How the vaxxx works; Why it fails.

[ThePythonicCow]

Someone who understands our immune system, viruses, vaccines and the COVID "vaxxx" provided a well written explanation of what's going on in our bodies with these vaxxx's.

Here's what he wrote, over on https://archive.4plebs.org/pol/thread/343850389. I've extracted the content from his 9 posts over on 4plebs.com, to become the 9 paragraphs below.

From what modest amount I know of such things, the author of this piece knows what he's talking about, and explains it well.

(Thanks to Clif High for the label "vaxxx" I used in this thread's title.)

=== ===

The mechanism behind vaccine side effects and the propaganda to hide them

Mon 18 Oct 05:53:44 2021

mRNA technology has been around for a while. What kept it from being used in widespread vaccination was lacking a way to protect the mRNA long enough to get inside of cells and to ribosomes, where it can be "read" to construct a protein. Instead of admitting this they (Moderna, Phizer, etc.) went ahead with an extremely lipid-soluble coating. That would guarantee the mRNA injected easily and quickly passed through cell membranes and gets to the site of action (ribosomes.) But it also meant that, unlike other vaccines, which have their particles taken up in normal lymph flow and end up in lymph-nodes local to site of injection where foreign, antigenic molecules are processed by dendritic cells and stay in the extracellular space otherwise (outside and in-between cells, the interstitium), the mRNA injected in these vaccines ends up everywhere, easily passing from the interstitium to the blood stream and across the blood-brain barrier.

Compared with getting a virus, the virus is only able to bond with and enter some cells; injecting its genetic material and taking over production to make more virus. It is limited to cells displaying molecules each virus is capable of binding to (in the case of SARS-CoV-2 this is a molecule called ACE2.) In "normal" vaccination only dendritic and a few other immune cells (which are designed to ingest and deal with antigenic molecules) end up with viral proteins in them. These specific cells are part of the immune reaction that ends up with long term and robust immunity. With mRNA vaccination the injection is in the deltoid (most of the time) but the particles of mRNA move easily in and out of cells and across biological membranes. Any cell, and subsequently its ribosomes, which come into contact with the exogenous mRNA will start to produce the altered SARS-CoV-2 spike proteins that the mRNA instructs for.

In the normal course of cellular function the master copy of your build and operating instructions (DNA) has a page or chapter photocopied as needed (mRNA) and sent out to factories (ribosomes) which read the instructions and build proteins according to them. During this process, whatever protein is being made is reported back to the immune system. This happens by each of your cells taking one of the things its factories are making and displaying them on the outside of their cell membrane. You can think of this as a sign at city limits which has an example of what each factory is making in a city. Security (T-Cells of the immune system) come by, but can't get inside, they just look at the sign to see if something is off. If something is, they can nuke the whole city (induce lysis) or tag the sign for other bulldozer immune cells to come by and level it. This function fights both cancer and viral infection. If either of those things cause a cell to start making abnormal or foreign proteins then the cell is instructed to kill itself (lysis) or tagged to be destroyed by other immune cells.

Up until now in human history you could only end up with antigenic (things which set off an immune response) molecules displayed to the immune system on subsets of cells. Either a virus infected your cells and that virus could only attach and enter a tiny number of overall cells in your body (like SARS-CoV-2 and cells which display ACE2) or you could get cancer (which is essentially one cell over and over and over.) Outside of that, antigenic molecules would be immediately destroyed by natural killer cells or would be collected through lymph and processed and displayed by dendritic cells in lymph tissue (nodes mostly). These dendritic cells look like massive tree root systems and all they do is process foreign material and display it on Major Histocompatibility Complex. That's the molecule complex that acts as the "signs at city limits" announcing what's going on inside a cell to the outside world. It is the sign security (the immune system) monitors to know if there is an issue inside, as security is a cell itself, and can't enter another cell. The immune system is blind to the intracellular environment besides these signs (MHC). One type of T-Cell, T-Helper Cells, move up and down the "root system" of the dendritic cell, just looking at all the signs. In this way, your lymph nodes and spleen (where this process mostly happens) act as security checkpoints, eventually coming across fragments of anything that ends up in your body. If they find something wrong, they induce an immune response to that thing which will eventually reach wherever the molecules they saw came from.

Back to what we are doing by injecting these lipid-soluble mRNA particles into peoples bodies; littering them throughout all tissue, dependent on each individuals weight, lipid %, hydration, cardiovascular state, anatomy, etc. Wherever concentrations of these end up you have random cells which will start to produce altered spike proteins and display them on their signs. The immune system notices this and starts attacking those areas. As each mRNA vaccinated cell is destroyed they spill their contents of altered spike protein (cytotoxic itself) into the local area. The vaccine makers know the path to immune activation is through MHC (signs), and don't really address or care about all the excess spike protein being made. The want the sign to say "altered spike protein" but in the background factories (ribosomes) are churning out actual spike protein into the inside of the cell. This is how virus reproduce as well; once infected more viral particles are constructed inside a cell, but they don't get release to go infect other cells until the infected cell is destroyed and they can escape.

Once these signs are made they are permanent, sort of, this is where the analogy breaks down. All the atoms in your body are replaced about once a decade. Even your bones are constantly re-structured by osteoclasts and osteoblasts, so every 10 years you have entirely different atoms making up those bones. Even cells that generally don't replicate or die until you do like neurons and muscle (muscle cells themselves get bigger when you work out, mostly, you don't get new muscle cells although nothing is ever 100%) constantly replace their constituent parts. The MHC displaying the product the factories are making will stay embedded in the cell wall until that section of the membrane is replaced due to other natural process (e.g. endocytosis.) This means that people who end up with persistent neurological or cardiac side effects may have them for years, until most of the signs stating the cell is making spike protein are torn down. For neurons in the brain, that could be years, not to mention the fact that in the mean time, the immune system is actively trying to kill off any of those cells, often successfully.

Humanity did this blindly. There is so much we don't understand about this. A gigantic portion of your genome is dedicated to MHC. We don't have any idea about the mechanisms we are playing with. Not only are large swaths of MHC black boxes but the whole question of Clonal Selection (how your body 'knows' what is you and what isn't you, and therefore what to attack) is an open question. There are no longitudinal studies on any of this, the safety data is non-existent beyond "it probably doesn't kill many of you in the first 90 days." Bankers, Government, and Corporations saw the opportunity to make hundreds of billions of dollars, and quickly grabbed whatever was on the shelf, dusted it off, and rushed it to market. It's one of the reasons that massive and rapid distribution is key. Not knowing what would happen, it was and is imperative to get as many doses injected as possible. While careful, isolated, controlled, longitudinal studies would easily recognize collective negative effects, even though the specifics differed, uncontrolled mass distribution during phase 4 study will make it easy to mask. Investigating any specific, like myocarditis, will only ever bring up a low level signal that's easily dismissed "COVID causes myocarditis too!" The collective information provided by all the signals would tell a different story. The VAERs database provides the strongest signal, but is easily ignored by propagandists due to its unverified nature. It will take years to collect the data and produce irrefutable results, which is why the normal process is around 6 years from a working product. Without control groups, even that data will be easy to skew in interpretation though.

These vaccines also have no hope of imparting robust long term immunity, and are effectively short term antibody therapy to one specific part of one specific strain. You need to have a broad spectrum of antigenic sites to induce robust and long lasting immunity. That's why vaccines are more complicated than re-producing a single bacterial protein and rubbing it on a cut. Although doing that with whiole dead bacteria (scabs) is where we saw inoculation first work. Whether the vaccines were attenuated, destroyed, or dead, the only vaccines we have ever seen impart robust and long lasting immunity provided the whole host of antigenic particles found in the wild. It's another reason why mRNA wasn't in widespread use in addition to the technical problem of a protective coating or encapsulation. They just don't work very well and are not vaccines. Mild endogenous antibody therapy would be a better description, which is why they had to change the definition of vaccine...

So here is where we stand. I'm not going to bother vaguely asserting some education, position of authority, or access to unavailable information. On the contrary, anyone who reads this will see I know what I'm talking about. I tried my best to both use proper technical terminology so all this can be easily researched, but to bridge the technical gap so a lay person could understand the mechanism behind the vaccine dangers. By their nature, these mRNA vaccines will only ever produce widespread, diffuse and low level specific signals. Every time anyone brings up a specific side effect they won't get anywhere and the MSM will always have the fallback of "basically the same as without the vaccine but having COVID." What about the risk before? Remember that time no one is allowed to talk about? When you could just say things like "myocarditis is nearly unheard of in children." I hope this helps someone explain to a loved one and win them over. As more and more shots are mandated to keep "antibody levels" high (since when are you supposed to walk around with high antibody levels? That's a sign of infection, not immunity, antibody levels should fade quickly and be replaced with primed memory cells), people lose their jobs, and anyone speaking out is silenced, people will have questions.

[Ewan]

Posted by ThePythonicCow (here)
Compared with getting a virus, the virus is only able to bond with and enter some cells; injecting its genetic material and taking over production to make more virus. It is limited to cells displaying molecules each virus is capable of binding to (in the case of SARS-CoV-2 this is a molecule called ACE2.)

Very good piece in total.

But the highlighet quote above makes me wonder if a current medication I am taking has led to protecting me from infection from SarsCov2.

Lisinopril is a angiotensin-converting enzyme (ACE) inhibitor. Which as I understand it reduces the quanity of cells with ACE receptors. Be interested in a Dr's view on that, though not my Dr. who is too busy spouting data from the NHS circulars he gets.

[ThePythonicCow]

P.S. to the article in my opening post: It doesn't cover the other crap in the clot shots, and of course it doesn't attempt to address the larger political, societal, economic, tyrannical, institutional, ... issues that threaten humanity.

[ThePythonicCow]

Posted by Ewan (here)

Posted by ThePythonicCow (here)
Compared with getting a virus, the virus is only able to bond with and enter some cells; injecting its genetic material and taking over production to make more virus. It is limited to cells displaying molecules each virus is capable of binding to (in the case of SARS-CoV-2 this is a molecule called ACE2.)

Very good piece in total.

But the highlighet quote above makes me wonder if a current medication I am taking has led to protecting me from infection from SarsCov2.

Lisinopril is a angiotensin-converting enzyme (ACE) inhibitor. Which as I understand it reduces the quanity of cells with ACE receptors. Be interested in a Dr's view on that, though not my Dr. who is too busy spouting data from the NHS circulars he gets.

According to this result on a search I just did for "lisinopril covid", yes, lisinopril can help. Quick thinking, Ewan!

• Blood pressure drug (Lisinopril) increases SARS-CoV-2 receptors in transmission and pathogenesis associated tissues

If I am reading this correctly, the study found that Lisinopril increased the proportion of ACE1 receptors, relative to the number of ACE2 receptors, and it's the ACE2 receptor that is targeted by the Sars-COV-2 spike protein, so Lisinopril might be helpful against COVID.

[norman]

Posted by ThePythonicCow (here)

. . . and it's the ACE2 receptor that is targeted by the Sars-COV-2 spike protein, so Lisinopril might be helpful against COVID.

. . . and don't stop there either, be a full blown, no holds barred, conspiracy theorist ( and sleep better at night ) . . . . https://www.sciencedirect.com/scienc...05580820301072

The study points a finger at the targets (white anglo saxons, forget all that fake racism about killing off the hat tipping yes-sir-no-sir 3rd world ) . . . .

BUT, oh maan . . . does it point a lazer pointer at the culprits.

[Mark]

This is awesome. Thanks, Paul.

[Sue (Ayt)]

Posted by Ewan (here)

Posted by ThePythonicCow (here)
Compared with getting a virus, the virus is only able to bond with and enter some cells; injecting its genetic material and taking over production to make more virus. It is limited to cells displaying molecules each virus is capable of binding to (in the case of SARS-CoV-2 this is a molecule called ACE2.)

Very good piece in total.

But the highlighet quote above makes me wonder if a current medication I am taking has led to protecting me from infection from SarsCov2.

Lisinopril is a angiotensin-converting enzyme (ACE) inhibitor. Which as I understand it reduces the quanity of cells with ACE receptors. Be interested in a Dr's view on that, though not my Dr. who is too busy spouting data from the NHS circulars he gets.

Ewan - I looked into this early on myself, wondering about the blood pressure drugs that some of my family are on.

I am not a doctor, but it appears to me that there is a big difference between ACE and ACE2, and there is a balance that is thrown off between the two functions when ACE inhibitors are used, that actually produces more ACE2 because it is the ACE part that is inhibited.

"The new coronavirus latches its spiky surface proteins to receptors on healthy cells, especially those in your lungs. Specifically, the viral proteins bust into cells through ACE2 receptors."

It was kind of confusing to me, but from the studies I read, I reached the opposite conclusion, that ACE inhibitors can make people more vulnerable to damage, as more ACE2 is produced.

Here are a couple such reports:
"There has been additional speculation that ACE inhibitors and ARBs may also increase the risk of SARS-CoV-2 infection and COVID-19.4 Like the original SARS-CoV described in 2003, data suggest that SARS-CoV-2 binds to ACE2 to gain entry to host cells on the respiratory tract epithelium. As select animal studies have demonstrated increased ACE2 expression with ACE inhibitor or ARB administration, a potential mechanistic link between SARS-CoV-2 infection, and these medications have been proposed (see below).
https://www.ahajournals.org/doi/10.1...NAHA.120.15291

"Hypertension and diabetes seem to stand out as the most common comorbidities in patients with more severe manifestations of the infection. An interesting hypothesis has emerged around the use of angiotensin converting enzyme (ACE) inhibitors to treat hypertension and diabetes to explain this phenomenon. ACE2 is the receptor for SARS-CoV2.5 The use of ACE inhibitors leads to increased expression of ACE2 making the cells more vulnerable to infection with the virus. Clinical studies are underway to test this hypothesis."
https://n.neurology.org/content/neur...09455.full.pdf

(I welcome medically trained people to comment on this, as I am unsure of my conclusion from what I have been reading.)

[Ewan]

Posted by Sue (Ayt) (here)

Posted by Ewan (here)

Posted by ThePythonicCow (here)
Compared with getting a virus, the virus is only able to bond with and enter some cells; injecting its genetic material and taking over production to make more virus. It is limited to cells displaying molecules each virus is capable of binding to (in the case of SARS-CoV-2 this is a molecule called ACE2.)

Very good piece in total.

But the highlighet quote above makes me wonder if a current medication I am taking has led to protecting me from infection from SarsCov2.

Lisinopril is a angiotensin-converting enzyme (ACE) inhibitor. Which as I understand it reduces the quanity of cells with ACE receptors. Be interested in a Dr's view on that, though not my Dr. who is too busy spouting data from the NHS circulars he gets.

Ewan - I looked into this early on myself, wondering about the blood pressure drugs that some of my family are on.

I am not a doctor, but it appears to me that there is a big difference between ACE and ACE2, and there is a balance that is thrown off between the two functions when ACE inhibitors are used, that actually produces more ACE2 because it is the ACE part that is inhibited.

"The new coronavirus latches its spiky surface proteins to receptors on healthy cells, especially those in your lungs. Specifically, the viral proteins bust into cells through ACE2 receptors."

It was kind of confusing to me, but from the studies I read, I reached the opposite conclusion, that ACE inhibitors can make people more vulnerable to damage, as more ACE2 is produced.

Here are a couple such reports:
"There has been additional speculation that ACE inhibitors and ARBs may also increase the risk of SARS-CoV-2 infection and COVID-19.4 Like the original SARS-CoV described in 2003, data suggest that SARS-CoV-2 binds to ACE2 to gain entry to host cells on the respiratory tract epithelium. As select animal studies have demonstrated increased ACE2 expression with ACE inhibitor or ARB administration, a potential mechanistic link between SARS-CoV-2 infection, and these medications have been proposed (see below).
https://www.ahajournals.org/doi/10.1...NAHA.120.15291

"Hypertension and diabetes seem to stand out as the most common comorbidities in patients with more severe manifestations of the infection. An interesting hypothesis has emerged around the use of angiotensin converting enzyme (ACE) inhibitors to treat hypertension and diabetes to explain this phenomenon. ACE2 is the receptor for SARS-CoV2.5 The use of ACE inhibitors leads to increased expression of ACE2 making the cells more vulnerable to infection with the virus. Clinical studies are underway to test this hypothesis."
https://n.neurology.org/content/neur...09455.full.pdf

(I welcome medically trained people to comment on this, as I am unsure of my conclusion from what I have been reading.)

Thank you Sue. It confounds my reasoning to explain my escape from infection though, very strange.

Around a month ago I considered that due to my daily exercise and improved diet I probably didn't need to keep taking the medication. I stopped for 5 days, noticing a little difference on the fourth day and increased signals on the fifth. Signs that were very concerning so I took a tablet as soon as i got home that day and again the next morning.

The symptoms were severe shortness of breath, intermittent increased heart rate and an inability to walk more then 50 yards without stopping for several minutes to recover energy and breathing. I also took Ivermectin for 2 days running as those symptoms felt more like Covid infection than a sudden increase in blood pressure.

[Sue (Ayt)]

Well, stopping something all at once can make for rebound effects too, Ewan. It can even be dangerous, cause our bodies have compensated for the meds actions by producing more or less of some other substance.
In my opinion, weaning slowly works best. Sometimes even very, very slowly. That is how my husband got off his plethora of meds that he was on at one time. My husband slowly weaned off 2 different high BP meds while adding a couple supplements at the same time. (hawthorn berry and olive root) He is still taking 1 of the BP meds, though, cut down to 1/2 the previous prescribed dose.