I've seen a lot of worry about the vaccine causing some prion disease. Do these fears have any basis in biology? Is there evidence to support these fears? Lets look at it a little bit.
The article put forth that discussed this makes several errors. It incorrectly states that the SARS-cov-2 vaccine has been shown to write to DNA. This is 100% false. The experiment cited begins with the premise that because people who have had Covid are later getting diagnosed with covid again (by the fraudulent PCR test!!!). They conjecture this is because the virus (not the vaccine) is being written to the DNA. The fact that the PCR test is shown to be completely fubar is not part of their discussion. This by itself is a huge red flag, but lets dig deeper.
The paper goes on to show that under lab conditions, when you take away the safeguards that exist in cells in vivo, inducing mitosis while under viral load, and introducing exogenous tools to make it happen (induced expression of HIV and LINE-1 Reverse Transcriptase) that the virus can write to DNA. Well of course it can, you just made it do it. It then showed that they got a positive result by only doing the first (induced mitosis while under viral load). But this is still the removal of a safeguard that is in place in vivo, and their positive results signal was so low as to be ridiculous. That doesn't mean it didn't happen, but if it did it was such a small occurrence as to have insufficient statistically meaningful results.
Then the other paper they are making the connection with to "prove" their overall theory of "causes neurodegenerative disease" is only showing a sequence similarity with another protein that can misfold, which can eventually lead to neurodegenerative diseases after the long term accumulation of these proteins. There are several problems with that paper as well, or at least with the conclusions that are being drawn from it:
- This theory ALSO requires the vaccine mRNA to write to DNA on a large scale. There is literally zero evidence to support such a claim, and biologically it makes zero sense
- it requires the same misfolding in the SARS spike protein as in the proteins that cause ALS etc. The problem here is two fold:
- The folding of proteins into their tertiary structure is a process that is dependent on OTHER parts of the protein. Just because there is a sequence similarity in one part, doesn't mean when it goes to fold up the forces of other domains will cause the same effect in the final structure. In fact, such a thing is very unlikely. More important, there has been no evidence to support such an idea. This was a THEORY put forth by someone who saw a sequence similarity.
- The spike proteins are TRANSMEMBRANE proteins, not cytosolic proteins. Transmembrane proteins are translated (created) directly into the membrane. This precludes them accumulating in the cytosol to cause the problems associated with these other diseases.
- The cell has an entire system put into place to take care of misfolded proteins. These misfoldings happen all the time. Pretty much all the time they are taken care of. The disease states from misfolded proteins are from the accumulation of such proteins, not in them existing in the first place. In these cases the misfoldings happen faster than the mechanisms in place can take care of them. There is not even a theoretical way that such accumulation can happen faster than their removal in the case of the vaccine mRNA.
- This effect would have to be taking place ON A LARGE SCALE, INSIDE THE BRAIN. This is incredibly unlikely, to the point of being absurd. There is no biological basis for such an effect to be happening in multiple, localized neurons. Even a single one of these lipid nanoparticles being transcytosed through the BBB is unlikely (though not impossible). This whole brain infection thing just adds several more biological improbabilities (virtual impossibilities in some cases) to the theory.
In order to show that the spike protein ACTUALLY misfolds in a similar manner, it would require doing ACTUAL experiments. Is it something worth looking into? Maybe, I guess, meh, but the paper did NOT show anything of the sort that is being claimed.
So both papers did not really say what the article writer is saying they said. The article both made mistakes (big enough to make the entire argument fall apart), AND false extrapolations (each of which also makes the entire argument fall apart).
This conjecture has no biological basis. That doesn't mean that biology can't be surprising. Biology is surprising more often than not. But without actual evidence of a problem, indulging in such fantasies to the point of being afraid of them is discrediting legitimate concerns. These ideas might be put forth in earnest, or they could be nefarious. Either way indulging in fantasies without evidence has a harmful effect on everyone.
The way I understand how this 'vaccine' works is that it uses mrna to make the spike protein. So it gets into a cell, makes this spike protein over and over, until the cell dies, releasing all the spike protein to make the immune response attack the spike protein, and it identifies that spike protein. couple of problems, how do you turn it off, and what happens to that spike protein when it attaches to cells in your lungs and other places, that have that receptor. Whos to say there's not some other engineered virus sitting back waiting to attach to that specialize spike receptor. Nope its still experimental, and I will choose to remain in the control group.
I'm not sure cell death is certain, though that is the most likely outcome of an immune response. Nevertheless, most of what you said up to this point is true enough.
It turns itself off. The half-life of the mRNA is about one day. Within a week or two its pretty much all gone, and is increasingly less effective every day.
In general, cells don't go attacking other cells. I'm not saying this is impossible, if say a cell of the immune system is the recipient of one of the lipid nanoparticles containing the mRNA, which almost certainly happens, but then it would need to go to the cell expressing the ACE-2 protein, for which there is no apparent motivation, then it would need to bind, and... Then what?
Unlike viruses or lipid-nanoparticles that are small enough to be endocytosed or otherwise be induced to release their contents into a cell, other cells interact by sending each other signals. They don't start eating each other. The ACE-2 expressing cell certainly isn't likely to be eating the mobile immune cell, on the contrary the opposite is likely to happen (and even then, there is no apparent motivation to begin this process). That unlikely hypothetical would result in the death of the ACE-2 expressing cell, not the creation of it becoming a spike protein factory.
In other words, there is no reason to think this could be cell-to-cell infectious.
These things don't stay "attached' forever... On the contrary, such attachment is very brief. If endocytosis doesn't start reasonably soon, its not likely to happen at all (with that specific connection). This idea just doesn't have any basis in biology. So I guess, biology would be the "who" who says.
I am 100% with you there. I am trying to reduce what I see as likely false fears, so we can remain focused on the real ones that exist. If easily proven false fears take root, it delegitimizes the real fears we discuss to externals who look in, i.e. new people, or active agents of the opposition.
In general, cells don't go attacking other cells. I'm not saying this is impossible, if say a cell of the immune system is the recipient of one of the lipid nanoparticles containing the mRNA, which almost certainly happens, but then it would need to go to the cell expressing the ACE-2 protein, for which there is no apparent motivation, then it would need to bind, and... Then what?
Unlike viruses or lipid-nanoparticles that are small enough to be endocytosed or otherwise be induced to release their contents into a cell, other cells interact by sending each other signals. They don't start eating each other. The ACE-2 expressing cell certainly isn't likely to be eating the mobile immune cell, on the contrary the opposite is likely to happen (and even then, there is no apparent motivation to begin this process). That unlikely hypothetical would result in the death of the ACE-2 expressing cell, not the creation of it becoming a spike protein factory.
In other words, there is no reason to think this could be cell-to-cell infectious.
However, no one mentions that cell death can result in over production of the spike protein, doesn't matter what cell it is. Now all these generated spike proteins are released into the body... looking for ACE-2 receptors. in theory..and yes this is a theory, the immune system will attack said spike proteins, no mention of where they might be when this happens. Stuck to an ace-2 receptor thats lung tissue...
I have no idea where you are getting such an idea, but even if true (for which there is no impetus nor evidence) then what?
Spike proteins are a transmembrane protein. They live INSIDE the membrane. So you are suggesting that a transmembrane protein that only can exist in a membrane is making little bubbles of cells float throughout the body?
Cell death is a process where the cell is broken up into small bubbles (blebs) and engulfed by the cells designed to eat them. The contents are then destroyed. They never enter the cytoplasm of the phagocyte (the cell doing the eating). There are no free floating spike proteins. Its basically impossible. Could there be free floating blebs with spike proteins? I find that extremely unlikely but I'll give it to you. What then? Why then it still gets eaten.
But lets say this hypothetical bleb escapes all that, what then? How does it find an ACE-2 receptor to dock to? That's a miracle worth solving.
So it goes into the blood stream (by some miracle) to seek out these receptors and gets eaten by cells in the blood designed for that express purpose. That's what happens to foreign bodies in the blood.
Bummer.
But this is the miracle bleb. Lets say it escapes all that.
Somehow it finds a path out of the blood vessels into the lumen of some tissue. Not going to happen, but I'll give it to you for this discussion.
Lets say, by some miracle it just so happened to be in a place with cells where ACE-2 is expressed and this theoretical bleb, that made it all this way, has finally found its mate.
Guess what happens? It gets eaten and destroyed. There is no mechanism on the spike protein to release anything into the cytoplasm of the new cells. That's what the rest of the virus is for. This miraculous spike protein expressing bleb would dock, be endocytosed, and consumed in the resulting lysosome.
Bummer.
The spike protein is not a virus. Its not a miracle. Its just a protein that docks to a receptor. What happens next is whatever would normally happen. If the spike protein is attached to a virus, it does its virus thing. If the spike protein is attached to the dead bleb, it gets eaten. Its that simple.
You know more about this than I do. So we get the terminology right, to make sure am expressing my view, and you can tell me thats not how it works. so the mRNA gets into a cell,and hijacks the manufacturing process like 'virus' to make the spike protein. how many will it make? if they are in the cell, won't they stay inside ( the manufactured spike protein) what causes them to be seen by the white blood cells,(again the spike protein). Once the body recognizes the spike protein it can make an antibody to gum it up and be removed as it is found (clumps of antibodies around that foreign protein. The problem I see is that there is no information on how this vaccine 'works' its a trust us kind of thing. I have listened to a few doctors explain how it works and that's where I have formed my hypothesis. the thing is we have seen evidence of blood clots in dead patients, so somehow its causing a immune response. with me so far?