Ebola or Marburg. Yet, bat viruses are perhaps THE BEST at spreading RAPIDLY in humans. Their virulence is testament to how difficult it is for our human immune systems to deal with bat viruses. Next. Let’s look at ACE2. As I have previously stated, and as I summarize (even this is only a partial summary) in the graphic, ACE2 is the foundation upon which virtually all diseases of old age are modulated. Remove ACE2 – and you are suddenly, biologically speaking, in your 90s.

It has already been observed that ACE2 autoantibodies develop after SARS-CoV-2 infection. This has been attributed to the abundance of antibodies that recognize the SARS- CoV-2 RBD (Spike Protein) and ACE2 protein in plasma or serum.

Also, it has been theorized that some of the Ab2 binding regions, or paratopes, can also mirror the spike protein itself and bind to the same target as the spike protein, the ACE2 receptor.

I cannot stress the importance of this. I also cannot express the utmost urgency to test those who have received Spike Protein therapies and the recovered for the presence of ACE2 Autoantibodies.

To me, this is too delicately horrific to have “evolved.”

Referenced/Related Papers

Bats’ immune defenses may be why their viruses can be so deadly to people

Development of ACE2 autoantibodies after SARS-CoV-2 infection

A Possible Role for Anti-idiotype Antibodies in SARS-CoV-2 Infection and Vaccination