re: Coworker got the Moderna shots in February

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Also, the warp speed Pres T was referring to caught Pharma off guard; therefore, the first 6 months of ppl being vax’d got a saline injection only. Pharma was not ready.

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Old people would be dropping like flies then because outside of healthcare workers, elderly people were the only ones eligible to get the vaccine at first.

I caught Covid in December of last year and got the J&J vaccine in February 1921. I am getting hey antibody test today at 2 PM. I will report my findings back to the poly board in a couple of days

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BECAUSE IT'S NOT A VACINNE!!!

IT'S GENE THERAPY!!!

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Delta, until these idiots get this through their heads it's not going to be good. Big Pharma is about making a profit not curing you.

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And yes I didn’t reference class 1 MHC being presented from an infected cell to activate cytotoxic T cells or macrophages presenting class II MHC post antigen introduction to activate the helper T cells…but apparently there is something you forgot as well

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I've actually written several posts on the immune response. You've missed lots of other relevant details too, but I should expect a lot from you in terms of rigor, obviously.

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Is just a fancy way of saying they got it close enough which is what I was saying -

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No. Think about each word I used very carefully, because I chose them carefully. We have no evidence of ADE yet either.

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I’m not sure how it doesn’t

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Describe the molecular process of this 'hijacking' of you could.

Good thing they’re wearing a mask- right?

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Oh Dear God, the studidity that has been exposed with this disease.

No you don't have antibodies for smallpox. You have memory cells that remember smallpox. Those cells then trigger the antibodies.

The MRNA shots do not create lifelong memory B cells.

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Ding ding.. We have a winner. Don't forget T cell memory as well.

My mechanic's brother in law got the Pfizer "vaccine" and soon after died of lung cancer. Coincidence? Maybe, but the risk is too high!

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All Covid tests are garbage. PCR. Rapid. Antigen.

All garbage. I wonder why that is?

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I've actually written several posts on the immune response. You've missed lots of other relevant details too, but I should expect a lot from you in terms of rigor, obviously.

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See - again - showing your inability to comprehend. You didn’t even quote my entire point: which was you forgot what OVER-SIMPLIFY means as I wasn’t trying to give a class or go out my way (like you’re apparently doing) to make people think I’m smart

Yet you jump in here lecturing all day about others being wrong always ending with - “now explain, in detail” pushing the burden of proving your own point back onto someone else - which is a lazy and dishonest

I could come on here ALL day proving half the Medical data people see is bullshite (because that’s been my specialty for two decades). But if I tell someone that they’re wrong, I don’t turn around and say - now prove my point by explaining your point. How about…just explaining your point? If you say antibodies can’t be used in viral replication in certain instances - YOU explain why

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No. Think about each word I used very carefully, because I chose them carefully. We have no evidence of ADE yet either

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I did consider them. Did you consider mine?

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I think what is happening

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I said I THINK. THINK. As in my opinion. I didn’t say it WAS that way.

And along those lines with ADE, as you said no one knows YET as you say. So stop jumping in these discussions claiming people are saying things they aren’t then projecting that failure at comprehension back on them.

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Describe the molecular process of this 'hijacking' of you could.

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There are several ADE mechanisms: in one, the constant region of the antibody binds to the fraction constant receptor of the macrophage in order to phagocytose the pathogen. The virus uses this antibody mediated entry to infect the macrophage. This was observed in SARS-COV-1 in cats. This can also cause M1 macrophage activation while M2 macrophages are not activated leading to an inflammatory response even though the viral load isn’t as high. These excited M1 macrophages then lead to more B cells, more antibodies and so on as the inflammatory reaction increases.

In another method, C3 dependent, the complement protein complex (C1Q, C1R, C1S) binds to the constant region of the antibody causing the activation of the C3B protein via C4 and C2. The C3B then binds with the pathogen and also, in turn, binds with the complement receptor on immune cells, smooth muscle cells etc to be hijacked for infection.

A third way is the C1Q pathway. Once the antibody binds to the virus, the C1Q can bind directly to the cells via the C1Q receptors. This can actually have in innate immune cells, and B cells leading to possible infection.

In another method, it is possible via the FCR receptors to bind to the antibody and this can be used to enter cells in place of the ACE2 receptors overloading the cell with virus leading to possible genetic suppression preventing the cell from warning nearby cells of dangers leading to accelerated replication.

In another mechanism, ADE occurs through when an antibody binds to the virus leading to conformational change in the virus’ ligand allowing for direct entry into the cell. This was observed in MERS-COV.

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Many people who got vaccinated early on are likely no more protected at this point than a non vaccinated person

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Exactly. The "vaccinated" are unvaccinated after less than 6 months.