Question about how mRNA vaccines work

Here's a link to a fully referenced, well annotated, detailed explanation of the Covid-19 'vaccines', how they differ from 'true' vaccines, and why they are dangerous -

- specifically, how the spike proteins end up damaging blood vessels and bodily organs.

It's very long, but I believe it answers any questions anyone might have.

doctors4covidethics link

I think what is odd here is that the spike alone shows inflammatory properties on a pseudo virus which is where all the fear of the spike protein is coming from. Since the vaccine is supposed to anchor it in a membrane, and then we see it going in other areas, there must be some form of exosome release with spike bound to the vesicle. That is unexpected but can happen with secreted proteins. Usually the cells adsorb these targets and take them back in.

The RNA genome of a positive strand virus like COVID is infectious no matter what because positive sense RNA genomes are constructed just like mRNA. It just has to get into the cell.

T cells do not recognize full antigen, I’m pretty sure it must be broken down in MHC. CD8 or cytotoxic T cells interact with MHC I which is the endogenous pathway meaning foreign proteins inside the cell like with a virus. Then CD4 or T helper cells target exogenous pathways from external antigens like bacteria or fungi. They also have overlapping functions.

I do think there is a way for CD8 T cells to recognize certain aspects of full antigen but I could be mixing up NK cells with them. I do remember papers where certain constructs of antigen could still generate a T cell response, I just can’t remember if it was with MHC I or II. Plus, there could be a PAMP component with innate pathways.

Coronavirus either uses membrane fusion and enters the cell at the membrane or endosomes to enter the cell and then releases as pH drops in the maturing endosome.

The spike was thought to work so well because it’s a conserved region. Combine that with coronavirus and the ExoN protein that error checks mutations and slows down attenuation, it should have been a long lasting vaccine target. You bind the spike with antibody it’s still going to stop the virus from reproducing later in infection.

Vaccines have never stopped a pathogen from entering the body or reproducing. They just give us a shortcut to clearing infection so our immune cells don’t have to guess. Plus we will still make other antibodies to other structures in the virus.

Corona is just really good at escape and ADE, it’s changing the shape of the spike to make it functional in different shapes or conformations. I guess it’s even making decoy spikes to bind antibody while still working at other spike proteins. Plus with furin cleavage at the spike when new virions are being produced and packaged in the Golgi, it needs less steps to bind ACE2. Making it even worse in the host.

All of this is surprising but the other SARS like coronaviruses showed very slow if any attenuation once they developed their traits. The seasonal coronaviruses did attenuate more quickly.

Coronavirus can also follow 2 virus release pathways. One slowly releases virions and primes them using the cell until it is exhausted or destroyed by the immune system. The other follows the lytic pathway and destroys the cell much more quickly and releases hundreds of virions at once, many of which aren’t infectious, but the inflammation is a problem. There was even talk of a latent type infection which would maintain the viral genome without virion and protein generation. That would be very odd because of the way RNA viruses reproduce when they use RdRp.

ExoN is also causing us problems because it can interfere with antivirals, repairing the mutagenic damage they cause and potentially helping the virus evolve. But this aspect is highly debated.

a reply to: ketsuko

Still, if the virus cannot enter the cell, it cannot replicate using the cell's internal mechanisms.

There are a lot of different steps a virus has to go through to replicate. Any one of those steps, if denied, stops the whole process. So far, we only know of the spike protein that can become an effective antibody target.

And really, that might be the reason this particular virus seems to take so long to produce antibodies for. Perhaps there just aren't a lot of protein configurations on it that can mate up with antibodies.

TheRedneck

a reply to: chr0naut

No, metaphors and a similes, often used to explain and simplify complex things, are not the facts that they try to explain.

Did you miss this?

originally posted by: TheRedneck
a reply to: chr0naut

I'm not going to argue semantics with you either. Learn English.

TheRedneck

a reply to: chr0naut

That is incorrect.

Toxoid
From Wikipedia, the free encyclopedia

I'm also not going to debate with someone who does not understand their own links.

TheRedneck

a reply to: TheAMEDDDoc

I need a little help making sure I understand this all correctly.

I think what is odd here is that the spike alone shows inflammatory properties on a pseudo virus which is where all the fear of the spike protein is coming from. Since the vaccine is supposed to anchor it in a membrane, and then we see it going in other areas, there must be some form of exosome release with spike bound to the vesicle. That is unexpected but can happen with secreted proteins. Usually the cells adsorb these targets and take them back in.

What I am taking from that is that the release of the spike proteins is indicative of a mechanism that was unexpected. This unexpected mechanism that releases the proteins from the cellular membranes is a concern because it indicates a potentially inflammatory nature.

The RNA genome of a positive strand virus like COVID is infectious no matter what because positive sense RNA genomes are constructed just like mRNA. It just has to get into the cell.

The virus is quite infectious due to the nature of the RNA strand(s) it carries. The best solution is to prevent it from entering a cell in the first place.

T cells do not recognize full antigen, I’m pretty sure it must be broken down in MHC. CD8 or cytotoxic T cells interact with MHC I which is the endogenous pathway meaning foreign proteins inside the cell like with a virus. Then CD4 or T helper cells target exogenous pathways from external antigens like bacteria or fungi. They also have overlapping functions.

I do think there is a way for CD8 T cells to recognize certain aspects of full antigen but I could be mixing up NK cells with them. I do remember papers where certain constructs of antigen could still generate a T cell response, I just can’t remember if it was with MHC I or II. Plus, there could be a PAMP component with innate pathways.

I'll admit it: this totally lost me. Can you break down some of those abbreviations?

Coronavirus either uses membrane fusion and enters the cell at the membrane or endosomes to enter the cell and then releases as pH drops in the maturing endosome.

The virus has two different pathways to enter a cell.

The spike was thought to work so well because it’s a conserved region. Combine that with coronavirus and the ExoN protein that error checks mutations and slows down attenuation, it should have been a long lasting vaccine target. You bind the spike with antibody it’s still going to stop the virus from reproducing later in infection.

The spike protein was not expected to mutate, but rather was expected to remain stable during mutations. That's why it was chosen as a target protein: so the vaccine would continue to be effective even after mutations like the Delta variant.

Vaccines have never stopped a pathogen from entering the body or reproducing. They just give us a shortcut to clearing infection so our immune cells don’t have to guess. Plus we will still make other antibodies to other structures in the virus.

Vaccines cause the creation of antibodies which allow the body to quickly clear any future invasions of the same pathogen. Natural immunity also tends to detect other antigens on the virus and create antibodies for them as well, thus causing multiple responses to a single virus.

Corona is just really good at escape and ADE, it’s changing the shape of the spike to make it functional in different shapes or conformations. I guess it’s even making decoy spikes to bind antibody while still working at other spike proteins. Plus with furin cleavage at the spike when new virions are being produced and packaged in the Golgi, it needs less steps to bind ACE2. Making it even worse in the host.

Are you saying that the spike protein actually changes independent of mutations? As in, the mechanisms in the host body that normally break down proteins are assisting the virus in deceiving the body's natural or acquired immunity?

Also, Golgi apparatus? I'm not sure of the significance of protein breakdown at the edge of the cell nucleus. Can you explain further?

All of this is surprising but the other SARS like coronaviruses showed very slow if any attenuation once they developed their traits. The seasonal coronaviruses did attenuate more quickly.

Here again, you lost me. What traits are you referring to?

Coronavirus can also follow 2 virus release pathways. One slowly releases virions and primes them using the cell until it is exhausted or destroyed by the immune system. The other follows the lytic pathway and destroys the cell much more quickly and releases hundreds of virions at once, many of which aren’t infectious, but the inflammation is a problem. There was even talk of a latent type infection which would maintain the viral genome without virion and protein generation. That would be very odd because of the way RNA viruses reproduce when they use RdRp.

So the virus can exit infected cells either individually or en masse. I was not aware of the individual mechanism; I assume it would be via the same mechanism that allows spike proteins to exit the cellular membrane.

I am also taking from that, that you don't expect latent infections to be an issue.

ExoN is also causing us problems because it can interfere with antivirals, repairing the mutagenic damage they cause and potentially helping the virus evolve. But this aspect is highly debated.

What is "ExoN" please?

Thank you in advance for an explanation. I am attempting to understand with limited medical knowledge, so please feel free to correct me where needed.

TheRedneck

a reply to: TheRedneck

The Golgi is an organelle in the cell the processes and packages proteins and lipids. Presumably it would be hijacked to finish off the production of new viruses.

From what I understand, latent infections are an issue because the spike protein destroys your immune system the longer you have covid and it progresses. Basically like a type of immune deficiency can occur as a sequella of poorly treated covid-19 that has enough time to compromise the immune system of a host.

The recovered host would then experience reinfection from latent viruses post recovery of covid-19, since their immune system wall has been deteriorated and they now have a weaker immune system compared to before covid-19 infection.

a reply to: natoshis

Latent infection with viruses usually means no protein generation so they maintain their genomes in the cell, usually the nucleus, and then there is some signal that changes that. So with EBV it’s B cell activation. Herpes it’s some type of stress response. HIV it’s CD4 cell activation etc. Then they make that jump, push the cell into S phase for gene replication and protein expression.

Corona can apparently do something similar in the nervous system and apparently the endothelial and cardiovascular systems and all these other areas which is weird, but ACE2 is a common receptor.

Bringing up latent got me thinking about HIV infection and T cell exhaustion and terminal differentiation. Corona doesn’t have the ability to integrate because it lacks markers for reverse transcriptase and integrase, plus doesn’t code for them. However, theoretically there are ways to induce terminal T cell differentiation incorrectly and if I remember right it’s using poor signaling with effector cells. That is your memory T cells, the stem cells with multipotency or the ability to self renew and differentiate into the specific cells required for antigen recognition start skewing towards specific targets. It shouldn’t happen because they self renew as they differentiate and are located with naive T cells but it could be something to explore.

We are actually shifting targets because it’s more effective to target these other cells since they have the potential to remember and self renew for the life of the organism.

With the spike protein, it should be temporary because your immune system rebuilds, there are far worse toxins and other inflammatory molecules and structures that we have recovered from. Aside from inflammatory damage and scar tissue. If you see issues with terminal T cell differentiation and effector cell signaling issues in these studies then yes it’s a possibility. I haven’t seen it with the current vaccines though, at least in peer reviewed literature.

a reply to: TheRedneck

except for verification that the correct target protein is being used.

Considering it was partly generated by a computer, I'm extremely skeptical of that.

a reply to: TheRedneck

Lol I’ll try but I only use my phone and most of what I post is from memory. We have spent the last month on SARS-CoV-2 and RNA viruses in a molecular virology course and that’s where most of this comes from since some of it is new to me as well.

I’ve been trying to figure out what’s going on with the vaccines. They’re finding movement of spike protein and it shouldn’t happen because they built it to anchor in the membrane if it gets secreted. So this can only be in cell membranes, membranes in the cell, or some type of vesicle with a membrane. I don’t think it is causing a B or T cell problem. With the clotting and similarities to active infection I’m guessing complement or innate signaling. Complement calls granulocytes and antigen presenting cells to sites of inflammation and pokes holes in pathogens or cells with protein, lectin or antigen targets. Granulocytes are secreting innate cells that can self sustain inflammation via complement pathways after inflammatory signaling is removed. They can also release respiratory bursts that damage pathogens and tissues.

MHC is major histocompatibility complex, it’s used to present pieces of antigen to CD8 or cytotoxic T cells and CD4 or helper T cells. PAMP is pathogen associated molecular pattern, in this case double stranded RNA. Corona blocks this by modifying the RNA to hide it by using a protein called EndoU that removes the identifying regions like polyU regions.

Vaccines produce antibodies from B and plasma cells. There are also general antibodies that slow down pathogens via common targets. They also train T cells and teach them antigen targets presented by MHC, dendritic cells are a common T-cell trainer. You can’t maintain antibody generation for specific pathogens forever, too energy intensive and potentially problematic because eventually immune cells may go after targets near the antigen. Natural immunity will give many more targets in a natural infection. Plus your antigen targets evolve with the virus and identify new targets inside infected cells and on the pathogen during cleanup.

There are studies showing that these new variants developed a way to trick our immune system. The spike changed shape, open and closed, to other shapes at a midpoint that is still functional. Antibodies don’t work as well, virus can enter cells or gets antibody dependent enhancement entry into antigen presenting cells and we’re back at starting all over again in generating antigen targets. It can also respond to its external environment like with pH in endosomes.

Golgi is like the packaging plant. It prepares proteins etc from the ER. They think furin cleavage at the S1/S2 region of the spike can prime it to enter cells. It also needs membrane from our cells so it takes that as it moves through interactions with the ER when it moves to the Golgi, and then buds from the cell, also tricking our immune system. Other viruses can take it from the cell membrane, not sure about corona. Dengue and Zika do the opposite in bypassing furin cleavage to get additional receptor targets. I would be curious if corona could as well. Virions aren’t usually immediately Infectious so they need help from somewhere.

RdRp is a polymerase generated from the ORF1b region. It generates RNA from an RNA template, something our cells can’t do. In most RNA viruses it cares about speed and lacks error correction which is why they mutate so quickly. ExoN is a unique exonuclease proofreading protein that works with RdRp and error checks the genome. Because it is larger it developed this ability to maintain the larger genome. This means attenuation is much slower. The seasonal Corona’s have attenuated, the SARS like, not so much.

Coronavirus has also shown an ability to infect other cells through membrane binding with cells, not sure about exosomes. This is because it’s RNA genome is built the same way as mRNA and can interact with ribosomes.

You definitely have scientific knowledge, you seem to grasp everything.

originally posted by: TheRedneck
a reply to: chr0naut

No, metaphors and a similes, often used to explain and simplify complex things, are not the facts that they try to explain.

Did you miss this?

originally posted by: TheRedneck
a reply to: chr0naut

I'm not going to argue semantics with you either. Learn English.

TheRedneck

I think I'm all good with the English language, thanks.

What you did is to suggest that someone had posted something that they didn't post. It has nothing to do with the understanding of the English language. It is something that I have observed you doing several times, on several threads.

Please prove me wrong by posting a link to where AaarghZombies specifically posted that "the vaccine is ineffective against the virus" and I will admit my error and apologize profusely. However, I have looked back through this topic thread and done a search on the phrase, and it only appears in your post or ones quoting your post.

a reply to: TheAMEDDDoc

Lol I’ll try but I only use my phone and most of what I post is from memory.

I tend to post a lot from memory as well, especially in my forte. So I can understand, and appreciate, your posting style. Unfortunately medical science is not one of my fortes; it appears to be yours.

Anyway, thank you for the further breakdown. It's starting to make a lot more sense to me now. My limited knowledge thus far has really been more a probability based on reports I have read about the Chinese virus than detailed understanding of the individual biochemical mechanisms. I have tried to consolidate those reports together based on my limited knowledge of the chemical actions inherent in the immune response. That (systems analysis) is one of my fortes.

However, any analysis of any system is dependent on the degree of basic knowledge of the system.

That's why I asked for clarification. I was able to look up some of the terms you use and understand the jist of your post, but a few of them were going right over my head. And of course I do not have the benefit of your technical vocabulary; medical is probably the most difficult science to grasp the terminology.

The good part of that is that as I look up terms, that leads me into areas I had not investigated well before, which leads to increased knowledge. So thank you!

Your explanation helped a lot to clear up my comprehension. I will need time to study it, of course, to ensure I am not misinterpreting something, but I do hope you will deem any future questions I have worthy of an explanation.

You definitely have scientific knowledge, you seem to grasp everything.

Well, thank you! Concepts are my strength; terminology is my weakness.

That was the one big disagreement I had with my graduate advisor. He was big on trying to make oneself look smart by using "big words"; I preferred to get my points across by using more common language when possible. LOL, you should have heard some of our discussions on that difference of outlook!

TheRedneck

a reply to: chr0naut

I think I'm all good with the English language, thanks.

I don't.

TheRedneck

originally posted by: TheRedneck
a reply to: chr0naut

I think I'm all good with the English language, thanks.

I don't.

TheRedneck

But you are an American.

LOL.

This doctors explanation for the blood clotting makes a lot of sense and lines up with what I've seen other doctors saying. It is about the spike protein causing damage to the inside of blood vessel walls, but not exactly the way I thought.

www.bitchute.com...

a reply to: ChaoticOrder
At the moment I am not convinced of the safety of the vaccines. Our immune system could be changed after the jab. This paper will never become peer reviewed. Fairly sure about that.

europepmc.org...

Asking questions is wrong, why can’t you be like most and just do what’s expected of you? Lols

a reply to: ChaoticOrder

You really think you are going to get your freedoms back if you get everyone vaccinated??? You must be the same person who thought the Patriot Act was a good idea too. If you want to be vaccinated fine. Do it. But please do not force anyone else to do it. From what I have seen since Covid became a thing, it’s not as dangerous or as contagious as we are made to believe. I do not need proof or a link to tell me that. I am from the Chicago area and it was never as bad as our dear leaders made it out to be. They were the ones that were fear mongoring and causing panic. Stop being afraid. Damn. a reply to: AaarghZombies