OF BATS, CORONAVIRUSES AND EXTREME HUMAN (INFLAMM)AGING

Why Bat Coronaviruses are Human Neutron Bombs

July 2, 2022

The world has been involved in heated and virulent (pun intended) debate over the origins of SARS-CoV-2. There have been scientists involved in explaining with great detail how this virus MUST be from a lab, and then there have been “scientists” that will defend to the death, and in the face of overwhelming evidence, that the virus has “naturally” evolved.

Regardless of where one stands (I don’t see how there are any options) with regards to the origins of the virus, one thing is absolutely certain. The United States has been funding gain of function research on Bat Coronaviruses both domestically and (when it became illegal to do so here) at the Wuhan Institute of Virology and other international locations.

Yet, nobody seems to have asked a very fundamental question: WHY is it that BAT coronaviruses have been targeted for such extreme study and manipulation?

The answer is found in the bat’s immune response to this type of virus.

NLR family pyrin domain containing 3 (NLRP3) is an important sensor that recognizes both cellular stresses (such as extracellular adenosine triphosphate (ATP), mitochondrial damage and oxidized DNA) and viral or bacterial infections. NLRP3-mediated inflammation has been causally linked to aging and multiple age-related chronic diseases. Over-activation of the NLRP3 inflammasome has been linked to a hyper-inflammatory state and immunopathology in viral infection with MINIMAL EFFECT ON THE VIRAL LOAD.

If we analyze NLRP3 inflammasome activation in humans and bats in (peripheral blood mononuclear cells) PBMCs, primed with LPS for 3 h, with or without stimulation by ATP or nigericin for 30 min, we notice a MASSIVE difference in the activation of this inflammasome within humans.

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What is most disturbing is that when exposed to MERS-CoV, humans have massive NLRP3 activation and ASTRONOMICAL levels of IL-1B, one of the most consistently upregulated cytokines in cachexia and other aging-related diseases.

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What I find fascinating, and hopeful, is that when human cells are primed with MCC950, THE NLRP3 INFLAMMASOME ACTIVATION AND IL-1B LEVELS ARE NOT SIGNIFICANT!!!

Why is MCC950 so important?

MCC950 significantly suppressed release of proinflammatory cytokines IL-1β, IL-18, IL1-α, IFNγ, TNF-α, IL6, IL17, chemokine MIP1a and Nitric Oxide in colonic explants.

Why has this therapeutic not been trialed in COVID-19 treatment?

Back to the depopulation and GOF game being played.

If a bat virus can induce such a massive amount of inflammaging age acceleration, how do you get it into humans?

YOU CREATE A SPIKE THAT HAS A PIT BULL ATTACK AFFINITY TO ACE-2!!!!!

Referenced/Related Papers

Dampened NLRP3-mediated inflammation in bats and implications for a special viral reservoir host
https://www.nature.com/articles/s41564-019-0371-3

The interplay of immunology and cachexia in infection and cancer
https://www.nature.com/articles/s41577-021-00624-w

MCC950, a specific small molecule inhibitor of NLRP3 inflammasome attenuates colonic inflammation in spontaneous colitis mice
https://www.nature.com/articles/s41598-018-26775-w