My bible on the C-19 mass vaccination experiment

My bible on the C-19 mass vaccination experiment. Nobody can conceal a scourge that Nature is now desperate to unveil. 

Summary

The cell-based innate immune system (CBIIS) is critically important for removal of most of the SARS-CoV-2 (SC-2) viral load upon primary infection and even re-infection (as infection-primed antibodies decline quite rapidly). Training of the CBIIS (i.e., comprising adaptation and functional reprogramming of innate Natural Killer [NK] cells via epigenetic imprinting) may even obviate the need for engaging the adaptive immune system. Population-level immune pressure on viral infectiousness following mass vaccination with S(pike) protein-directed C-19 vaccines during a pandemic eventually sidelines this vitally important first line of immune defense against SC-2. As large-scale suboptimal humoral immune pressure on viral infectiousness drives natural selection and expansion of immune escape variants that the C-19 vaccine-induced antibodies (Abs) cannot sufficiently neutralize, infection-enhancing polyreactive, non-neutralizing Abs (PNNAbs) come into effect and cause PNNAb-dependent enhancement of viral infectiousness. Omicron became the first dominantly circulating SC-2 variant that managed to cause large-scale PNNAb-dependent breakthrough infections in highly vaccinated populations.
PNNAb-dependent vaccine breakthrough infections (VBTIs) are responsible for steric immune refocusing (SIR), a phenomenon which occurs when anti-S Abs bind with low affinity to S protein and thereby sterically mask the immunodominant S-associated epitopes. This allows immune subdominant epitopes to seek noncognate T help from recalled, previously induced CD4+ T memory cells to prime new, S-specific Abs targeting S-associated antigenic domains that are more conserved but less immunogenic. This explains why I have been wrong regarding my predictions on the timeline for ‘vaccinocidal’ variants to emerge as SIR enabled the immune system of vaccinees to elicit new functional immune responses that could even prevent productive infection. However, as the corresponding Abs have only short-lived neutralizing capacity and take several months to mature, the protective effect of VBTIs (and mRNA boosters: see below) was only short-lived. Because these short-lived, broadly functional Abs exerted suboptimal immune pressure on these epitopes, they eventually precipitated viral immune escape dynamics. 

My analysis unambiguously proves that the mass vaccination experiment has been responsible for selecting and promoting dominant propagation of Omicron in highly vaccinated populations. Whereas ‘original antigenic sin’ has been expediting immune escape during the pre-Omicron phase of the pandemic in countries with increasing vaccine coverage rates, a combination of ‘original antigenic sin’ with   ‘steric immune refocusing’ (SIR) has been the key driver of the spectacular evolutionary dynamics of this pandemic during the Omicron phase. As Omicron causes SIR-enabling VBTIs and as SIR caused highly vaccinated populations to exert immune pressure on more conserved, subdominant S-associated domains, circulation of Omicron was required but sufficient to drive large scale immune escape. However, this evolution has been expedited by the continued mass vaccination program as booster doses and growing vaccine coverage rates enabled more widespread and increased immune pressure on shared cross-functional S-associated epitopes. Since the advent of Omicron, however, mRNA-based C-19 vaccines have dramatically expedited the pace and magnitude of viral immune escape as—in contrast to the other, non-mRNA C-19 vaccines—they elicit low affinity anti-S Abs(1) directed at S protein that is expressed on the surface of the mRNA-transfected host cells and thereby allow steric masking of the immunodominant epitopes expressed on the surface of free-circulating S protein once the latter is released from the transfected cells. mRNA-based C-19 vaccines are therefore SIR-enabling in their own right.

SIR-enabling VBTIs and SIR-enabling vaccines (i.e., mRNA-based C-19 vaccines) cause vaccinees to bypass the CBIIS and inevitably drive the emergence of large-scale immune escape mutations that eventually converged to the receptor-binding domain of spike protein (S-RBD) to confer a high level of intrinsic viral infectiousness. As these highly infectious Omicron descendants are now no longer sustaining elevated concentrations of PNNAbs, the trans infection-inhibiting effect of PNNAbs is weakened whereas the uptake of these highly infectious SC-2 virions into antigen(Ag)-presenting cells (APCs) is enhanced. Consequently, current co-circulation of new highly infectious variants is accompanied by attenuation  of disease symptoms and diminished viral transmission. However, as no selective immune pressure can be exerted on viral transmission, Nature has coupled enhanced CTL (cytolytic T lymphocyte)-mediated activity on viral transmission with growing immune pressure on viral trans infectiousness(2): all highly vaccinated populations are now separately exerting steadily increasing immune pressure on viral virulence. Consequently, vaccinees have now started to breed a multitude of SC-variants that pickup mutations that will allow them to break through the last mechanism of vaccine-mediated adaptive immune defense that protects vaccinees against (severe) disease, i.e., PNNAb-dependent inhibition of trans infectiousness/ virulence.  I have no doubt that this will soon lead to the independent emergence of a diversified spectrum of a new generation of SC-variants that are fully capable of causing enhanced viral virulence in vaccinees (through PNNAb-dependent enhancement of severe C-19 disease) whereas the unvaccinated will be resistant to these ‘vaccinocidal’ variants. Since mRNA vaccines trigger immune refocusing as of the first injection following natural productive infection or as of the first exposure after the first injection,  they not only expedite immune escape but also prevent training of the CBIIS by natural infection as of the first injection.  It is therefore undeniable that usage of mRNA vaccines has significantly contributed to the tragic evolution of this pandemic.  

Given that SIR is triggered by mRNA-based vaccines at an early stage of mRNA vaccination and irrevocably sidelines the CBIIS, and individuals vaccinated with non-mRNA-based C-19 vaccines required high titers of poorly neutralizing Abs  to develop SIR-enabling VBTIs upon exposure to Omicron, it is fair to conclude that the following vaccinees will still have been able to train their CBIIS and can therefore rely on its protective capacity:

All healthy individuals who:
i) got symptomatic infection with pre-Omicron variants prior to their booster with non-mRNA-based C-19 vaccines or prior to their second injection with an mRNA-based C-19 vaccine(3), whichever came first,
and
ii) refrained from booster doses with mRNA-based C-19 vaccines before Omicron dominantly circulated in the population

PNNAb-mediated inhibition of viral trans infectiousness and enhanced CTL activity towards SC-2-infected cells is currently still protecting vaccinees from (severe) C-19 disease and thus still supports the mainstream narrative. However, both of these immune mechanisms are T help-independent and therefore both short-lived and not robust.

Although I keep warning the world that ‘society will be caught by surprise’, it is difficult to imagine that our leading scientists and public health experts are not aware of the threat that viral immune escape is currently posing to highly vaccinated populations and that they truly believe that infections with Omicron and its descendants are a blessing because of their modest impact on public health (as side effects are largely denied anyway). However, if they truly believe this, their narrative is not only an unforgivable insult to the science but also a profoundly unethical and despicable blow in the face of all those who have been coerced into vaccination by their employer, governments, health authorities, educational institutions or other influential bodies.    

(1) During natural infection, viral protein expressed at the surface of virus-infected cells cannot prime an immune response because the virus (but not mRNA-based vaccines!) synthesizes peptides that prevent antigen presentation at an early stage of infection. Hence, no CD4+ T helper cells are induced. In the absence of helper T cells, the cell surface-expressed protein cannot prime an immune response. 

(2) Diminished PNNAb-mediated inhibition of viral trans infectiousness leads to increased PNNAb-mediated immune pressure on viral trans infectiousness and therefore on viral virulence

(3) However, any symptomatic SC-2 infection that occurred before the first injection, should have been mild for mRNA-based C-19 vaccination after CD4+ T help priming following symptomatic SC-2 infection will prime low-affinity memory B cells and thereby trigger SIR upon subsequent infection