Chemaitelly et al.: "COVID-19 primary series and booster vaccination and immune imprinting"; what? 3 dose (includes 1st boost) elevates risk of re-infection vs 2 doses? Original antigenic sin (OAS)?

by Paul Alexander

These results once again raise serious questions as to the repeated injections & boosters for it is clear that antigenic sin operates; immune imprinting, fixation to the initial prime exposure

Yes, OAS in full force! The original prime or exposure prejudices the subsequent immune response to that exposure or similar and potentially life-long.

The potential nightmare is if the virus overcomes the sub-optimal population immune pressure on virus virulence and selects for sub-variants that could cause severe illness in the lower distal lung. Increased infectiousness in the upper respiratory tract is one huge challenge yet it is severe illness in the lower respiratory tract that keeps us up at night and it can happen with this sub-optimal non-sterilizing non-neutralizing vaccine and induced vaccinal antibodies that puts selection pressure on the spike and binding sites (infection and virulence) yet does not eliminate the virus.

This statement by the authors makes no sense when you consider the results, and typical woke writing, politicized garbage:

“These findings do not undermine the short-term public health utility of booster vaccination.”


Bottom line is that the 3rd dose enhanced infection (re-infection) in the vaccinee to omicron (and it’s subvariants) and this is exacerbated with each additional dose. It is classic OAS yet one can argue it is beyond OAS (immune imprinting and thus biased and prejudiced immune response/recall antibodies). Why? What we are finding is that the vaccine is actually causing the virus to become highly infectious as if gaining a property it did not have. The vaccinated are and became infected/re-infected especially in high vaccine coverage nations. With that is the increased risk of illness, severe outcome and death. We have seen this.

This study was an observational, matched, retrospective, cohort design and conducted to investigate differences in incidence of SARS-CoV-2 reinfection in the national cohort of persons who had a primary omicron infection, but different vaccination histories. History of primary-series (two-dose) vaccination was compared to that of no vaccination, history of booster (three-dose) vaccination was compared to that of two-dose vaccination, and history of booster vaccination was compared to that of no vaccination.’

It is clear that the repeated shots and boosters are subverting the immune system and deranging the response. The virus has become largely resistant to the potentially neutralizing vaccinal antibodies (that are now dominated by largely non-neutralizing vaccinal antibodies) and especially omicron and it’s sub-variants. It appears that the vaccinal antibodies are giving the virus properties it did not have prior in terms of enhanced infectivity and re-infection of the vaccinee. We are looking at classic antibody-dependent enhancement of infection (ADEI), viral immune escape and original antigenic sin (role of immune prejudice due to the initial prime or exposure). No doubt, immune imprinting OAS is in full force here with re-infection risk dramatically elevated with the 3rd dose vs 2nd dose.

See Liu et al. below as part of this debate.

Liu et al. (I bold the key statement of the study as it appears that binding to the N-terminal domain binding site and not the receptor binding domain binding site, induces greater infectivity by causing conformational changes to the RBD e.g. goes into the ‘up and out’ posture etc.):

‘Antibodies against the receptor-binding domain (RBD) of the SARS-CoV-2 spike protein prevent SARS-CoV-2 infection. However, the effects of antibodies against other spike protein domains are largely unknown.

Here, we screened a series of anti-spike monoclonal antibodies from coronavirus disease 2019 (COVID-19) patients and found that some of antibodies against the N-terminal domain (NTD) induced the open conformation of RBD and thus enhanced the binding capacity of the spike protein to ACE2 and infectivity of SARS-CoV-2. Mutational analysis revealed that all of the infectivity-enhancing antibodies recognized a specific site on the NTD.

Structural analysis demonstrated that all infectivity-enhancing antibodies bound to NTD in a similar manner. The antibodies against this infectivity-enhancing site were detected at high levels in severe patients. Moreover, we identified antibodies against the infectivity-enhancing site in uninfected donors, albeit at a lower frequency. These findings demonstrate that not only neutralizing antibodies but also enhancing antibodies are produced during SARS-CoV-2 infection.’