You can divorce T Cells from your concept of mucosal immunity, if you'd like. Resident (migrated into respiratory / gut tissues) T Cells (memory immunity) and Natural Killer Cells (innate immunity) put out small fires, they don't necessarily create a "sterilizing" immunity condition. And antibodies fade, though we don't know as much about IgA mucosal antibody immune response as we should, since we're obsessed over IgG. Asymptomatic "reinfection" becomes possible after a resting period; again, this seems to be by design and thus is probably the most desirable outcome.
This creates a win-win for the virus and the host and still looks like sterilizing immunity from 1,000 feet above - i.e., you get a sniffle and probably pass on the virus at sub-clinical viral loads, until seasonality kicks in and everyone's transmitting with high loads at the same time.
But if loads are high all the time, or if "shedded" spike exposure is persistent, it's easy to imagine that mucosal IgA antibodies stay high and this might create spike escape pressure (however, it could just as easily stimulate an ADE-priming IgE response).
1. "This is the idea behind a self-spreading viral "coronavirus vaccine," and may be what SARS-CoV-2 was actually designed to be
Self-spreading but non-replicating?
How would it spread? If it spread, that would mean it would be replication competent no? and that would then involve an actual infection and T-cells and all.
What I had in mind is understanding would just having high levels of ambient but not acute exposure mean for a human upper respiratory tract and mouth as well. Would it be like being exposed to multiple viral proteins but not a whole virus being expelled from someone's body? Would the encapsulation have dramatic influence on what another immune system sees? As in what is the signal that a body picks up if it seems viral protein encapsulated within saliva vs mucus vs sputum vs fecal dust vs exosome (at least proven to be in Pfizer MRNA)
Can you follow what i'm saying until now? I'll proceed to the next point then. Sorry for being slow, I'm learning as much as I can and I appreciate someone holding my hand through it.
"It" would replicate - in other words, "it" literally is SARS-CoV-2 (or any other coronavirus "vaccine" that was idiotically designed to create antibodies against something else, like HIV).
So, that's not the same means as "mRNA-injection-induced exosome secondary vaccination," just the same ends. It seems plausible that someone wanted to "vaccinate the world against coronavirus" even without having to inject everyone, and when the first platform didn't pan out they released it to sell the second platform. It seems equally plausible the end-game of global vaccination was global ADE. However, I rate all this as not a strongly likely origin story since the end result is that even the designers get their immune systems busted.
"What is the signal" is indeed the pressing question. I keep returning to "allergic" IgE sensitization because "exosome vaccination" means antigen presenting cells do not have any viral contextual signals to pick up (DAMP pathways that detect cellular destruction, etc) so they will just think "ok, allergen."
Then the respiratory epithelium gets loaded up with receptor-bound IgE antibodies for spike. Then the virus comes along and you get cytokine storm from go.
so, f'ing up the natural (worked for eons) immune process so that we go into self-damaging mode disaster mode immediately? Isn't that what has been happening with all these vaccinations and antibiotics for the past century? (all the auto immune diseases?) or am I misunderstanding?
It's obviously complex since not all viruses are alike - otherwise you would be able to say, well if nothing bad came from the polio vaccine, escape-mutant-wise, than every kind of vaccine is hunky-dory; or, if things are going so badly with coronavirus, we should be able to find disaster results from every vaccine ever.
But we know that coronavirus vaccines all flunk in animal trials for ADE. Here is a reallllllly damning one from 2019 that JJ Couey recently highlighted - https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC6478436/ - "In SARS-CoV/macaque models, we determined that antiтАУspike IgG (S-IgG), in productively infected lungs, causes severe ALI [acute lung injury] by skewing inflammation-resolving response."
You can divorce T Cells from your concept of mucosal immunity, if you'd like. Resident (migrated into respiratory / gut tissues) T Cells (memory immunity) and Natural Killer Cells (innate immunity) put out small fires, they don't necessarily create a "sterilizing" immunity condition. And antibodies fade, though we don't know as much about IgA mucosal antibody immune response as we should, since we're obsessed over IgG. Asymptomatic "reinfection" becomes possible after a resting period; again, this seems to be by design and thus is probably the most desirable outcome.
This creates a win-win for the virus and the host and still looks like sterilizing immunity from 1,000 feet above - i.e., you get a sniffle and probably pass on the virus at sub-clinical viral loads, until seasonality kicks in and everyone's transmitting with high loads at the same time.
But if loads are high all the time, or if "shedded" spike exposure is persistent, it's easy to imagine that mucosal IgA antibodies stay high and this might create spike escape pressure (however, it could just as easily stimulate an ADE-priming IgE response).
Give me a second to process this, it's so much I can't follow. Thanks for your explanation and patience.
Okay, one by one.
1. "This is the idea behind a self-spreading viral "coronavirus vaccine," and may be what SARS-CoV-2 was actually designed to be
Self-spreading but non-replicating?
How would it spread? If it spread, that would mean it would be replication competent no? and that would then involve an actual infection and T-cells and all.
What I had in mind is understanding would just having high levels of ambient but not acute exposure mean for a human upper respiratory tract and mouth as well. Would it be like being exposed to multiple viral proteins but not a whole virus being expelled from someone's body? Would the encapsulation have dramatic influence on what another immune system sees? As in what is the signal that a body picks up if it seems viral protein encapsulated within saliva vs mucus vs sputum vs fecal dust vs exosome (at least proven to be in Pfizer MRNA)
Can you follow what i'm saying until now? I'll proceed to the next point then. Sorry for being slow, I'm learning as much as I can and I appreciate someone holding my hand through it.
"It" would replicate - in other words, "it" literally is SARS-CoV-2 (or any other coronavirus "vaccine" that was idiotically designed to create antibodies against something else, like HIV).
So, that's not the same means as "mRNA-injection-induced exosome secondary vaccination," just the same ends. It seems plausible that someone wanted to "vaccinate the world against coronavirus" even without having to inject everyone, and when the first platform didn't pan out they released it to sell the second platform. It seems equally plausible the end-game of global vaccination was global ADE. However, I rate all this as not a strongly likely origin story since the end result is that even the designers get their immune systems busted.
"What is the signal" is indeed the pressing question. I keep returning to "allergic" IgE sensitization because "exosome vaccination" means antigen presenting cells do not have any viral contextual signals to pick up (DAMP pathways that detect cellular destruction, etc) so they will just think "ok, allergen."
Then the respiratory epithelium gets loaded up with receptor-bound IgE antibodies for spike. Then the virus comes along and you get cytokine storm from go.
so, f'ing up the natural (worked for eons) immune process so that we go into self-damaging mode disaster mode immediately? Isn't that what has been happening with all these vaccinations and antibiotics for the past century? (all the auto immune diseases?) or am I misunderstanding?
It's obviously complex since not all viruses are alike - otherwise you would be able to say, well if nothing bad came from the polio vaccine, escape-mutant-wise, than every kind of vaccine is hunky-dory; or, if things are going so badly with coronavirus, we should be able to find disaster results from every vaccine ever.
But we know that coronavirus vaccines all flunk in animal trials for ADE. Here is a reallllllly damning one from 2019 that JJ Couey recently highlighted - https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC6478436/ - "In SARS-CoV/macaque models, we determined that antiтАУspike IgG (S-IgG), in productively infected lungs, causes severe ALI [acute lung injury] by skewing inflammation-resolving response."
Also, I've read that the first Polio vaccine had to be pulled because it killed and paralyzed so many people.
Further illustrating your point that not all vaccines are alike, since the second one seemed to work better.
ЁЯШп
Intriguing, do you know if someone who is sleeping ever sneezes?
Google says no.
What do you think it means, in terms of inference we could draw about involvement of infection blocking or infection attack rates?