Jan 14, 2023·edited Jan 14, 2023Liked by Joomi Kim
I'm no immunologist, but the whole "presence of antibodies" thing seems silly to me.
There was a study published in Nature early in the pandemic that showed that people with exposure to the original SARS had T-cell immunity based on a common N protein some 17 years later.
If you have long lasting T cell immunity that can request that the B cells generate anti-bodies when needed, why would the lack of antibodies when not infected be predictive of anything?
Hi Joomi, very nice summary as always. I had not seen the studies on response and recovery in B cell depleted individuals. Very interesting. Do you have plans to dive into detail on mucosal immune response (eg IgA) as immune correlates vs IgG subclasses? As a general statement, it has driven me crazy that the discussion about immune correlates of protection, disease severity etc, has been dumbed down to “you need a high IgG titer or you are not protected”. The organization and magnitude of the cell mediated response appears much more predictive of disease outcomes and protection against serious disease. Thank you for the great work sand looking forward to the next articles!
In 1908, Elie Metchnikoff and Paul Ehrlich both received the nobel price for their works on immunology. Metchnikoff discovered phagocytosis and innate immunity. Ehrlich discovered antibody formation (what he called the "magic bullet").
Later, when the pharma industry discovered that they can make much more money with following Ehrlich, they completely forgot Metchnikoff
From what I understand, you don't get B-cell memory formation without being triggered by Tcells through "linked recognition "which shows that Tcell activation comes generally BEFORE Bcell activation. Also, only NK cells and Tcells are able to identify non-self proteins displayed on the surface of infected cells (on MHC receptors). During initial infection these are non-structural proteins and these are highly conserved across viruses. Thus the idea that sars- cov2 was "novel" and there was no background immunity is a stretch, to say the least.
"Class switch towards non-inflammatory, spike-specific IgG4 antibodies after repeated SARS-CoV-2 mRNA vaccination"
Not all IgG are the same. There are four classes. And the IgG4 have recently been shown to be involved in turbo charging cancer growth because IgG4 can interact with IgG1.
Nice approach, Joomi. So then next up could be risk for patients already getting Campath/alemtuzumab, which depletes both B and T lymphocytes. As always, nothing is simple; but at least here's a very small study, 2020, showing that subjects weren't decimated: https://www.sciencedirect.com/science/article/pii/S2211034820303734
"Potential COVID-19 infection in patients with severe multiple sclerosis treated with alemtuzumab"
Their lowest abs Lymphs were <=600 (with ~normal range 1000 to 4800).
"Conclusions
Our data suggest that patients receiving alemtuzumab showed very mild symptoms of COVID-19. "
I think I remember reading similar material from sources such as WDDTY many years ago, indicating that immune compromised people can survive viral infections even as you say, without antibodies. It’s perhaps also more correct to talk about “immune systems”, because there are other mechanisms involving in immunity beyond antibodies.
What tends to determine the severity of symptoms is the nature of response to the infection a person develops. Viral replication itself does not on its own necessarily produce dangerous symptoms anymore than replication in normal cells, the bodies ability to manage the response moderate’s symptoms.
Isn’t a Corona, basically an undetectable “common cold”?
With all this research, as a layperson when all is said and done…
Still sounds like “well, we are close, but still don’t know anything?” Seems the whole idea…. This “thing “ is attached to something common and insidious… it’s difficult to track…
Corona’s seem common, and difficult to track…
It seems something bad has been attached to the Common Corona…(one one bad actor) and results may be bad for some, not others (as is the case with Corona/common cold) yet the synthetic bad actor has been attached and is doing its stuff…
I'm no immunologist, but the whole "presence of antibodies" thing seems silly to me.
There was a study published in Nature early in the pandemic that showed that people with exposure to the original SARS had T-cell immunity based on a common N protein some 17 years later.
If you have long lasting T cell immunity that can request that the B cells generate anti-bodies when needed, why would the lack of antibodies when not infected be predictive of anything?
"Shhh, antibodies are what we can sell!"
Hi Joomi, very nice summary as always. I had not seen the studies on response and recovery in B cell depleted individuals. Very interesting. Do you have plans to dive into detail on mucosal immune response (eg IgA) as immune correlates vs IgG subclasses? As a general statement, it has driven me crazy that the discussion about immune correlates of protection, disease severity etc, has been dumbed down to “you need a high IgG titer or you are not protected”. The organization and magnitude of the cell mediated response appears much more predictive of disease outcomes and protection against serious disease. Thank you for the great work sand looking forward to the next articles!
Most helpful and educational to a lay person, such as myself.
Will Part 2 be discussing the role of the different IgG's 3 and 4?
Covered here: https://igorchudov.substack.com/p/immune-tolerance-igg4-class-switch
In 1908, Elie Metchnikoff and Paul Ehrlich both received the nobel price for their works on immunology. Metchnikoff discovered phagocytosis and innate immunity. Ehrlich discovered antibody formation (what he called the "magic bullet").
Later, when the pharma industry discovered that they can make much more money with following Ehrlich, they completely forgot Metchnikoff
From what I understand, you don't get B-cell memory formation without being triggered by Tcells through "linked recognition "which shows that Tcell activation comes generally BEFORE Bcell activation. Also, only NK cells and Tcells are able to identify non-self proteins displayed on the surface of infected cells (on MHC receptors). During initial infection these are non-structural proteins and these are highly conserved across viruses. Thus the idea that sars- cov2 was "novel" and there was no background immunity is a stretch, to say the least.
I think you should also look into this study: https://www.science.org/doi/10.1126/sciimmunol.ade2798
"Class switch towards non-inflammatory, spike-specific IgG4 antibodies after repeated SARS-CoV-2 mRNA vaccination"
Not all IgG are the same. There are four classes. And the IgG4 have recently been shown to be involved in turbo charging cancer growth because IgG4 can interact with IgG1.
https://pubmed.ncbi.nlm.nih.gov/32819973/ "An immune evasion mechanism with IgG4 playing an essential role in cancer and implication for immunotherapy"
Read this as a potential example: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8656165/ "Rapid Progression of Angioimmunoblastic T Cell Lymphoma Following BNT162b2 mRNA Vaccine Booster Shot: A Case Report"
♥️🙏
Nice approach, Joomi. So then next up could be risk for patients already getting Campath/alemtuzumab, which depletes both B and T lymphocytes. As always, nothing is simple; but at least here's a very small study, 2020, showing that subjects weren't decimated: https://www.sciencedirect.com/science/article/pii/S2211034820303734
"Potential COVID-19 infection in patients with severe multiple sclerosis treated with alemtuzumab"
Their lowest abs Lymphs were <=600 (with ~normal range 1000 to 4800).
"Conclusions
Our data suggest that patients receiving alemtuzumab showed very mild symptoms of COVID-19. "
well you already see some serious backtracking here:
"large randomized clinical trials similar to the initial trials of the currently authorized or licensed vaccines for COVID-19 will be required.”
Marks et al. JAMA commentary from Dec 2022
This is a bit off topic, but I’m curious about why the PCR test is STILL being used as a diagnostic? Is RT-PCR any more useful?
To the vaxaholics, antibodies are like electrolytes ~ https://www.youtube.com/watch?v=ZMHfBobgLSI
I think I remember reading similar material from sources such as WDDTY many years ago, indicating that immune compromised people can survive viral infections even as you say, without antibodies. It’s perhaps also more correct to talk about “immune systems”, because there are other mechanisms involving in immunity beyond antibodies.
What tends to determine the severity of symptoms is the nature of response to the infection a person develops. Viral replication itself does not on its own necessarily produce dangerous symptoms anymore than replication in normal cells, the bodies ability to manage the response moderate’s symptoms.
Isn’t a Corona, basically an undetectable “common cold”?
With all this research, as a layperson when all is said and done…
Still sounds like “well, we are close, but still don’t know anything?” Seems the whole idea…. This “thing “ is attached to something common and insidious… it’s difficult to track…
Corona’s seem common, and difficult to track…
It seems something bad has been attached to the Common Corona…(one one bad actor) and results may be bad for some, not others (as is the case with Corona/common cold) yet the synthetic bad actor has been attached and is doing its stuff…
A
Is everyone following a red herring…”Corona”?
Don’t know much about anything here…
Just wondering…