What happens if a pandemic involving a virus naturally causing acute self-limiting infection fails to generate herd immunity?

And this is how it all started…..and how it is likely to end….

What’s your Reaction?


What happens if a pandemic involving a virus naturally causing acute self-limiting infection fails to generate herd immunity?


General considerations

Ab: Antibody
APC: Antigen (Ag)-presenting cell
C-19: Covid-19
CII: Cell-based innate immunity
CTL: Cytotoxic T lymphocyte
DC: Dendritic cell
NAb: Neutralizing Ab
NK cell: Natural Killer cell
PNNAB: Polymeric non-neutralizing Ab
RBD: Receptor-binding domain
S: Spike (protein)
SC-2: SARS-CoV-2
SIR: Steric immune refocusing
(V)BTI: (Vaccine) breakthrough infection

A lack of comprehensive understanding of immunology poses a significant hurdle to the development of effective public health interventions and prevention strategies during pandemics.

  • Key stakeholders in pandemic management, including epidemiologists, virologists, public health
    experts, and authorities, lack profound insights into the adaptive dynamics of the host immune
    response that develops during a pandemic. Even the concept of herd immunity isn’t correctly
  • Any (large-scale) intervention in population immunity that does not prevent viral transmission
    may have catastrophic consequences on public and individual health. The idea that viruses
    evolve to become benign — like the coronavirus evolving into the “common cold” — is a “myth”
    and was never guaranteed.
  • Implementing widespread measures to impede viral growth —i.e., viral transmission in the case
    of an acute self-limiting viral infection— eventually drives a spectacular gain in viral fitness. This
    can manifest as gain in resistance to NAbs in the case of large-scale immune pressure on virus
    neutralizability (e.g., Omicron BA.1) or gain in intrinsic viral infectiousness in the case of largescale immune pressure on viral infectiousness (e.g., BA.2.86).
  • Failure to comprehend the impact of adaptive, population-level immune pressure has resulted
    in failure to understand why and how mass vaccination has transformed a natural pandemic
    into one marked by more infectious variants.


  • In the context of acute, self-limiting infections, herd immunity refers to a level of
    population-level immunity that reduces the level of (viral) transmission down to a
    threshold where individuals who have not been immunized (for lack of exposure to
    wild or live attenuated vaccine) are protected against infection. Herd immunity
    therefore stops viral spread in the population.
  • Herd immunity is achieved when a sufficiently large portion of the population
    develops sterilizing immunity towards the circulating virus/ pathogen.
  • No pandemic of an acute, self-limiting viral infection can be contained without herd
  • Due to its self-limiting nature, a pandemic of an acute self-limiting viral infection
    can never be considered a health emergency of international concern!
  • Because the threshold for seroconversion (SC) to attain herd immunity following
    natural infection varies based on pre-existing population-level innate immunity and
    viral transmissibility, the SC rate is not be a reliable metric for assessing herd
    immunity. Conversely, vaccine-induced SC rates are not a reliable metric either as C19 vaccines do not stimulate cell-based innate immunity.

As some so-called ‘experts’ are confounding herd (i.e., population-level) immune pressure
with herd immune protection, they have claimed that the ‘acute phase’ of the pandemic is
over. They don’t seem to understand that when the acute phase of a pandemic involving a
virus causing acute self-limiting infection were over, this would mean that the pandemic is
over altogether!

  • As others ignore how adaptive immune responses evolve as a consequence of mass
    vaccination, they consider the emergence of Omicron BA.1 and BA.2.86 ‘unnatural’ and rely
    on conspiracy theories or scapegoat immune-suppressed individuals to explain the sudden
    dominant propagation of these highly mutated, highly transmissible immune escape variants*.
  • When a virus reaches peak infectiousness while still facing sustained immune pressure on its
    transmissibility, it may unleash the brakes on systemic viral dissemination to increase viral
    replication and propagation within the host → enhanced viral virulence.
  • Contrary to being a blessing, Omicron must be considered a scourge, triggering vaccine
    breakthrough infections that shift immune responses from suboptimal S variant-specific NAbs
    to suboptimal S variant-cross-reactive, infection-inhibiting Abs. This perpetuates a cycle of
    suboptimal immune pressure, facilitating ongoing viral immune escape.
  • As infection-mitigating Abs lose efficacy, Ab-mediated immune pressure increasingly shifts to
    CTL-mediated immune pressure.

What you need to know about immune steric refocusing (SIR)

  • Immune refocusing is triggered by VBTIs and updated vaccine boosters;
    mRNA vaccines promote SIR in their own right, even in the absence of
  • Immune refocusing drives immune escape
  • Infections with newly emerging variants in C-19 vaccinees inevitably cause
    SIR-enabling VBTIs. Highly C-19 vaccinated populations are therefore
    driving irreversible viral immune escape.
  • SIR makes the host immune response not only weaker (less affinity), but
    also broader (less specific) and eventually shifts the immune response from
    humoral to cell-mediated.

Avidity is a measure of the overall strength and stability of interactions between multiple binding sites on a bivalent or multivalent Ab and its corresponding multivalent Ag. Low-affinity Abs cover a broader scope of variants and can stabilize viral particulates over a broader range of dilutions. These Abs can, therefore, exert much broader and stronger immune selection pressure on viral infectiousness (via their prolonged infectionmitigating activity) compared to high-affinity Abs. At excessively high concentration, though, the latter have much higher pseudo-neutralizing capacity than low-affinity Abs

  • CTL-mediated abrogation of viral transmission becomes suboptimal as more infectious
    virus increasingly adsorbs to APCs instead of being internalized into these cells. This lowers
    the concentration of PNNAbs down to suboptimal levels, thereby leading highly C-19
    vaccinated populations to exert immune selection pressure on viral virulence.
  • Finally, as immune refocusing promotes the recognition of more conserved S-associated B
    cell epitopes with degenerate specificity^, VBTIs (and mRNA vaccines!) likely promote an
    increased incidence of autoimmune diseases and cancers.
  • In essence, a comprehensive understanding of immunology is crucial for understanding
    that the collective natural immunity within a population (i.e., herd immunity) is the most
    effective immune strategy to combat pandemics and avoid the emergence of more
    infectious viral variants.

^Flexibility in MHC and TCR Recognition: Degenerate Specificity at the T Cell Level in the Recognition of Promiscuous Th Epitopes Exhibiting No Primary Sequence Homology:

And this is how it all started…..and how it is likely to end….

  • Large-scale immunization against S protein (responsible for viral infectiousness) during
    an acute viral pandemic fails to generate herd immunity and instead generates ‘herd’
    immune pressure.
  • Collective (mass vaccination!), highly selective immune pressure exerted by
    ‘neutrali ation-mitigating’ A s on the specific immunodominant domain of the
    ‘infectious’ protein i.e., -RBD) eventually promotes dominant propagation of an
    immune escape variant (Omicron) that collectively resists S-specific NAbs (> 30 mutations).
  • Diminished neutralizing capacity of previously primed Abs promotes production of PNNAbs
    (IgMs), thereby triggering PNNAb-dependent VBTIs (
    The latter restimulate previously vaccine-primed Abs at high titers, thereby triggering SIR,
    while PNNAbs inhibit viral trans infectiousness.
  • SIR leads to boosting of previously primed, broadly cross S variant-reactive B cells, which
    produce low-affinity Abs with suboptimal neutralizing capacity. These low-affinity Abs
    stably mitigate viral infectiousness while recognition of more conserved S-associated B cell
    epitopes with degenerate specificity promotes early onset autoimmune diseases and
    cancers (IgG4 Abs)
  • Suboptimal S variant-nonspecific immune pressure exerted y ‘infection-mitigating’ A s on
    viral infectiousness promotes co-circulation of a diversified spectrum of newly emerging,
    more infectious immune escape variants, thereby ensuring perpetuation of VBTIs and
    immune refocusing.
  • Collective (large-scale VBTIs), suboptimal immune pressure on viral infectiousness promotes
    natural selection of highly immune evasive variants that have incorporated additional
    mutations enabling their resistance to infection-mitigating S variant-cross-reactive Abs and
    nonS-specific CTLs. These mutations have been found in proteins responsible for viral entry
    (> 30 mutations) and productive viral infection and are driving dominant propagation of
    these variants (BA.2.86/ JN.1 clan).
  • Enhanced intrinsic infectiousness of the BA.2.86 clan triggers Ab-independent VBTIs and
    thereby causes PNNAb concentrations to collectively decline, thereby causing highly C-19
    vaccinated populations to exert S variant-cross-reactive immune pressure on viral virulence
    (i.e., on the specific infection-enhancing site within S-NTD).
  • Suboptimal S variant-nonspecific immune pressure collectively exerted on viral virulence
    likely promotes dominant propagation of an immune evasive, highly infectious immune
    escape variant that collectively resists the virulence-mitigating, S variant-cross-reactive
    PNNAbs. This could occur through a conformational change in the infection-enhancing site
    of SC-2 particles adsorbed on migratory DCs, thereby allowing the new variant to unleash
    the PNNAb-mediated blockade on viral trans infection/ virulence.

Why could Omicron not train the CII of non-previously exposed C-19 vaccinees?

  • Following its initial VBTI (or 2nd mRNA dose), Omicron was readily
    neutralized by high concentrations of mismatched, previously vaccine-
    (SIR-)primed Abs that bind with low affinity to S-associated
    immunodominant epitopes (thereby triggering SIR). Prevention or
    mitigation of infection of susceptible cells following initial VBTI
    prevented training of naïve/ unexposed innate immune systems
  • Subsequent exposure to newly emerged immune escape variants boosts
    previously SIR-primed cross-reactive Abs at high titers, thereby ensuring
    strong infection-mitigating activity and further preventing triggering and
    training of CII

How are the unvaccinated protected from highly infectious variants?

  • Their innate immune system is able to quickly lower viral loads and kill
    virus-infected cells (via trained, i.e., epigenetically re-programmed,
    innate immune cells) without causing a strong recall of previously
    infection-primed pNAbs (and, therefore, preventing SIR).
  • The better the innate immune system is trained, the weaker the recall
    effect and the lower the likelihood of PNNAb-dependent BTI.
  • Unvaccinated individuals who are in good health and avoiding
    overcrowding can now successfully rely on their innate immune system
    to handle their immune defence entirely

Never immunize during a pandemic!

  • Work on prevention:
    ➢ Avoid overcrowding (especially of vulnerable people),
    ➢ Foster good health practices
    ➢ Apply standard hygiene/ sanitation
  • Let the (asymptomatically/ mildly) infected spread and treat
    vulnerable people with antivirals

How will the outcome of the C-19 pandemic be described in future science books?

“Due to suboptimal neutralization of its infectiousness, SC-2 acquired enhanced intrinsic infectiousness. As enhanced intrinsic infectiousness led to suboptimal neutralization of its trans infectiousness in C-19 vaccinees, SC-2 acquired enhanced intrinsic virulence in C-19 vaccinees.”
“Th C-19 mass vaccination program will indisputably be remembered as the largest and most dangerous gain-offunction experiment ever conducted in the history of biology- one which mankind has unleashed to his own species.”

C-19 vaccination does not promote herd immunity!

  • mRNA vaccines and vaccine breakthrough infections promoted resistance of new
    Omicron sublineages to previously SIR-induced antibodies and therefore expedited
    viral infectivity instead of developing herd immunity
  • Highly C-19 vaccinated populations exert herd immune pressure on viral
    infectiousness instead of generating herd immunity against productive infection.
  • Mass vaccination programs imposed by health authorities and policy makers have
    turned highly C-19 vaccinated populations into a breeding ground for immune
    escape variants and thereby transformed a natural pandemic into a pandemic of
    immune escape variants. Pretending that a pandemic of immune escape variants
    generates herd immunity is a contradictio in terminis….. and without herd immunity
    a pandemic cannot transition into endemicity….
  • Natural infection/ immunization during a natural pandemic prevents immune
    escape and thereby generates herd immunity while providing long-lived sterilizing
    immune capacity to the individual. In contrast, mass vaccination during a natural
    pandemic drives natural immune selection of non-neutralizable and more infectious
    immune escape variants and, therefore, fails to generate herd immunity or provide
    long-lived sterilizing immunity to the individual.

In the case of a pandemic, natural immunity, including trained innate immunity, is far more efficient (and safe!) than vaccine-induced immunity!

  • In the absence of a robust adaptive immune mechanism that protects against
    viral virulence, the best alternative to protect against severe C-19 disease during
    an immune escape pandemic is to avoid breakthrough infection via trained cellbased innate immunity.
  • Whereas both cell-based innate immunity and virulence-inhibiting, nonneutralizing antibodies (NNAbs) are S variant-nonspecific, the cell-based innate
    immune system (CBIIS) is endowed with adaptive memory whereas deficient T
    help will eventually prevent recall of NNAbs.
  • Due to their thoroughly trained CBIIS, healthy unvaccinated people are
    protected from severe C-19 disease and will likely improve their protection when
    highly infectious SC-2 variants evolve to exhi it high virulence in ‘untrained’ C-19
  • In conclusion: Large-scale natural immunity is required but sufficient to durably
    protect an individual from a virus causing ASLVI and to end a natural pandemic.

Why and how is the majority of vaccinees still protected against (severe) C-19 disease?

  • The currently observed protection against (severe) disease in C-19
    vaccinees fully relies on short-lived NNAbs and strong activation of
    CTLs. (Re-)exposure to circulating Omicron descendants or vaccine
    booster doses initially extended this protection, but only temporarily
    and not without enhancing large-scale immune selection pressure on
    viral virulence.
  • However, once the NNAbs collectively decline below an optimal
    threshold, the virus will likely break through their virulence-inhibiting
    capacity and unleash a major wave of severe C-19 disease in highly C19 vaccinated populations.

Where has all the science gone?

  • Key opinion leaders and health experts are erroneously interpreting
    diminished pathogenicity as an indication that the virus is transitioning into
    endemicity. They do not understand that reduced pathogenicity of SC-2
    does not result from herd immunity but is triggered by broadly infectionmitigating immune response. Repeated activation of broadly infectionmitigating CTLs upon re-exposure to highly infectious circulating variants
    results in enhanced immune selection pressure on the virus’ capacity to
    prevent NNAb-mediated inhibition of viral virulence. This is now preparing
    the virus to lift the immune blockade on severe C-19 disease.
  • Massive exercises in mutational stamp collection combined with ad hoc
    interpretations of epidemiological, biological and clinical data have
    prevented scientists from seeing the forest for the trees and are the biggest
    obstacle for them to understand the disastrous consequences of this mass
    vaccination experiment; their mutational analyses and predictive
    epidemiological models merely reflect snapshots and don’t consider the
    immunologic dynamics that are driving natural adaptation of the virus.
  • Although scientists seem to agree that Spike (S)-associated viral mutations are
    driven by population-level immune selection pressure, none of them dares to
    mention that mass vaccination and subsequent booster immunizations caused
    populations to exert large-scale immune pressure on viral infectiousness.
    Why does no one investigate the origin of this large-scale immune selection
    pressure placed on the virus?
  • While our experts claim that mRNA vaccination and vaccine breakthrough
    infections (VBTIs) protect against severe C-19 disease, they seem to ignore that
    both prevent or even abrogate training of the cell-based innate immune system
    and promote viral immune escape.
  • Not understanding that updated vaccine booster doses will only recall
    previously primed Abs, thereby expedite immune refocusing and leading to
    immune escape, is one of the most blatant examples of immunological
    illiteracy. On the other hand, VBTI infections fail to prime new NAbs towards
    the infecting circulating variant.
  • Neither health experts nor scientists seem to understand how enhanced susceptibility to Omicron infection can be reconciled with prevention against (severe) disease in C-19 vaccinees whose antibodies no longer possess sufficient neutralizing capacity.
  • No scientist even seems to be considering the risk of this virus evolving
    a major – but immunosilent (glycan-based!)- shift transforming it into a
    variant that enhances viral virulence in highly vaccinated populations.
  • Regardless of their astonishing lack of understanding and insight, many
    scientists continue to blindly endorse the proposal of incompetent
    public health experts and authorities to continue the mass vaccination
    experiment with mRNA-based vaccines and to even recommend use of
    the latter for fighting other diseases.

Many experts pretended Omicron would end the pandemic. Why have they been wrong?

  • Since the advent of Omicron, the pandemic has evolved into a self-catalyzing
    chain of large-scale immune escape instead of transitioning into endemicity.
  • Because Omicron self-catalyzed its evolution into a series of highly infectious
    co-circulating descendants, it rapidly caused immune escape dynamics to reach
    a point of no return. What this means is that Omicron descendants are now
    paving the way to the likely emergence of a naturally selected immune escape
    variant with high virulence potential in highly C-19 vaccinated populations
  • In conclusion: Early Omicron descendants, the infectiousness of which could
    no longer be sufficiently neutralized by pre-existing potentially neutralizing Abs,
    acquired enhanced infectiousness in vaccinated individuals whereas subsequent
    Omicron descendants, the trans infectiousness of which can no longer be
    sufficiently inhibited by pre-existing non-neutralizing Abs, will likely acquire
    enhanced virulence.

Vaccinated -but not unvaccinated people – in highly C-19 vaccinated populations have turned the natural pandemic into a pandemic of immune escape variants

  • Because trained cell-based innate immunity provides strong
    sterilizing immunity the unvaccinated did not contribute to
    viral immune escape and were not responsible for turning
    the natural SARS-CoV-2 pandemic into a pandemic of
    immune escape variants.
  • Each highly C-19 vaccinated population is now planting the
    seeds for the emergence of a new Omicron descendant with
    high virulence potential (HI-VI-CRON).

What’s your Reaction?


Click to comment

You must be logged in to post a comment Login

Leave a Reply

To Top