How is it mechanistically possible that the jab has negative efficacy for transmission yet somehow appears to do something with respect to hospitalization and death?
I really appreciate detailed footnotes and references.
Some random questions that I hope will be explored further:
1. What does "trained" innate immunity really mean? To me it really can only work if you are exposed to small amounts of virus/bacteria. Just enough that your immune system can handle it.
2. Sometimes I am puzzled by claims about how good children's innate immune system is.
Is it really? Aren't kids sick all the time? Come beginning of school year and until the end of
flu season, children were the biggest vector of spread of colds/flu.
3. I am still confused by "asymptomatic". And the fact that "experts" cannot definitively answer
questions, it only means that a) they don't know or b) science is not settled.
So, you are infected, but you are asymptomatic. What does that mean? Did your natural innate immunity stop the virus in time? If yes, then the adaptive immune system wasn't even engaged and therefore no specific antibodies (and further down memory cells) were generated.
Has this been cleared up? I haven't seen any compelling papers discussing this.
4. What happens if you are vaccinated and then you get infected? Do you actually develop
any long term immunity? Or vaccinal antibodies completely prevent you from developing
any sort of robust immunity (as you would if you weren't vaccinated)?
5. It seems that Omicron is the end of the line. There have been some reports that after Omicron infection there appears to be immunity against other variants as well. So, my interpretation is the following:
a. Boosters won't have any effect: either in positive sense (Omicron largely evades it) or negative (no extra evolutionary pressure since Omicron can already evade it)
b. If getting Omicron develops long-term immunity (despite being vaccinated), it means this
is the best-case scenario. By end of the spring, we'll all either get it or be exposed to it
that fairly robust herd immunity should emerge.
Where is the flaw in this logic?
6. Omicron appears mild (to me, this is the first time in the pandemic where number of
cases and hospitalizations/deaths is clearly decoupled) at the moment. What is the
evolutionary environment where another variant emerges that is as infectious *and* more virulent? From evolutionary perspective, more virulent virus would have hard time becoming dominant (it of course can emerge, but it wouldn't become dominant if equally infectious
The difference between ''inoculated'' and congenital immunity is equivalent to a package vacationer posing as a native speaker in the country of the body, so to speak.
Ah, it's sentences like these that make my days more shiny and liveable:
''No wonder modern medicine’s fixation on detectable serum antibody - induced via vaccination - has been a perpetual, Quixotic campaign targeting the wrong dragons.''
Dec 24, 2021·edited Dec 24, 2021Liked by Brian Mowrey
I have read so many pages of a number of immunology books and this is the first time I ever have heard of "natural antibodies". Roitt's doesn't mention them until page 302.
"The ideal spectrum of epitopes for antibody targeting cannot be created; the immune system must focus exclusively on the spike and may target host-homologous epitopes that otherwise would not have been “of notice,” leading to autoimmune antibodies. The spike protein is a smorgasbord of such potential epitopes."
Oh yeah. They used pseudoiridine, which can apparently lead to stop codons failing.
Wow. This was a fantastic read. It drives home the point that for all of the advances in medicine, we essentially are throwing a monkey-wrench into a highly complex system in order to loosen one stuck gear and not giving consideration to where the wrench may end up and what damage it may inadvertently cause along the way.
I suppose now if this becomes a noticeable enough problem the solution will be to simply "upregulate" the suppressed immunity in some way via the development of a new, proprietary expensive drug that you then have to take within X days of your fifth/eighth/fourteenth/[insert number here] booster shot. Never mind what inadvertent effects this new "innate booster" drug will cause as there will be a fix for that too in time.
"This new study confirms, again, that these groups are night and day in their protection against infection"
is that confirmed? Or is it protection against symptoms of infection, an easily confused metric unless they are tested directly for infective particles?
2. probably jabbed in high viral load/dose traffic locales
3. human, and unlikely to retain the "I am not vaccinated [sic] until 14 days time" info in their "jabbed = freedom" minds...
I would seriously love to see the stats of that 1-14 day post jab VE rate and the impact in general on cases, etc. It almost feels like cheating to exclude that period of time.
It could well be that prior memory cells or existing Ab would prevent the needed innate response.
The survey article linked below talks about the relationship between innate and adaptive immune response to SARS-CoV-2, and notes that failure to mount an appropriate innate response prevents the development of a T-Cell response and predicts more severe or fatal illness.
"In an idealized example of a generic viral infection, the innate immune system rapidly recognizes the infection and triggers the “alarm bells” of type I IFN expression and related molecules (Weaver and Murphy, 2016) (Figure 2 A). This can occur within a couple of hours of infection. The innate immune response serves three main purposes: (1) restriction of viral replication within infected cells, (2) creation of an antiviral state in the local tissue environment, including recruitment of effector cells of the innate immune system, and (3) priming the adaptive immune response. The first two activities of the innate immune system slow down the viral replication and spread. The third is a critical requirement of the innate immune system to trigger the adaptive immune response."
Re: Footnote 1, I find repetition helps me with comprehension and retention, so I appreciate your persistence with any of your topics, especially for the complexities of immune responses. Exercise makes most things better.
But it occurs to me that just as some people comprehend quicker and retain longer, so do people have varying immune competence. Discussions like this one seem to describe how these activities are supposed to perform, but apparently some people perform better than others. Perhaps the key to solving this is determining why some people have poor outcomes while (most?) others are more successful, though still with varying difficulty. If we can figure out what makes the successful people perform better, maybe we can help the weaklings adjust themselves.
I'm currently experimenting with keto diet, using Saladino's Carnivore Code as a guide. His book is extensively researched, with about 700 citations of published research. His theories are based on LDL being a principal transport for delivering immune cells and excreting the waste from successful engagements. LDL reduction is an obsessive target for cardiologists particularly, and doctors generally, which might account for the observations of cardiac conditions being a co-morbidity. He cites studies that show improved immunity in people with higher LDL levels. Mine is high enough to cause mild panic in my doctors, but my experience during the pandemic has been so successful, I wonder if my high LDL is indeed protective, and all those statins my friends gorge on are actually increasing their risk.
Thanks for your well-reasoned take on this, and for a more helpful explanation of how "natural antibodies" work than Geert has ever offered.
Although I think your two possible explanations probably rank higher at this point, I would like to offer a third that may rise in relevance as more people get 3, 4, or more injections of the same genetic spike vaccines.
Specific Spike Tolerance
Foreign proteins can function as both antigens (generating an antibody and inflammatory response) and tolerogens (generating a tolerance response that inhibits inflammation). We are constantly exposed to foreign proteins that are not associated with pathogens, and when our immune system treats them as antigens the result is an allergic reaction.
Allergic reactions can often be treated by regular controlled injections of the offending protein, which activates tolerance mechanisms. I had this experience personally after developing an allergy to bee stings, which was successfully treated by allergy shots.
My concern is that the mechanism of delivery of the spike protein in genetic vaccination does not "look" to the immune system like a viral infection, and also that the ensuing antigenic response and attack on spike beating cells "looks" like an autoimmune reaction.
One expected outcome of this, which would be exacerbated by boosters, would be the activation of tolerance pathways that counteract and ultimately downregulate the initial immune response to spike protein, even as antibody levels remain high and receive a boost upon further injections.
The cells to keep an eye on here are regulatory T cells (Tregs or FoxP3+), which are well studied in cancer research (because they can prevent the immune system from recognizing and destroying metaplastic cells) but so far not much examined in the context of SARS-CoV2 vaccination.
How is it mechanistically possible that the jab has negative efficacy for transmission yet somehow appears to do something with respect to hospitalization and death?
I really appreciate detailed footnotes and references.
Some random questions that I hope will be explored further:
1. What does "trained" innate immunity really mean? To me it really can only work if you are exposed to small amounts of virus/bacteria. Just enough that your immune system can handle it.
2. Sometimes I am puzzled by claims about how good children's innate immune system is.
Is it really? Aren't kids sick all the time? Come beginning of school year and until the end of
flu season, children were the biggest vector of spread of colds/flu.
3. I am still confused by "asymptomatic". And the fact that "experts" cannot definitively answer
questions, it only means that a) they don't know or b) science is not settled.
So, you are infected, but you are asymptomatic. What does that mean? Did your natural innate immunity stop the virus in time? If yes, then the adaptive immune system wasn't even engaged and therefore no specific antibodies (and further down memory cells) were generated.
Has this been cleared up? I haven't seen any compelling papers discussing this.
4. What happens if you are vaccinated and then you get infected? Do you actually develop
any long term immunity? Or vaccinal antibodies completely prevent you from developing
any sort of robust immunity (as you would if you weren't vaccinated)?
5. It seems that Omicron is the end of the line. There have been some reports that after Omicron infection there appears to be immunity against other variants as well. So, my interpretation is the following:
a. Boosters won't have any effect: either in positive sense (Omicron largely evades it) or negative (no extra evolutionary pressure since Omicron can already evade it)
b. If getting Omicron develops long-term immunity (despite being vaccinated), it means this
is the best-case scenario. By end of the spring, we'll all either get it or be exposed to it
that fairly robust herd immunity should emerge.
Where is the flaw in this logic?
6. Omicron appears mild (to me, this is the first time in the pandemic where number of
cases and hospitalizations/deaths is clearly decoupled) at the moment. What is the
evolutionary environment where another variant emerges that is as infectious *and* more virulent? From evolutionary perspective, more virulent virus would have hard time becoming dominant (it of course can emerge, but it wouldn't become dominant if equally infectious
virus is less virulent).
Again, where is the flaw in my thinking?
The difference between ''inoculated'' and congenital immunity is equivalent to a package vacationer posing as a native speaker in the country of the body, so to speak.
Ah, it's sentences like these that make my days more shiny and liveable:
''No wonder modern medicine’s fixation on detectable serum antibody - induced via vaccination - has been a perpetual, Quixotic campaign targeting the wrong dragons.''
Please, please, mor of it ...
Have you seen this article? Some very scary stuff. Not sure what to make of it.
https://www.thailandmedical.news/news/omicron-might-cause-mild-symptoms-in-a-large-percentage-but-the-long-term-health-implications-are-far-worse-than-delta,-be-warned
I have read so many pages of a number of immunology books and this is the first time I ever have heard of "natural antibodies". Roitt's doesn't mention them until page 302.
Thanks for the lesson.
"The ideal spectrum of epitopes for antibody targeting cannot be created; the immune system must focus exclusively on the spike and may target host-homologous epitopes that otherwise would not have been “of notice,” leading to autoimmune antibodies. The spike protein is a smorgasbord of such potential epitopes."
Oh yeah. They used pseudoiridine, which can apparently lead to stop codons failing.
https://twitter.com/JikkyKjj/status/1472805357747523586
Wow. This was a fantastic read. It drives home the point that for all of the advances in medicine, we essentially are throwing a monkey-wrench into a highly complex system in order to loosen one stuck gear and not giving consideration to where the wrench may end up and what damage it may inadvertently cause along the way.
I suppose now if this becomes a noticeable enough problem the solution will be to simply "upregulate" the suppressed immunity in some way via the development of a new, proprietary expensive drug that you then have to take within X days of your fifth/eighth/fourteenth/[insert number here] booster shot. Never mind what inadvertent effects this new "innate booster" drug will cause as there will be a fix for that too in time.
"This new study confirms, again, that these groups are night and day in their protection against infection"
is that confirmed? Or is it protection against symptoms of infection, an easily confused metric unless they are tested directly for infective particles?
Given the freshly jabbed are
1. not sequestered from society
2. probably jabbed in high viral load/dose traffic locales
3. human, and unlikely to retain the "I am not vaccinated [sic] until 14 days time" info in their "jabbed = freedom" minds...
I would seriously love to see the stats of that 1-14 day post jab VE rate and the impact in general on cases, etc. It almost feels like cheating to exclude that period of time.
"Illness is a viscous cycle" was not an intentional pun.
Very interesting/helpful article, thanks!
It could well be that prior memory cells or existing Ab would prevent the needed innate response.
The survey article linked below talks about the relationship between innate and adaptive immune response to SARS-CoV-2, and notes that failure to mount an appropriate innate response prevents the development of a T-Cell response and predicts more severe or fatal illness.
"In an idealized example of a generic viral infection, the innate immune system rapidly recognizes the infection and triggers the “alarm bells” of type I IFN expression and related molecules (Weaver and Murphy, 2016) (Figure 2 A). This can occur within a couple of hours of infection. The innate immune response serves three main purposes: (1) restriction of viral replication within infected cells, (2) creation of an antiviral state in the local tissue environment, including recruitment of effector cells of the innate immune system, and (3) priming the adaptive immune response. The first two activities of the innate immune system slow down the viral replication and spread. The third is a critical requirement of the innate immune system to trigger the adaptive immune response."
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7803150/
Re: Footnote 1, I find repetition helps me with comprehension and retention, so I appreciate your persistence with any of your topics, especially for the complexities of immune responses. Exercise makes most things better.
But it occurs to me that just as some people comprehend quicker and retain longer, so do people have varying immune competence. Discussions like this one seem to describe how these activities are supposed to perform, but apparently some people perform better than others. Perhaps the key to solving this is determining why some people have poor outcomes while (most?) others are more successful, though still with varying difficulty. If we can figure out what makes the successful people perform better, maybe we can help the weaklings adjust themselves.
I'm currently experimenting with keto diet, using Saladino's Carnivore Code as a guide. His book is extensively researched, with about 700 citations of published research. His theories are based on LDL being a principal transport for delivering immune cells and excreting the waste from successful engagements. LDL reduction is an obsessive target for cardiologists particularly, and doctors generally, which might account for the observations of cardiac conditions being a co-morbidity. He cites studies that show improved immunity in people with higher LDL levels. Mine is high enough to cause mild panic in my doctors, but my experience during the pandemic has been so successful, I wonder if my high LDL is indeed protective, and all those statins my friends gorge on are actually increasing their risk.
Thanks for your well-reasoned take on this, and for a more helpful explanation of how "natural antibodies" work than Geert has ever offered.
Although I think your two possible explanations probably rank higher at this point, I would like to offer a third that may rise in relevance as more people get 3, 4, or more injections of the same genetic spike vaccines.
Specific Spike Tolerance
Foreign proteins can function as both antigens (generating an antibody and inflammatory response) and tolerogens (generating a tolerance response that inhibits inflammation). We are constantly exposed to foreign proteins that are not associated with pathogens, and when our immune system treats them as antigens the result is an allergic reaction.
Allergic reactions can often be treated by regular controlled injections of the offending protein, which activates tolerance mechanisms. I had this experience personally after developing an allergy to bee stings, which was successfully treated by allergy shots.
My concern is that the mechanism of delivery of the spike protein in genetic vaccination does not "look" to the immune system like a viral infection, and also that the ensuing antigenic response and attack on spike beating cells "looks" like an autoimmune reaction.
One expected outcome of this, which would be exacerbated by boosters, would be the activation of tolerance pathways that counteract and ultimately downregulate the initial immune response to spike protein, even as antibody levels remain high and receive a boost upon further injections.
The cells to keep an eye on here are regulatory T cells (Tregs or FoxP3+), which are well studied in cancer research (because they can prevent the immune system from recognizing and destroying metaplastic cells) but so far not much examined in the context of SARS-CoV2 vaccination.