Seminal research show you Original Antigenic Sin (OAS) which I have now termed 'Mortal Antigenic Sin' (MAS) (Aguilar-Bretones et al. Seasonal coronavirus–specific B cells); the imprint is 'fatal'

by Paul Alexander

I argue that in original sin, you absolve yourself with baptism that wipes the child of the original sin, but the case of immunology & virology/vaccinology, initial prime/exposure/imprint is 'fatal'

I am arguing or stating firmly, IMO, that the vaccines are subverting the immune response to SARS-2 and the OAS/MAS can explain this. We are actually witnessing this in the UK, Scottish, Israel data, where there is massive infection in the vaccinated persons over the unvaccinated persons. The vaccinated persons then are getting sicker in the deeper respiratory tract and lungs and actually transmitting virus.

What I am referring to surrounds the initial priming or exposure or imprinting of the immune system; if the initial prime or exposure is optimal or sub-optimal, then that would be the immunological response to that pathogen life-long; in other words the immune system is prejudiced or biased to that prime; if the initial prime is to vaccine the the immune response is antibody systemically, then that is the response even when you are exposed to localized infection in the respiratory tract; the response demands localized cytolytic cytotoxic cellular response e.g NK cells etc. to clear out the site of infection, but you may have prejudiced and convinced the immune system to respond with antibodies and not the correct Ab and NK response etc. at the localized site of the mucosal lining/barrier etc. where the virus usually lands etc. This initial prime is set and in this case this is a sub-optimal ‘incorrect’ response. I argue this too is OAS/MAS.

The following is an example also of OAS where the immune system developed an Abs response to circulating coronaviruses that cause common colds and this is seen to prejudice the immune response even when now exposed to SARS-CoV-2…in other words, the immune system is responding as if it were facing the initial exposed to coronaviruses.

OAS/MAS study one example:

Study “Seasonal coronavirus–specific B cells with limited SARS-CoV-2 cross-reactivity dominate the IgG response in severe COVID-19” , Muriel Aguilar-Bretones et al.

Summary to consider how OAS works here:

They assessed antibody reactivity to nucleocapsid and spike antigens and correlated this IgG response to SARS-CoV-2 neutralization. Patients with COVID-19 mounted a mostly type-specific SARS-CoV-2 response. Additionally, IgG clones directed against a seasonal coronavirus were boosted in patients with severe COVID-19. These boosted clones showed limited cross-reactivity and did not neutralize SARS-CoV-2. ‘This study included 20 patients with severe COVID-19 who had reverse transcription-PCR–confirmed (RT-PCR–confirmed) SARS-CoV-2 infection and were admitted to the ICU with ARDS. Additionally, 12 RT-PCR–confirmed SARS-CoV-2 patients with COVID-19 who had only mild coronavirus infection–related symptoms and 6 RT-PCR–negative disease controls with similarly mild symptoms were included. None of the patients with mild disease was admitted to the hospital.’

What they found was that in severe COVID patients vs the milder patients, the response was mainly IgG Abs geared towards seasonal coronaviruses. This meant that the severe patients were responding immunologically NOT to SARS-CoV-2 (COVID) virus (via what we would expect e.g. naïve B cells imprinting on SARS-CoV-2 COVID virus) but rather long lived memory B cells that were generating Abs against common cold coronaviruses (more common circulating and benign coronavirus that they were exposed to prior in their lives). This is what OAS/MAS is, for the immune system is now trained or learnt and imprinted a memory based on the initial prime or exposure to prior coronaviruses that were circulating. So now that they are exposed to COVID virus, the immune system has a memory to the initial coronavirus and these are the Abs being churned out by the B-cells as part of the present response. The ‘WRONG’ Abs. Importantly, it is beyond that they are the wrong Abs being produced and sent to respond, but it is that they subvert a more robust and accurate naïve B-cell response to the existing COVID virus.

This is why I have renamed OAS the MAS, for the flaw or initial imprint prime is fatal…it prejudices and biases and determines all future responding to that pathogen or similar. In this case the immune system is recognizing COVID as a coronavirus as it should, and it is so similar to the prior coronaviruses exposed to with immune memory, that the immune system is sending that initial response. This is very problematic and we (Dr. Dan Stock and me) have argued that we can extend this OAS/MAS model to if the initial prime or exposure to COVID antigen (spike protein) was not virus (actual virus spike antigen) but actual VACCINE (and your immune system then made the artificial spike and immune response); your immune system may have built the Abs systemically to the artificial spike, but when you are then exposed to the actual respiratory COVID virus in the wild (which you will given we vaccinated during the ongoing pandemic), then that initial systemic Ab (in your blood) response would be sent again and again, when the correct localized response in the respiratory tract (mucosae) is not sent which allows virus to build up, the lungs get sicker, and you are then capable of transmitting virus.

Bhakdi has gone as far to posit that the vaccinal Abs can never reach the mucosal layer and thus why the vaccine can never work and never did work. I find very plausible. There is also Marek’s disease Read et al. at play here that could explain this (vaccinated chickens model).

It is near certain in my mind that OAS and the initial prime/exposure/imprint being to vaccine and thus vaccinal Abs being produced, that subsequent exposure to the virus as it circulated e.g. Delta and the predominant OMICRON, has the virus building up in the naso-pharyngeal; passage while the immune response is systemic into the blood stream (circulating IgGs) where it is not needed. Coupled with the vaccinal Abs cannot reach the mucosal layer. We needed a vaccine that was nasal, introducing nasal antigen to provoke a localized mucosal response e.g. Secretory IgG, etc.

What was done with these vaccines seems as if they were designed to fail. They never worked!

The researchers concluded:

“In conclusion, we found robust OAS in patients with severe COVID-19. Boosted CCC-specific IgGs did not substantially contribute to SARS-CoV-2 neutralization, which is considered key in immune protection. Moreover, recent studies showed that the rise in CCC-specific IgG titers does not contribute to CCC neutralization and is not associated with protection (33, 34). These findings mitigate any positive effect of CCC antibody backboost in maintaining broad immunity to preceding infections, as was described for influenza virus (12). We believe that the detailed insights into the kinetics and cross-reactivity patterns of N- and S-reactive IgGs presented in this study will aid in the interpretation of serological studies and further expand our understanding of how the CCC-experienced humoral immune system responds to SARS-CoV-2. Our study underscores the notion that the immunological background of individuals needs to be considered an important factor in assessing the quality and quantity of a newly initiated antibody response to SARS-CoV-2, either by infection or vaccination.”