I have been re-reading this series of postings and have derived a lot of benefit from them.
However, I watched the Pillai video (because you insisted I do so) and one thing struck me.
He tells us that the wiruses go through a Darvinian process and damage to our innate immune system can prevent the ewolution of our development of the appropriate antibodies.
However, you have made a strong case, and I find it persuasive for a number of reasons, that the virus cannot mutate much and remain functional. Sure, it can change its Spike protein (possibly the S1 most) but it will not be able to do much to the N protein, and if you have ever been exposed to a Corona Wirus in the past then you likely have memory T cells that recognize it and can cleanup cells infected with SARS-CoV-2 as well.
So, is that a good explanation or is it simply that, as you seem to point out, it just shuts down the adaptive immune system for a period of time?
One thing I was confused about was the use of ADE in this post as it seemed atypical to its normal use.
I took ADE to refer to effector function as a method of mediating the enhancement, and strangely ADE appears to be found mostly with infection of effector cells. So would the case of IgG4 be appropriately termed as ADE or more like kooky "I don't see anything" immune tolerance.
Feb 13, 2023·edited Feb 13, 2023Liked by Brian Mowrey
Great series of posts Brian! It's probably tough catching flak from both sides, but ultimately I think this process is producing the strongest arguments.
Regarding testing, especially in the US, almost all testing is nasal swabs which is of the mucus membranes. My understanding is IgM dominates the response there. It seems that response will be identical in both Vaccinated and Unvaccinated. If the immune tolerancing theory is correct and the Vaccinated start having persistent infections, would it continue to show up in the nasal swab tests or would anal swab tests or blood serum tests be more accurate?
Anecdotally, I have seen a case where a "vaccinated"19 year old healthy BMI female has had a persistent cough for 1.5 months. Tests "negative" for Covid with a nasal swab and has no other symptoms. I also see plenty of anecdotes about persistent viral infections "but it's not covid". Is it possible that we are already seeing persistent infections but our testing regime is failing us? Keeping in mind of course that there really are other viruses out there that we routinely do not test for.
Feb 13, 2023·edited Feb 13, 2023Liked by Brian Mowrey
It's very weird to me that current events have made amateur immunologists out of every thinking person in the world. Very weird.
But what I took away from that, is that when the virus and the immune system reach their stalemate, this is worse than is obvious. Even if the virus is not rapidly infecting and destroying cells there is a baseline load of spike that is still proinflammatory and still doing random vascular damage possibly in the brain. Tolerating spike in the body is always a mistake unless the things I have read about spike on its own are in error.
So two questions:
1 Does free spike have the destructive potential to we have heard it does?
2 What is the 'half life' of spike without the rest of the virus? Or of free floating virus in the body, if it can't find a target for whatever reason?
Being an ignorant virus denier person I have 33% of my brain circuitry overwhelmed by this post, but I am doing a sincere effort to understand as much of this as possible.
In the spirit of the old "Remember, there are no stupid questions, only stupid people" I bring you two questions:
First. I don't know if I understand the metaphor at the end, the one about deputizing the raccoons. I understand it to mean a grim future where the body never stops attacking itself. That's his new programming: destroy yourself slowly, with the help of these well trained police raccoons. Did I understand that correctly, or is it the other way around, that is, deputizing the raccoons is a good situation?
Second question: I understood somehow that the cytokines act as a drug that sends the adaptive immune response to sleep, and the lack of adaptve immune response fosters more viral damage in more healthy cells. (I doubt I got that right.) But this happens only in that stage of "severe covid." But severe covid is rare. Most people never got there. What piece fails so that mild covid finally expands into in that severe covid which causes that adaptive response suppression? I'm guessing that there is a "race condition" here, as in electronics: if T cells mature before the lymph nodes freeze, there is no severe disease, and if they fail to mature in time, their maturation process will be shut down even harder.
So ::dons the conspiracy hat:: it seems there is a physical exploit built in into the pseudovaccines. They learned how the immune system fails sometimes, and designed a drug to make that effect more likely to happen in some people. Maybe it was a fluke that they are so bad?
I'm sorry to complicate this even more by summoning here the one of the most esoteric parts of electronics design. Immunology is already difficult as it is, no one needs more metaphors.
I get the IGG4 elevation. Question I have is how strong is the igG4 and how much of the iGg1 does it suppress? Does it suppress enough to truly depress immune reactions?
I'm on board with everything you are saying. Makes sense.
About a week ago, a commenter (Massimaux) called attention to a study from the European Journal of Internal Medicine: "Serum IgG4 level predicts COVID-19 related mortality" (https://doi.org/10.1016/j.ejim.2021.09.012)
Have you seen this study?
From said study: "[A] concentration of serum IgG4 > 700 mg/dl and an IgG4/IgG1 ratio > 0.05 were associated with a significantly increased mortality at 30-days . . . . Of note, a significantly positive correlation was found between serum IgG4 and IL-6 level, an established predictor of COVID-19 related mortality . . . . In this prospective study we found that serum IgG4 level predicts a poor COVID-19 outcome. Based on the available literature, IgG4 antibodies may contribute to COVID-19 progression . . . ."
Their findings seem to support what you are saying. However, the head-scratcher here is that the patients in this study had Covid between June and December 2020, prior to the rollout of the mRNA vaccines. Thoughts?
I'm starting to really appreciate Brian Mowrey's contribution to this whole Covid-19 topic. His explanation as to the myth of the cytokine storm (as opposed to DAD) was welcomed. Now, I wish I have more of a serviceable grip on "all-things virology and vaccinology" but...
I have been re-reading this series of postings and have derived a lot of benefit from them.
However, I watched the Pillai video (because you insisted I do so) and one thing struck me.
He tells us that the wiruses go through a Darvinian process and damage to our innate immune system can prevent the ewolution of our development of the appropriate antibodies.
However, you have made a strong case, and I find it persuasive for a number of reasons, that the virus cannot mutate much and remain functional. Sure, it can change its Spike protein (possibly the S1 most) but it will not be able to do much to the N protein, and if you have ever been exposed to a Corona Wirus in the past then you likely have memory T cells that recognize it and can cleanup cells infected with SARS-CoV-2 as well.
So, is that a good explanation or is it simply that, as you seem to point out, it just shuts down the adaptive immune system for a period of time?
(/cease-indian-accent-now)
One thing I was confused about was the use of ADE in this post as it seemed atypical to its normal use.
I took ADE to refer to effector function as a method of mediating the enhancement, and strangely ADE appears to be found mostly with infection of effector cells. So would the case of IgG4 be appropriately termed as ADE or more like kooky "I don't see anything" immune tolerance.
Great series of posts Brian! It's probably tough catching flak from both sides, but ultimately I think this process is producing the strongest arguments.
Regarding testing, especially in the US, almost all testing is nasal swabs which is of the mucus membranes. My understanding is IgM dominates the response there. It seems that response will be identical in both Vaccinated and Unvaccinated. If the immune tolerancing theory is correct and the Vaccinated start having persistent infections, would it continue to show up in the nasal swab tests or would anal swab tests or blood serum tests be more accurate?
Anecdotally, I have seen a case where a "vaccinated"19 year old healthy BMI female has had a persistent cough for 1.5 months. Tests "negative" for Covid with a nasal swab and has no other symptoms. I also see plenty of anecdotes about persistent viral infections "but it's not covid". Is it possible that we are already seeing persistent infections but our testing regime is failing us? Keeping in mind of course that there really are other viruses out there that we routinely do not test for.
It's very weird to me that current events have made amateur immunologists out of every thinking person in the world. Very weird.
But what I took away from that, is that when the virus and the immune system reach their stalemate, this is worse than is obvious. Even if the virus is not rapidly infecting and destroying cells there is a baseline load of spike that is still proinflammatory and still doing random vascular damage possibly in the brain. Tolerating spike in the body is always a mistake unless the things I have read about spike on its own are in error.
So two questions:
1 Does free spike have the destructive potential to we have heard it does?
2 What is the 'half life' of spike without the rest of the virus? Or of free floating virus in the body, if it can't find a target for whatever reason?
Being an ignorant virus denier person I have 33% of my brain circuitry overwhelmed by this post, but I am doing a sincere effort to understand as much of this as possible.
In the spirit of the old "Remember, there are no stupid questions, only stupid people" I bring you two questions:
First. I don't know if I understand the metaphor at the end, the one about deputizing the raccoons. I understand it to mean a grim future where the body never stops attacking itself. That's his new programming: destroy yourself slowly, with the help of these well trained police raccoons. Did I understand that correctly, or is it the other way around, that is, deputizing the raccoons is a good situation?
Second question: I understood somehow that the cytokines act as a drug that sends the adaptive immune response to sleep, and the lack of adaptve immune response fosters more viral damage in more healthy cells. (I doubt I got that right.) But this happens only in that stage of "severe covid." But severe covid is rare. Most people never got there. What piece fails so that mild covid finally expands into in that severe covid which causes that adaptive response suppression? I'm guessing that there is a "race condition" here, as in electronics: if T cells mature before the lymph nodes freeze, there is no severe disease, and if they fail to mature in time, their maturation process will be shut down even harder.
So ::dons the conspiracy hat:: it seems there is a physical exploit built in into the pseudovaccines. They learned how the immune system fails sometimes, and designed a drug to make that effect more likely to happen in some people. Maybe it was a fluke that they are so bad?
I'm sorry to complicate this even more by summoning here the one of the most esoteric parts of electronics design. Immunology is already difficult as it is, no one needs more metaphors.
Thank you for the post!
I get the IGG4 elevation. Question I have is how strong is the igG4 and how much of the iGg1 does it suppress? Does it suppress enough to truly depress immune reactions?
Pardon the digression, Brian, but did you ever get around to having a Zoom chat with Nick? If so, can the public access it?
I'm on board with everything you are saying. Makes sense.
About a week ago, a commenter (Massimaux) called attention to a study from the European Journal of Internal Medicine: "Serum IgG4 level predicts COVID-19 related mortality" (https://doi.org/10.1016/j.ejim.2021.09.012)
Have you seen this study?
From said study: "[A] concentration of serum IgG4 > 700 mg/dl and an IgG4/IgG1 ratio > 0.05 were associated with a significantly increased mortality at 30-days . . . . Of note, a significantly positive correlation was found between serum IgG4 and IL-6 level, an established predictor of COVID-19 related mortality . . . . In this prospective study we found that serum IgG4 level predicts a poor COVID-19 outcome. Based on the available literature, IgG4 antibodies may contribute to COVID-19 progression . . . ."
Their findings seem to support what you are saying. However, the head-scratcher here is that the patients in this study had Covid between June and December 2020, prior to the rollout of the mRNA vaccines. Thoughts?
I'm starting to really appreciate Brian Mowrey's contribution to this whole Covid-19 topic. His explanation as to the myth of the cytokine storm (as opposed to DAD) was welcomed. Now, I wish I have more of a serviceable grip on "all-things virology and vaccinology" but...