Watch the Snake Water
How venom was found in COVID and ended up on the kitchen table. An analysis and where it fits.
If you have been sorting through channels seeking the latest research on COVID, you have probably come across an interview by Stew Peters with Dr. Brian Artis titled “Watch The Water” recently. This has spurred a number of “conspirasee theereeze” on how snake venom is in Covid, and ending up in our drinking water.
I will be focusing on the specific snake venom genes, where they are located in Covid, and how a doctor may come to this conclusion, but first want to note the correlation the doctor makes to Remdesivir and how that drug operates similarly to the snake venom as well. Its use in a clinical setting has proven to be “problematic” at best and criminal in reality.
With the wide ranging scope of the interview I was left with the question, “Where did this guy get his info on how snake venom was in COVID?”, and tracked down the study out of Arizona State he referred to titled:
COVID-19 and Cholinergic Anti-inflammatory Pathway: In silico Identification of an Interaction between α7 Nicotinic Acetylcholine Receptor and the Cryptic Epitopes of SARS-CoV and SARS-CoV-2 Spike Glycoproteins
If you have no clue what that means, no worries, neither did I… 😂
The first thing to notice is the call to a7 nAChRs, the Nicotinic Cholinergic System (NCS), and their regulation by the Vagus nerve. Up to this point spike protein interaction has been exclusively within the domain of ACE2 receptors, so to suggest a completely different pathway upends most of the current research, but may still be relevant to Covid’s pathophysiology.
In Silico (i.e. Computer Algorithm), the authors found a “toxin-like” epitope, with homology (similarity) to a sequence of snake venom toxin that coincides with CR3022 and COVA1-16 antibodies. These antibodies do NOT interact with ACE2 nor inhibit infections (which may explain their lack of study).
Location of the peptide/amino acid(aa)/protein/gene sequences becomes relevant in finding where interactions may occur. The “Spike Glycoprotein” of Covid19 has THE MOST interaction with the human body and is one of, if not THE MOST studied protein sequences in all of human history. Spike, and its S1/S2 subdomains are pharmacology’s foundation for the therapeutic benefit of vaccine immunogenicity, upon which all “mandates” have been issued.
The association with specific antibodies provides precedent by which to observe their character, nature, and biomechanisms. Focus on the Receptor Binding Domain (RBD) of Spike’s S1 subdomain in an “open” and “closed” position was conducted to determine their interactivity with the nAChR alpha subunit (mainly aa 189-192) extracellular domain (ECD). ECD is the specific “binding domain” where the receptor interacts with another protein, like the end of RBD is known to attach to ACE2.
Current understanding of how Covid damages the body relies on RBD in an open/up position, binding to ACE2. RBD does NOT BIND to ACE2 when in a closed position, so the general thought is that S1/RBD is “benign” in a closed/down position. For this reason alone it would appear easy to discount any suggestion a closed S1/RBD has the potential for pathogenicity, and many, it seems, have not even thought to look…🤔
What do they mean by "venom-like" homolog anyway?🤷♂️
Now that we understand the experiment as being a study of how the S1/RBD interacts with NCS receptors in both an open and closed position, let’s get into “Cryptic Epitopes”.
Cryptic in this sense means “currently unknown”. The epitope is the specific piece of the antigen to which an antibody binds. Antigens are any protein sequence capable of binding to an antibody. Hence Cryptic Epitopes are pieces of the RBD protein that bind to antibodies. Viewing the terrain of the body with antibodies as a baseline, the authors zeroed in on conformational changes those antibodies are associated with.
They found this “toxin-like” fragment, containing an amphipathic sequence of alternating polar and hydrophobic amino acid residues with selectively charged amino acids in a conserved order, lies on the spike protein surface and is NOT buried in the domain core. Neighboring the ACE2 binding motif, this entity may interact with the human α7 nAChRs in a manner similar to neurotoxins. Meaning this NL1 homolog sequence may interact with α7 of the NCS when RBD is in a closed/down position. No Bueno. 😬
I have not reviewed any In Vitro or In Vivo studies, and welcome any links or suggestions to extensions of this research. With an understanding of the background and implications of the study, it provides a compelling lens as to how someone may say that Covid is “snake venom”. However, it is important to keep in mind it was never stated that Covid is ONLY snake venom.
Allusions to water monitoring for future infectious outbreaks by the CDC, begs the question as to what peptides they are testing for? The presence of spike protein in the food chain is going to be endemic for a while, especially with people reupping their bodies with a fresh dose of spike mRNA formula every 4 to 6 months… 🤦♂️
In addition to the extracellular interactions with the NCS this NL1 homolog may have, what happens intracellularly when this compound is produced in ribosomes via mRNA injection? 🤷♂️
How is it possible to introduce the production of a spike protein, with elements that cause dysfunction of the cholinergic anti-inflammatory pathway, resulting in cytokine storm and failure for the immune response to return to homeostasis, as a therapeutic? 🤷♂️
These are all great questions that should have been answered before someone wrote an article about research conducted last year as a result of a viral conspiracy video to explain the research behind how someone could come up with them, yes? 🤣
I will admit my bias upon first being presented with the notion of “Covid Snake Venom” was to discount it due to my understanding of the inflammatory and fibrinogenic response due to S1/RBD attaching to the ACE2 receptor. However, upon reviewing this article I can see how this specific sequence may be involved in cytokine storm.
NL1 homolog is exposed to a7 NCS receptor while RBD is in closed position. However, the sequence may have additional means of exposure when S1 is separated from S2 by TMPRSS2 at the Spike Furin Cleavage Site (FCS). When S1 is separated from the rest of the virus it means the NL1 sequence no longer has to rely on a “closed/down” position as the frame of reference to be open or closed to is gone…
This implication is also present for all vaccines whose therapeutic target is the production of the spike S1 subdomain.
The only thing that remains to be seen is if the computer models and subsequent confirmation of the author’s hypothesis In Silico bares itself as true in reality. It is easier to discount something at first glance than to dig into the implications of its possibility. Hopefully this article helped to “clear the waters” a bit for you.
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