are covid vaccines causing persistent covid?
and might a shift in antibody response be the piece at the center of the mosaic?
well, getting back on twitter sure gets gallons of research sprayed at you like a firehose at a teacup. i am still getting up to speed on this, but the implications are vast and the eerie perfection of the way this piece seems to slot into the center of several puzzles makes me want to take this discussion out into realm of unfettered review so we can hash it through and see if this is, indeed, what it appears it is.
i want to caveat this is still somewhat speculative on my part and i want to urge more work here not over rapid acceptance/concern, but it’s such an odd shaped piece fitting so perfectly into such an odd shaped hole that i cannot quite get over the sense that there is something here.
it’s just going to take some time to get comfortable with.
thanks to RINTRAH who put together a great piece here that pointed me in some very useful directions.
i like to read all the source material myself to be sure i’m getting it right, so we start HERE in some pretty detailed immunology (which, believe me, is a VERY difficult discipline and far less well understood than most realize)
but what’s going on here is, while a complex system, actually remarkably simple and may well be the mechanism that ties together antigenic fixation/OAS to long covid effects, organ damage, and persistent excess deaths in the covid vaxxed world.
we have been repeatedly told that “these vaccine boosters induce antibody response” as though that proves efficacy and in order to sidestep a need for clinical data. but the reality is much more complex.
just making antibodies means little. you need to know how well they work. produce the wrong ones and you get antigenic fixation and vaccine advantaged virus. this is a known and knowable problem with “leaky” vaccines.
but there are other issues one can run into as well, particularly what the types and roles of antibodies elicited are.
and what’s going on in boosters appears worrying.
so let’s look.
volunteers received three doses of the mRNA vaccine Comirnaty as detailed in Table 1. Serum samples were collected at a median of ten days after each vaccination (post first, post second, post third) as well as during follow-up visits at 210 days after the second vaccination (FU second) and 180 days after the third vaccination (FU third). Ten individuals experienced a breakthrough infection in the time frame between post third and FU third (indicated by grey circles). The different IgG subclasses were quantified by flow cytometry using recombinant monoclonal receptor binding domain (RBD)-antibodies as a standard.
this is the outcomes data:
this looks like 3 out of 4 IgG antibodies are up. so if we accept “antibodies = efficacy” this looks great.
but what if it means something very different?
as we can see HERE effective response to covid is more about quality than quantity.
IgG3 is 42% of neutralization, but only 3% of mass.
this means 2 things:
1. IgG3 is a big part of the ballgame.
2. it’s easy to miss or swamp by changes in other volumes.
consider that as single figure “mouse data” is used to validate booster efficacy.
Fig 4. Comparison of neutralization capacity against total Ig mass.
(A) Contribution of Ig classes to the neutralization of SARS-CoV-2 (percentage contribution) based on experimental data depicted in Table 1. (B) The abundance of Ig classes as percentage of total Ig in convalescent plasma pool are based on quantitative nephelometric results.
and that gets worrying.
jumping back, the irrgang study, like many of its ilk, buries the really interesting stuff in the supplemental data (can be downloaded at the end of the link above)
red boxes/lines are added by me.
what the “mouseketeers” want you to see is the red line. that is being pushed as “efficacy.”
but what looks like it matters is figure C.
what we are seeing here is the near total elimination of IgG3 response in the boosted, especially in those (gray circles) who got breakthrough infections. as that was the most potent vector, that’s a big loss.
IgG4 response is way up, especially in the gray dots which indicate a breakthrough infection. is this post boost infection unlocking this effect or this effect making post boost infection more likely? i’m not really sure and we’d sort of need to see some more longitudinal study there for me to make a confident call.
one can tell from the supplement that the 4 highlighted subjects had breakthrough infections post d3 and before follow up. i’m not exactly sure how this maps to the gray dots as clearly, there are more than 4. i am guessing those were earlier breakthroughs but the fact that the gray dots have such high IgG4 response (and half the IgG3) is provocative.
it potentially represents a real problem because, in many cases, IgG4 is not your friend.
•The role of IgG4 in IgG4-RD could be pathogenic, protective, or a fortuitous marker of an aberrant inflammatory response.
•Beekeepers and patients after allergen immunotherapy possess high serum IgG4 protective against anaphylactic reactions.
•IgG4 autoantibodies are pathogenic in immune-mediated pemphigus vulgaris, pemphigus foliaceus and MuSK-myasthenia gravis.
•IgG4 antibodies inhibit clearance of tumor cells or the invader, respectively, in melanoma or helminthic infections.
•In IgG4-RD, IgG4 alone can be pathogenic, but may also dampen the more harmful effects of IgG1 when directed against the same epitopes.
IgG4 acts as a form of “shepherd” for chronic exposure to things that should not always be pathogens. you get irritated by cat dander and your body responds with histamines and inflammation. but binding by something like like IgG4 would attenuate or even stop that response.
IgG4 is not about removing a pathogen, it’s about creating a “tolerance” by preventing your body from attacking whatever it has bound to. this may be fine for peanuts, but for a replicating respiratory pathogen with high organ affinity, it could be an all access arson pass to burn you down while you fail to elicit any effective immune response.
mistaking a virus for an allergen is a very, very bad outcome.
and this is where you get the nasty OAS issues i’ve been banging on about for a year or more and that keeps showing up in the data
over and over in dozens of places including this dire outcome in the UK data
and it may explain the surge in relative risk when boosters were applied. (it really is a shame they stopped providing this series)
this also coincided with shift in variant (chart in link above).
i had been presuming that we’ve been looking at viral escape as evolutionary forcing selected for vaccine advantaged viral strains, but this IgG4 issue adds a whole new wrinkle on just what this pathway may be.
whether this same issue would have happened vs earlier strains (alpha, beta, delta, etc) would be a highly illuminating experiment to run, but there is sound reason to presume viral evo as a driver.
leaky (non-sterilizing) vaccines are exceedingly dangerous. there is a reason we don’t use them. viruses that can still replicate and spread get forced toward variants that take advantage of the vaccine and its having locked you into one, narrow response vector. and if they can find variants that elicit no IgG3 and lots of IgG4, they get to run riot.
and if you have created a widespread homogeneous herd immunity profile that can be taken advantage of, you’re really in for it.
everybody gets this and no one can generate sound immunity.
this would be entirely unprecedented in human history.
this proposed method of action could be telling us a ton about all the observed issues with excess mortality all over the high vaxx regions, about the fact that it takes the vaxxed longer to clear covid virus, that they carry higher viral loads, AND that they experience “mild” seeming symptoms but then often see some other pathology emerge with sudden severity.
if your immune system is being told to stand down and ignore virus, the virus can hang around a long time and do A LOT of damage and you’re not really going to notice. you won’t get the inflammation and perhaps fever. you’re walking around infected and contagious, but with no sense that you are.
it explains the cleveland clinic data showing that more doses of vaxx leads to more covid that so many have been passing around of late.
and the higher covid hospitalization rates in the vulnerable we’re seeing year on year in many bellwether locations. (far right data is still incomplete)
there is clearly something very wrong going on with the covid vaccines. if ever they reduced spread or contraction of covid, they now seem to multiply it.
if ever they reduced all cause mortality (not proven at all in their approval studies) they now seem associated with higher society scale mortality rates and these rates appear persistent.
it’s time the health agencies, especially those with really good data like in the UK, sweden, israel, etc, stopped playing “hide the ball” and started releasing all cause mortality data stratified by vaccine status.
if these hypotheses are inaccurate, then let’s put them to bed. i really do not want to see this outcome proven out. it’s objectively awful and the ramifications would be horrific. but given that health officials, especially in the US are still pushing these products aggressively, if this is going on, we need to know. this is not something you want to be in the dark about.
this is not a difficult analysis, but we need the data to make it definitive.
the ongoing failure to provide it or even seem interested really starts to seem to stand as indictment.
the purpose of public health is supposed to be to serve the public, not to keep it in the dark.
I didn't go through the entire paper yet, but this quote from the abstract is interesting, "This induction of IgG4 antibodies was not observed after homologous or heterologous SARS-CoV-2 vaccination with adenoviral vectors."
It goes along with a comment I had on the post from the other day "did covid vaccines prevent covid deaths in the US?", in terms of different non-specific effects (NSE) of different types of vaccines, including mRNA, adenovirus vectored, subunit, and whole virion (including distinctions among 'adjuvants').
The paper I posted was specific to covid and looked at mRNA vs adenovirus...
Beyond that, I think watching India may be interesting since, while highly vaxxed, it did use primarily adenovirus (Covidshield aka Astra Zeneca) and whole virion (Covaxin) vaccines. In my view the latter may be particularly interesting regarding the IgG4 issues since it should overcome the spike-only fixation (being whole virion), but also its adjuvant (a TRL7/8 agonist) predicates more of a Th1 response (i.e. cell mediated) vs. a Th2 response (i.e. antibody) typical in an alum (only) adjuvanted vaccine (e.g. the Chinese whole virion vaccines). I have wondered for a time if this could enable it (Covaxin) to 'fix' the immune suppression of the mRNA shots from both an OAS perspective (fixaxtion to spike) and innate suppression (inherent w/mRNA shot design w/pseudouridine modification, etc.). Allegedly Phase 3 'immunobridging and broadening' trial data may come out in January (homologous and heterologous w/mRNA or adenovirus).
Irregardless, I think the potential angle (in terms of remediation) may be along the lines of other work from Christine Stabell Benn (author of paper above) which suggests negative NSE of certain vaccines could be undone by other vaccines/protocols (https://pubmed.ncbi.nlm.nih.gov/32645296/).
N.B. Novavax also contains an adjuvant biased towards Th1 response as well.
Thanks for taking us a little deeper into this. Jeff Childers' substack ("Coffee & Covid") had a great layman's explanation today, which was the perfect lead-in to your piece just as it landed in my inbox. You guys are doing such GREAT WORK educating the public on all of this. Thank you, thank you, thank you.