Let’s talk about sin, baby (the original antigenic variety)

28 February 2022

I’ve discussed the problem of original antigenic sin in relation to experimental COVID-19 injections here, here, here and here, but with the recent publication of an article in the prestigious scientific journal Cell, it’s time to revisit the topic.

First, a quick refresher on original antigenic sin (OAS). As I wrote in Lies, damned lies, and ATAGI statements, OAS

“is a type of ‘programming of the immune system by its first exposure to a particular antigen. When it subsequently encounters a similar pathogen, it attempts to respond using the same strategy as it used to defeat the first pathogen, but this response will be ineffective if the new pathogen has evolved different strategies to establish infection.”

First proposed by Thomas Francis in 1960 to explain why susceptibility to (apparently) new strains of influenza varied by birth year, OAS is also thought to account for vaccine failure in human papillomavirus (HPV) and influenza vaccination campaigns.

In a nutshell, if

a) a person is exposed to a viral antigen (a part of the virus that triggers the immune system’s defence mechanisms), either by infection with the virus itself or through vaccination, and

b) the virus subsequently develops significant mutations in this antigen, and

c) the person is exposed to the mutated virus, then

d) the antibodies produced by the person’s immune system may not be capable of neutralising the virus, which is what antibodies are meant to do, and may in fact produce a worse outcome by triggering a hyperinflammatory response (“disease enhancement”).

Now, let’s take a look at that new paper in Cell. Titled ‘Immune imprinting, breadth of variant recognition, and germinal center response in human SARS-CoV-2 infection and vaccination‘, it’s a long and technical read, but worth ploughing through in order to grasp how comprehensively the authors studied human immune responses to SARS-CoV-2 infection and COVID-19 inoculations.

The study’s authors conducted detailed analyses of:

• The quantity and types of antibodies formed after either infection with SARS-CoV-2, or inoculation with the Pfizer, Moderna, AstraZeneca, Sputnik V or Sinopharm injections;
• The level of spike protein in lymph nodes and bloodstream after injection with an mRNA product (Pfizer or Moderna);
• The effect of infection or inoculation with the Pfizer injection on production of antibodies to other types of coronavirus, including SARS-CoV-1 and the four endemic coronaviruses that cause 15-30% of common colds.

And here’s what they found:

1. The injection-induced immune response is narrower than the infection-induced response

In contrast to the broad and balanced immune response induced by infection with SARS-CoV-2, which stimulated antibodies of multiple types (immunoglobulins A, M and G, respectively abbreviated IgA, IgM and IgG) to both the spike protein and nucleocapsid or core protein of the virus, the Pfizer COVID-19 injection “induced a highly IgG-polarized serological response with minimal IgM- and IgA-binding spike and RBD [receptor binding domain]… Principal component analysis (PCA) showed clustered and homogeneous SARS-CoV-2 spike and spike-domain-specific serological responses in BNT162b2 vaccinees compared with infected patients.”

Or, in plain English, people who received the injection made only one class of antibodies – IgG – to only one part of the virus – the spike protein, which is the most rapidly-mutating part of the virus. On the other hand, people who got infected with the virus made multiple types of antibodies to multiple parts of the virus, auguring well for their immune system’s ability to recognise and fend off infection with variants.

2. The Pfizer injection induces levels of IgG antibodies to spike protein that are as high as those in people with severe COVID-19 (but that’s not necessarily a good thing)

“BNT162b2 [Pfizer] vaccinee RBD and spike IgG concentrations were comparable to those of severely ill patients [people who got COVID-19] and higher than those of mildly or moderately ill patients for anti-RBD antibodies at day 42.”

Immune imprinting, breadth of variant recognition, and germinal center response in human SARS-CoV-2 infection and vaccination

The authors presented this finding as if it was a selling point for the injection, but other research has found that high levels of IgG to spike protein in COVID-19 patients actually causes lung damage, by forming immune complexes with the viral spike protein that trigger the hyper-inflammatory state known as a cytokine storm:

“In COVID-19 patients, high anti-Spike IgG titers are associated with disease severity… anti-Spike IgG from severely ill COVID-19 patients does not only induce hyperinflammation by macrophages, but also may contribute to permeabilization of pulmonary endothelium and microvascular thrombosis… anti-Spike IgG from serum of severely ill COVID-19 patients induces a hyper-inflammatory response by human macrophages, which subsequently breaks pulmonary endothelial barrier integrity and induces microvascular thrombosis.”

Anti-SARS-CoV-2 IgG from severely ill COVID-19 patients promotes macrophage hyper-inflammatory responses

The Cell study authors acknowledge that their ability to detect spike protein in injection recipients’ bloodstreams after the second shot is likely hindered by this very process of circulating immune complex formation, but they neglect to discuss the worrying implications of their own conclusions:

“The detection of spike antigen in plasma samples is impeded after second dose BNT162b2 vaccination, likely due to the formation of circulating immune complexes of anti-spike antibodies and spike protein.”

Is this immune complex formation why we see such high rates of immune-mediated disorders such as myocarditis after the second shot?

And are there adverse immunological consequences of becoming infected with SARS-CoV-2 whilst IgG antibodies are highly elevated? Is that why we’re seeing outcomes like this:

… and this:

… indicating increasing rates of severe COVID-19 among the fully jabbed?

And then there’s the role that IgG can play in generating pain. Does this help explain the massive number of reports of chronic pain submitted to pharmacovigilance systems after COVID-19 injections?

A quick search of OpenVAERS, for instance, turns up over 1 million submissions that include the term “pain”.

While some of these reports describe temporary injection site pain that resolved within days, many others tell harrowing tales of body aches, shooting pains that come and go without apparent cause, unrelenting stabbing pain, and pain in the injected limb that has persisted for months post inoculation, hampering or even preventing normal activities of living. Is there a connection between persistently elevated IgG levels post-injection and these reports of chronic pain?

The taxpayer-funded National Institutes of Health isn’t interested in finding out, although they acknowledge that the horrific symptoms suffered by AstraZeneca trial victim Brianne Dressen, and many thousands of others like her (some of whom have been driven to suicide by their intractable pain), are “an immune mediated response to the spike protein”:

But somehow the NIH has plenty of that lovely taxpayer money to throw at woke issues:

3. Natural immunity develops over time to more effectively target SARS-CoV-2 variants and other coronaviruses, whilst injection-induced immunity remains ‘fixated’ on the original Wuhan strain

“Viral variant infection elicits variant-specific antibodies, but prior mRNA vaccination imprints serological responses toward Wuhan-Hu-1 rather than variant antigens.”

Infection with SARS-CoV-2 initially stimulates the production of antibodies that target the variant with which one was infected, with the immune response broadening over time to recognise other SARS-CoV-2 variants (as well as two of the four endemic coronaviruses to which SARS-CoV-2 is most closely related):

“Over time, infected patient plasma samples showed improvement in variant RBD binding relative to Wuhan-Hu-1 RBD, suggesting evolution of the antibody response through at least 7 weeks post-onset of symptoms.”

“Infected patients showed greater boosting of spike IgG and IgA for endemic human betacoronaviruses OC43 and HKU1.”

However, the immune systems of people who received a COVID-19 injection and subsequently became infected with a variant of SARS-CoV-2 only produced antibodies targeted to the spike protein of the Wuhan strain of the virus, on which the injections were based:

“BNT162b2 vaccinee IgG Wuhan-Hu-1 to variant RBD binding ratios did not change from day 21 onward… We quantify a strong imprinting effect of prior vaccination with Wuhan-Hu-1 spike antigen on antibody specificities following breakthrough infection with viral variants… Despite breakthrough infection with Alpha or Delta viral variants, the vaccinated individuals showed patterns of IgG binding to viral variant RBDs similar to those of individuals exposed to only Wuhan-Hu-1.”

Notably, original antigenic sin (which the authors of this paper call “immune imprinting”) was only evident in people who had received COVID-19 injections:

“We find that prior vaccination with Wuhan-Hu-1-like antigens followed by infection with Alpha or Delta variants gives rise to plasma antibody responses with apparent Wuhan-Hu-1-specific imprinting manifesting as relatively decreased responses to the variant virus epitopes, compared with unvaccinated patients infected with those variant viruses.”

The authors of the Cell study claim that

“Although susceptibility to infection by viral variants is common to both vaccinated and convalescent populations, particularly as antibody titers decrease over time (Israel et al., 2022; Levin et al., 2021), our findings lead to the prediction that antibodies derived from infection may provide somewhat decreased protection against virus variants compared with comparable concentrations of antibodies stimulated by vaccination.”

However, this assertion does not accord with real-world outcomes.

Until the appearance of the Omicron variant (which, judging by the dramatic difference in its genetic sequence to other strains, may in fact not be a variant of SARS-CoV-2 at all), it was exceptionally rare for anyone who had recovered from infection with SARS-CoV-2 to become reinfected with either the same variant or any subsequent one, whilst “breakthrough infections” (infection after receiving a COVID-19 injection, otherwise known as “vaccine failure”) is common and increasing in frequency.

Furthermore, a follow-up study of infected individuals found that their “memory B cells display clonal turnover after 6.2 months, and the antibodies they express have greater somatic hypermutation, increased potency and resistance to RBD mutations, indicative of continued evolution of the humoral response.” In other words, no matter what variant of SARS-CoV-2 you were infected with, in the weeks and months after recovery, your immune system develops broad immunity to other variants.

4. COVID-19 injections induce elevated levels of B cells, and this may contribute to OAS

The Cell study authors note that “elevated frequencies of GC [germinal centre] B cells are seen after mRNA vaccination in healthy individuals” (N.B. germinal centres, which are located in secondary lymphoid organs such as the lymph nodes and Peyer’s patches of the intestine, are like nurseries for B cells, helping them mature and training them to make antibodies more effectively.)

Contrasting this to the decreased B cell count found in severely ill COVID-19 patients, they imply that increased B cells post-injection are favourable to the development of immunity.

However, excessive formation of B cells may contribute to OAS:

“It has been speculated that overproduction of memory B cells could compromise the activation of naïve B cells capable of producing efficient and novel antibodies.”

“Original antigenic sin”: A potential threat beyond the development of booster vaccination against novel SARS-CoV-2 variants

The sins of the pharmas shall be visited upon the injected

In summary, while original antigenic sin has been observed after either infection with, or vaccination against, other types of virus (most notably influenza viruses), in the case of SARS-CoV-2 there is no evidence of OAS occurring after infection, but mounting evidence that it is induced by COVID-19 injections.

But that’s not all that the Cell study revealed.

Contrary to assertions by “fact checkers”, public health bodies and the vaccine manufacturers themselves, the genetic material in mRNA shots (Moderna and Pfizer) is not quickly broken down and removed from the body.

In fact, the researchers found mRNA from the injections in the germinal centres of lymph nodes for as long as 60 days (beyond which the researchers stopped testing for it) after the second shot:

“We performed in situ hybridization with control and SARS-CoV-2 vaccine mRNA-specific RNAScope probes in the core needle biopsies of the ipsilateral [same side as injection] axillary [armpit] LNs [lymph nodes] that were collected 7–60 days after the second dose of mRNA-1273 [Moderna] or BNT162b2 [Pfizer] vaccination and detected vaccine mRNA collected in the GCs [germinal centres] of LNs on days 7, 16, and 37 postvaccination, with lower but still appreciable specific signal at day 60.”

They also detected genetic material from the injections at other sites besides the lymph nodes, albeit rarely:

“Only rare foci of vaccine mRNA were seen outside of GCs.”

And they found spike protein – which the mRNA in the shots instructs the recipient’s cells to make – in the bloodstream of the vast majority of inoculees, at essentially the same levels as in people severely ill with COVID-19:

“We detected spike antigen in 96% of vaccinees in plasma collected 1–2 days after the prime injection, with antigen levels reaching as high as 174 pg/mL. The range of spike antigen concentrations in the blood of vaccinees at this early time point largely overlaps with the range of spike antigen concentrations reported in plasma in a study of acute infection (Ogata et al., 2020) although a small number of infected individuals had higher concentrations in the ng/mL range. At later time points after vaccination, the concentrations of spike antigen in blood quickly decrease although spike is still detectable in plasma in 63% of vaccinees 1 week after the first dose.”

Injection-induced spike protein persisted in the germinal centres of lymph nodes for much longer – up to two months after the second shot:

“Spike antigen in mRNA-vaccinated patient LNs [lymph nodes] varied between individuals but showed abundant spike protein in GCs [germinal centres] 16 days post-second dose, with spike antigen still present as late as 60 days post-second dose.”

What does it all mean?

The short answer to that question is “pretty much everything you were told about COVID-19 injections is untrue”.

The longer answer is, we don’t know what the effects of provoking an unbalanced and narrowly-focused immune response to SARS-CoV-2, inducing elevated levels of IgG antibodies, and having mRNA and spike protein hanging around in people’s bodies for weeks to months after injection will be.

We may already be seeing the impact of original antigenic sin, immune-mediated and spike protein-induced pathologies on vast numbers of people.

But health authorities and regulatory agencies aren’t showing any interest in investigating the extreme safety signals being thrown off by pharmacovigilance databases like VAERS:

I’ll leave you to draw your own conclusions about what this stony-faced indifference to the suffering and death unleashed by experimental, inadequately tested, rushed-to-market COVID-19 injections by the health agencies that are supposed to be protecting us might mean. Here’s a hint about mine:

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