(Not) Coming Up
Another tiresome look at the UK data! Or not. Plus: Original Antigenic What Now?
A sentence contained in the latest UK Human Surveillance Agency Sorry Health Security Agency Haha Isn’t That Funny, It Just Slipped Out; No But Seriously We’re Going to Put All of You in the Camps Quite Shortly Updatehas set off a barrage of alarmist posts in “Covid-vax skeptic world.” I wish to downplay it briefly, and move on. I am still mentally drained from the fugue which resulted in Wednesday’s post; forgive the tepid tone.
The sentence concerns charts on prevalence for antibodies to the spike protein (the target of the pseudo-vaccines) and the nucleocapsid protein (“N,” which would only be derived from natural infection) in highly Covid-vaccinated blood donations. Despite the tsunami of cases in the UK’s “summerautumn wave,” levels of “N” protein in sampled blood donations don’t seem to be coming up very much. Is this because the infected (especially elderly infected), among other possible changes in behavior, are less likely to continue donating blood - or has something “broken” in the memory immune response of the Covid-vaccinated?
The sentence (emphasis added):
Seropositivity estimates for N antibody will underestimate the proportion of the population previously infected due to (i) blood donors are potentially less likely to be exposed to natural infection than age matched individuals in the general population (ii) waning of the N antibody response over time and (iii) recent observations from UK Health Security Agency (UKHSA) surveillance data that N antibody levels appear to be lower in individuals who acquire infection following 2 doses of vaccination.
“Recent observations” does not mean observations of recent outcomes. Plenty of “recently” published studies have been time capsules of post-Covid-vaccination infections from the spring. In the review of the “swab” study in September, I lamented that such out-of-date studies could easily be used to unwrite the admission that the Covid-vaccinated can catch and transmit the virus as easily as their unpersoned peers.This has indeed been the case.
Just as easily, such a study could have been used to provide grounds for the comment above, and thus seeded the subsequent declaration that post-“breakthrough” immunity is kaput - in advance of a single shred of evidence that “breakthrough” convalescents are becoming reinfected.
In fact, in reviewing the Security Agency statement as evidence that “Mass vaccination may permanently attenuate population-wide immunity to SARS-2,”the blogger eugyppius alludes to a letter to the editor published in the Brit-centric Journal of Infection on the 1st (but posted online in August) that finds deficient generation of N protein antibodies after “breakthrough” infection by looking, quite predictably, only at early results:
For these 23 participants, the median number of days between second vaccine dose and positive PCR was 30 days (IQR 25–50 days)
Note that the referenced study (which actually took place in Ireland) was published in July, so there isn’t actually much reason to suppose that the letter to the editor quoted above is the source of the Security Agency statement. Nonetheless, it exemplifies the type of “breakthrough” infection research that can still be classified as recent. Thus, in advance of knowing the actual source of the Security Agency “observations,” there is no reason to use them as a basis for concluding anything. Early “breakthrough” infections are less symptomatic, and more prone to false positives; post 4-month “breakthrough” infections are more likely to be the real deal.
The other portions of the statement, meanwhile, strongly argue against extrapolating from the blood donor seroprevalence charts to the rates that would be found in the general population. The sample, again, likely selects both for high rates of Covid-vaccinated and low rates of post-infection donors (with the latter bias increasing with age). The chart has no value anymore. It has ceased to be a window into reality; it is a mirror reflecting the observer.The coverage that the Security Agency’s throwaway statement has nonetheless generated is slathered with one term in particular: “Original Antigenic Sin.” But this term, like so many others in “leaky vaccine” discourse, is limited in application. Not all viruses are alike; not all “vaccines” are alike; and not all vaccinees are alike. (Further, viral encounters in youth are not the same as vaccinations in youth.)
Inoculation of adults, outside of certain historical contexts, is a fairly novel phenomenon. With it, has come the (re-)discovery that the adult immune system is not as easy to edit as the immune system of children. The pseudo-vaccine for flu is not the only example. A 2016 study by Wiedermann, et al., which reviewed modern difficulties in adult vaccination, noted:
Non-responsiveness increases with age and in particular vaccination to a novel vaccine in persons > 65 years is associated with a high low/non-responder rate, indicating that vaccine schedules and doses (at least for primary vaccination) should be adapted according to age. [...]
The reduced responsiveness of the aged immune system is responsible for both increased susceptibility toward infectious and pathological events and suboptimal responsiveness to vaccination. […]
Generally very few vaccination studies exist in obese people, but it has been documented for some vaccines that an elevated body mass index (BMI) is associated with poor vaccine responsiveness.
In a sense, the ossification of the adult immune system is a double-edged sword. Certainly it contributes to less flexibility - T Cells in the elderly don’t expire as quickly,implying slower rates for remodeling immune response - but it also implies less impressionability. Is it really plausible that the immune system of adults is as easy to “set in stone” as the immune system of children?
Because “Original Antigenic Sin” has been applied to both infection and vaccination in modern research, I am not sure what use it really has as a term. It can mean, both, some type of memory immunity inflexibility following first exposure to a viral antigen of which there are other variants in the wild, or some type of “fooled me once” effect when the immune system cannot be forced to take interest in more than one version of a viral antigen via vaccination. In either case, the variant antigen, out there in the wild, is in a sort of unhappy valley between familiarity and distinction; encounter it at your peril. Both the infection and vaccination context of the term come into play with Dengue Virus.Thus, to say that the Covid vaccines might cause “Original Antigenic Sin” - which now also means “might cause difficulty in immunizing against something else similar” - is an ambiguous claim. And neither outcome suggested by that ambiguity is strong cause for alarm.
The Covid vaccines are probably not so dramatically imprinting the immune system to begin with - to say that they are requires asserting that they rewrite lifelong familiarity with coronavirus. They might disable immunity against coronavirus, but that doesn’t mean they have done so via imprinting (rather than other mechanisms of antibody dependent enhancement, namely IgE sensitization, that are more commonly mentioned in coronavirus vaccine research failures).
The Covid vaccines might, on the other hand, be “using up” the one chance to synthetically trick the immune system into generating a custom coronavirus spike antibody - but does this have any significance? Coronaviruses are respiratory infections; they do not appear in the body by being injected into the blood by mosquitoes. Prior immune familiarity to coronavirus proteins does not depend on anti-spike antibodies - the spike protein, in fact, is akin to an “afterthought” when the immune response is observed on the level of T Cells, which appear to focus predominately on “structural” proteins. And if Covid-vaccinated “breakthrough” immune responses turn out to be deficient in sensitivity to these structural proteins, does that really mean it’s because they were too similar to the spike? Again, it’s more likely that another mechanism of antibody dependent enhancement would be the more appropriate description here.
These mechanisms, quite critically, would resemble something that is already so familiar to humanity’s experience with SARS-CoV-2 that it is as omnipresent as the Google logo - i.e., “(Severe) Covid-19”: Inflammation-enhanced infection, as if due to previously-primed IgE antibodies or some other similar immune dysfunction. The Covid vaccines, if they do cause antibody dependent enhancement, will likely do so in a way that responds to the same therapeutics that have already been found effective in naive infection.
(For further discussion, see “(Non-) Update to ‘(Not) Coming Up.’”)
Ah, but what to make of the rest of the Security Agency report? Shall we not dive back into the “real-time” efficacy rates - shall we not gawk at the surge in unvaccinated hospital admission rates? No. Rather, I think it is time to move on. The reason is threefold:
I have become skeptical of the accuracy of the Agency’s figures for unvaccinated populations in each age group. Incorrect population counts, obviously, would distort the per-100k rates.
The boosters - rolled out starting September 16 - make it unclear how many doses individuals in the “fully vaccinated” category have actually had.
The world, at the moment, has become a choose-your-own-reality book. Post Covid-vaccine patterns of viral spread have become quite altered in places that are not even heavily vaccinated (Russia); they have reverted to normalcy in other places that are (Florida); and, of course, the reverse can be observed in both categories as well. Anyone who believes anything only needs to set their view-finder to the appropriate region, and they will find support for their belief. One could rewrite the map of Earth so that the names of countries are replaced with the names of theories for how the Covid vaccines are working.
As I remain sanguine on antibody dependent enhancement - I think it will happen, but that it will be manageable wherever effective therapies are not suppressed - I see little reason to focus on controversies of the virus itself, for the moment.
The triplet of catastrophes which will determine the short-term fate of humanity are the probable direct harms from the Covid-vaccines- especially cancer, which I will be writing about next week - the likely widespread use of Molnupiravir this winter, and the passports which are paving the way for state violence and civil war. Hopefully my sense of humor will be replenished in time to tackle the cancer bit.
Play us out, Paul!
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Referring to “Scienceme Street.”
From the Week 42 report:
“Seropositivity estimates for S antibody in blood donors are likely to be higher than would be expected in the general population and this probably reflects the fact that donors are more likely to be vaccinated.”
See “Travels to Maskladesh.”
Here, naturally, The Asylum has risen the occasion. See: Spencer, Craig. “No, Vaccinated People Are Not ‘Just as Likely’ to Spread the Coronavirus as Unvaccinated People.” (2021, September 23.) The Atlantic:
“Even in the United States, where more than half of the population is fully vaccinated, the unvaccinated are responsible for the overwhelming majority of transmission. […]
[The Covid-vaccinated] are likely contagious for a shorter period of time when compared with the unvaccinated, and they may harbor less infectious virus overall.”
This claim stupidly links to an irrelevant study from China and a study which seems to blend early and later “breakthrough” infections, with the natural result that the averages for clearance are lowered in the Covid-vaccinated group, but the surprising result that the vaccinated score lower for peak cycle counts (implying potentially higher peak viral load), which totally contradicts the hyperlinked claim. (Kissler, SM. et al. “Viral dynamics of SARS-CoV-2 variants in vaccinated and unvaccinated individuals” - Figure 2 A and E display peak viral loads. B, C, and D hint at a relation between time from Covid-vaccination and length of “breakthrough” infection, if Alpha is a correlate for spring infections and Delta a correlate for summer infections. However, no actual values for days since 2nd dose appear to be provided.)
eugyppius. “Mass vaccination may permanently attenuate population-wide immunity to SARS-2.” (2021, October 21.) eugyppius.substack.com.
Allen, N. et al. “Serological markers of SARS-CoV-2 infection; anti-nucleocapsid antibody positivity may not be the ideal marker of natural infection in vaccinated individuals.” Journal of Infection. Volume 83, Issue 4, E9-E10, October 01, 2021.
(index link anchor)
Wiedermann, U. et al. (2016.) “Primary vaccine failure to routine vaccines: Why and what to do?” Human Vaccines and Immunotherapeutics. 2016 Jan; 12(1): 239–243.
And may be heavily “colonized” by immune-evading viruses that favor less dynamic remodeling, such as by betaherpesvirus 5. For more on this impressive and nearly-universal genetic visitor, which I believe cannot be anywhere near as malicious as it is believed to be, see “Crackpot Corner: Marekspocalypse Edition.”
However, the application of the term to describe the infection dynamics of Dengue Virus isn’t really helpful, anyway. Again, the context is unique - Dengue Virus is spread by mosquitos, so exposure is often delayed into adulthood. Dengue antigen “imprinting” leading to later ADE is thus frequently a feature of primary (i.e., “original”) infection in adults, and it isn’t clear (to me, because I forgot my own research) whether it is as serious a problem for primary infection during childhood. Dengue secondary infection outcomes are better described as a form of ADE (with attendant implications for coronavirus vaccination). “Original Antigenic Sin” should probably remain limited to it’s original application, the flu virus. At which point it becomes questionable (to me, because I have done little research on influenza) whether Francis’ original results (from literally 1960) can even still be reproduced.
Including the immortal controversy of its origins. Nonetheless, I cannot help but recommend today’s overview, by Mathew Crawford, of the evidence that SARS-CoV-2 was already widespread in China as early as 2018: “The Earlier Lab Leak Hypothesis.”
It is excellent reading, and the implications are beyond intriguing - it would imply that California, and much of the west coast by extension, had already acclimated to SARS-CoV-2 in the years before 2020, perhaps in the form of an earlier variant that just fails to be reflected by antibody testing (and widespread antibody levels already would have dropped, by that point). Similar possibilities would explain India’s resilience, urban Bangladesh’s high seropositivity rates, etc. It could even account for a brief illness that knocked me out in October 2018, just after a few months spent in the Bay Area (I’ve never bothered getting an antibody test)!
Two posts hot off the presses worth reading on the subject:
Kilpatrick, Joel. “Ventura County Nurses Blow the Whistle on Crisis in Local Health Care.” (2021, October 21.) The Conejo Guardian.
“One fit, healthy nurse in her twenties whom Daniel knows went into cardiac arrest three weeks after she received the Pfizer shot. An aortic dissection ruptured a portion of her aorta like a balloon. She was resuscitated, underwent open-heart surgery and made a full recovery. But she could not abide the suggestion that the COVID vaccine shots had caused it.”
el gato malo. “did covid vaccines cause a spike in cardiovascular and neurological issues?” (2021, October 22.) bad cattitude.
German hospitalizations for cardiovascular and neurological issues show a clear, aberrant elevation starting in the spring. (This mirrors the signal observed during the roll out of triple-dosing in Israel. See “Dashboard Divinations, take 5.”
For my list of the likely dangers of Molnupiravir, see “Doppelgänger” (now updated with a cover graphic!).
As someone who relies quite heavily on the Seroprevalence data in my own analysis - I don't know that I can argue with your conclusion that it's becoming something that's not worth what it used to be. Not only is there a time dependent peak and fade in antibodies in even the S protein (with no mention similar to the N antibodies), their shift from 4 to 12 week sampling (and once monthly reporting) is mystifying to me in a report that it all about looking at the recent timeframe. If I were a suspicious man, I'd say it's to use the peak antibody levels from 8-10 weeks back to mask a rapidly fading level in their oldest populations long enough to get the booster campaign really going. I suspect it might have been stealth enough that many of their target demographic weren't really aware of it.
Their new antibody level charts do show some evidence of their silent booster campaign, but it really isn't marked at the moment aside from the 70-84 year-old group.
But this all adds up to the data possibly undergoing more manipulation that was originally the case. And data manipulated before it gets to us in unknown ways is kind of useless for analysis.
I really really wish you were wrong, but I've got a sneaking suspicion that you aren't.
Excellent reading - thank you Brian. I apologize that I will have to read more than once in order to fully digest. I keep going back to Footnote #13. Your surmising is supported by Peter Doshi https://www.bmj.com/content/370/bmj.m3563 who articulates evidence of SARS-CoV-2 T-Cell reactivity in US blood specimens between 2015 and 2018. If you REALLY want to find out whether you caught it, https://www.t-detect.com/ allows for T Cell testing. Sadly, mine was negative. But I was happy to know either way.