I'm sure many of the regular readers have come across the Medium article but if not I suggest you read it here. Prepare a drink, it's long, which is why I did not post it earlier. Read, then post, is my rule. I also suggest you save a copy as a PDF because of the penchant of website to remove or alter data based on pressure from outside groups. In terms of content, it adds a lot to my previous posting in regards to the lab origins of this virus. And makes it that much more likely to be correct. Fortunately the article is not written in science jargon so anyone of decent intelligence can follow along. That said there is one part I'd like to point out:
3) The furin cleavage site.
The furin cleavage site is a minute part of the virus’s anatomy but one that exerts great influence on its infectivity. It sits in the middle of the SARS2 spike protein. It also lies at the heart of the puzzle of where the virus came from.
The spike protein has two sub-units with different roles. The first, called S1, recognizes the virus’s target, a protein called angiotensin converting enzyme-2 (or ACE2) which studs the surface of cells lining the human airways. The second, S2, helps the virus, once anchored to the cell, to fuse with the cell’s membrane. After the virus’s outer membrane has coalesced with that of the stricken cell, the viral genome is injected into the cell, hijacks its protein-making machinery and forces it to generate new viruses.
I won't get into how this is probably the most damning portion of the paper but I think it underlines why there are two means of dealing with this (or any) virus. So as I discussed in my last posting on the subject, the "spike protien" which is nasty on it's own has multiple parts. The mRNA vaccines causes the hosts cells to create one of these parts, supposedly the S1. If the S1 is THE cause of the spike protien's ability to cause problems, then such a "vaccine", in my opinion, is not a good idea. But that's not really what this post is about. The interaction between the S1 and S2 parts of the spike is interesting. Per the article I think we can look at it like a car with a manual transmission.
The S1 protein is like having a key to a car door (or any door but go along with me). The S2 portion is like turning the key. Have you ever had a key that fit into a keyhole but you either could not turn it OR you could turn it but the lock doesn't disengage? Right. If a key cannot open a door, it's not all that useful. Similarly having the ability to turn the key is useless unless you have the right key.
The current mRNA vaccines, as I understand them is like having the key and not being able to turn the lock. We don't know if that makes the key useless in and of itself. Now the S2 portion allows the virus to fuse to the cell membrane (open the car door) and allow entry of the RNA.
One could argue that a natural infection would be preferable than an S1 derived vaccine because the host may develop the ability to recognize both S1 AND S2 as well as produce epitopes that can recognize variants of both which is likely why people exposed to SARS1 and other coronaviruses have T-cell responses to SARScov-19 even though they've never had it.
So we understand what the "vaccine" end of the "solution" is. It's very specific to one part of the virus. Now lets look at the other side. Theraputics.
We know that vitamin D levels affects who gets bad Wuhan and who doesn't. We know it is because D modulates ACE2 receptors, low in some places high in others. Hence a Vitamin D directly affects S1's ability to bind to a cell. If it cannot bind it cannot cause disease. Period.
But lets say that enough virus has entered the body and therefore simply on the basis of probability enough virus can bind to enough ACE2 receptors, S2 then opens the cellular door and the viral RNA enters. Now what?
Enter zinc, the manual transmission.
We know that Zinc inhibits viral replication. (that link from 11 years ago).
Increasing the intracellular Zn(2+) concentration with zinc-ionophores like pyrithione (PT) can efficiently impair the replication of a variety of RNA viruses, including poliovirus and influenza virus. For some viruses this effect has been attributed to interference with viral polyprotein processing. In this study we demonstrate that the combination of Zn(2+) and PT at low concentrations (2 µM Zn(2+) and 2 µM PT) inhibits the replication of SARS-coronavirus (SARS-CoV) and equine arteritis virus (EAV) in cell culture. The RNA synthesis of these two distantly related nidoviruses is catalyzed by an RNA-dependent RNA polymerase (RdRp), which is the core enzyme of their multiprotein replication and transcription complex (RTC).
being unable to replicate is like a person who breaks into a car with a manual transmission but doesn't know how to drive one. You're not getting far and if you persist, the police (T-Cells) will eventually find you. If no police show up you will eventually abandon the vehicle because you can't drive it. Similarly a virus that breaks into your cell but cannot replicate has only left a mess of it's RNA in the cell, soon to be given the lysosome treatment.
More specifically, Zn(2+) was found to block the initiation step of EAV RNA synthesis, whereas in the case of the SARS-CoV RdRp elongation was inhibited and template binding reduced.Translation, in the presence of zinc, replication cannot be initiated. Virus is stopped dead.
And so we see that there is indeed a means to handle Covid without a vaccine. This information has been known for years. I also think this zinc approach is probably better than a vaccine because it is not specific to any particular strain of virus. So any new variant that happens to be "better" at fusing with cells still has the zinc problem. Until or unless the zinc barrier to replication is overcome zinc should continue to be invaluable.
Why no discussion of this in the public by "health officials"? Well there is no money in zinc and vitamin D (though Quercetin is apparently quite a profit center). There is also no government power to be had.