immune pressure or adaptation, any mutation or combination that further suppresses both antiviral and inflammatory components of innate immunity could severely weaken this most nonspecific line of immune defense.

Geert Vanden Bosshe again provoked deep and serious thought. He cannot be disregarded. He has led the way in our understanding of the evolutionary dynamics when you mass vaccinate across all age-groups into the midst and teeth of a pandemic or virus outbreak using a ‘leaky’ imperfect non-sterilizing vaccine (that does not stop infection or transmission as the Malone mRNA vaccine failed to do); the result can only be viral immune escape, original antigenic sin/immune imprinting/priming, pathogenic priming, antibody dependent enhancement of infection (ADEI) and of disease (ADED) etc…

Geert:

‘For example, suppression of humoral innate immune responses in XFG descendants may facilitate the stochastic emergence and accumulation of additional mutations in chronically infected individuals, some of which could enhance the virus’s ability to evade interferon-mediated innate immunity and/or innate immune sensing without compromising intrinsic viral infectiousness. When combined with failing adaptive immunity, this would inevitably result in immune tolerance and consequently trigger unchecked viral replication and dissemination of the virus within the host — and even on a large scale due to the associated increase in inter-host transmission of the virus.”’

‘The hoarse voice—without accompanying sore throat—regularly caused by infections with XFG (sub)variants (the so-called Stratus variant) is a clear sign of suppressed local inflammatory symptoms. As long as the remaining cell-mediated innate immunity (mainly in the unvaccinated) or adaptive immunity (mainly in the vaccinated) is still strong enough to eliminate the virus in time or to prevent symptoms, respectively, hoarseness remains practically the only notable sign of an XFG infection.’

A pat on the back on the way to the gallows…

“As the vaccine-induced antibodies (i.e., humoral immunity) exerted growing selective pressure, viral variants were selected that increasingly escaped this pressure, became more infectious, and thereby sustained viral transmission. As vaccine-induced antibodies lost their neutralizing capacity, T cells were increasingly recruited in an attempt to control rapid intra-host viral replication. However, these T cells were equally ineffective at controlling inter-host transmission. Because this T cell recruitment resulted from immune refocusing, the newly mobilized immune responses became progressively less specific—that is, increasingly less directed against the intended target antigen (e.g., the receptor-binding domain of the spike protein).Whereas the initial vaccine-driven immune selection pressure was very high—resulting in the rapid and spectacular emergence of Omicron—the subsequent immune pressure, driven by less target-specific antibodies and T cells, led to the selection of an increasingly broad spectrum of circulating immune escape variants (i.e., causing large-scale immune escape). Despite their genetic diversity, these variants shared one key trait: enhanced intrinsic infectivity. As the prevalence of vaccine breakthrough infections (VBTIs)—and consequently, immune refocusing—increased, a growing number of immune effector cells were recruited that exerted little or no impact on viral infectivity, thereby further reducing the immune selection pressure exerted by highly C-19 vaccinated populations. This explains the observed decline in the rate of emergence of new viral immune escape variants in the post-Omicron era.”

and

Viral gain-of-function is associated with immunological pain-of-function as mass C-19 vaccination turned an acute, self-limiting pandemic into a chronic, self-perpetuating immune escape epidemic

‘Scientists and so-called public health experts have fundamentally misjudged the Covid-19 (C-19) pandemic because they remain blinded—fixated on snapshots rather than analyzing the evolutionary dynamics that govern its course. This explains why they have long lost sight of the forest for the trees, mistaking the immune system’s final convulsions for a stable form of protective herd immunity—one they believe can be sustained through continued vaccination and boosters. Yet, it has become unmistakably clear that, compared to the early stages of the pandemic, the virus has grown increasingly infectious, while the collective immune defense in highly C-19-vaccinated populations has become progressively less effective.

As the vaccine-induced antibodies (i.e., humoral immunity) exerted growing selective pressure, viral variants were selected that increasingly escaped this pressure, became more infectious, and thereby sustained viral transmission. As vaccine-induced antibodies lost their neutralizing capacity, T cells were increasingly recruited in an attempt to control rapid intra-host viral replication. However, these T cells were equally ineffective at controlling inter-host transmission. Because this T cell recruitment resulted from immune refocusing, the newly mobilized immune responses became progressively less specific—that is, increasingly less directed against the intended target antigen (e.g., the receptor-binding domain of the spike protein).Whereas the initial vaccine-driven immune selection pressure was very high—resulting in the rapid and spectacular emergence of Omicron—the subsequent immune pressure, driven by less target-specific antibodies and T cells, led to the selection of an increasingly broad spectrum of circulating immune escape variants (i.e., causing large-scale immune escape). Despite their genetic diversity, these variants shared one key trait: enhanced intrinsic infectivity. As the prevalence of vaccine breakthrough infections (VBTIs)—and consequently, immune refocusing—increased, a growing number of immune effector cells were recruited that exerted little or no impact on viral infectivity, thereby further reducing the immune selection pressure exerted by highly C-19 vaccinated populations. This explains the observed decline in the rate of emergence of new viral immune escape variants in the post-Omicron era.

Moreover, the exuberant stimulation of dysfunctional T cells—often cross-reactive with self-antigens—has led to a slowly evolving immune pathology, commonly referred to as ‘Long COVID’. This syndrome involves autoreactive immune responses that target one or more organs. Notably, certain subsets of autoreactive regulatory T cells can suppress anti-tumor immunity, and their hyperstimulation during VBTIs—and thus immune refocusing—has undoubtedly played a role in the explosive emergence of multi-organ cancers in highly C-19 vaccinated populations. VBTI-mediated immune refocusing following Omicron emergence has therefore turned what were once beneficial immune responses into harmful, dysfunctional immunity.
The immuno-virological trajectory depicted above illustrates how an acute, self-limiting pandemic has been irreversibly transformed into a chronic, progressive one—where acute symptoms increasingly evolved into chronic disease.

Based on the above, it is reasonable to conclude that the emergence of more infectious immune escape variants has unambiguously led to a less targeted and therefore less effective immune response—characterized by increased viral immune escape and a shift from acute to chronic symptomatology.

Voice for Science and Solidarity by Geert Vanden Bossche is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.

We have now entered a phase in which the combined forces of the adaptive immune system (humoral and cellular) suppress viral transmission to such an extent (as evidenced by prolonged periods of low viral concentrations in wastewater) that the virus must exploit a further weakening of immune protection to ensure its survival. Since the virus has already maximized its escape from adaptive immunity through antigenic variation, its continued propagation and transmission now hinges on suppressing non-antigen-specific innate immunity.
Highly infectious variants that have evolved to suppress antiviral innate defenses by compromising interferon (IFN) signaling—such as NB.1.8.1, and likely also XFG—have already gained a clear competitive advantage. Nevertheless, their increased viral replication capacity and infectivity tends to be ‘neutralized’ by enhanced local inflammatory symptoms in the upper respiratory tract (URT), which promotes adsorption of infectious virus particles by URT-patrolling dendritic cells, thereby somewhat curbing viral transmission. Due to its ability to significantly suppress IFN signaling, NP.1.8.1, for example, exhibits increased replicative capacity and strongly induces local immune inflammation at the URT level, thereby causing the so-called ‘razor blade throat’ symptom. XFG, which incorporates combinations of mutations presumed to weaken both IFN signaling and upstream innate immune sensing (i.e., via non-IFN pathways), appears to enjoy an additional fitness advantage and consequently seems to be on track to become globally dominant.

Although mutations in circulating variants—and combinations thereof—that suppress the antiviral and anti-inflammatory components of the innate immune system are purely stochastic in nature, the growing number of chronically infected individuals in highly C-19 vaccinated populations (which now serve as the breeding ground for new variants) is leading to an ever-increasing diversity of highly infectious SARS-CoV-2 (SC-2) variants. Even in the absence of immune pressure or adaptation, any mutation or combination that further suppresses both antiviral and inflammatory components of innate immunity could severely weaken this most basic, nonspecific line of immune defense. For example, suppression of humoral innate immune responses in XFG descendants may facilitate the stochastic emergence and accumulation of additional mutations in chronically infected individuals, some of which could enhance the virus’s ability to evade interferon-mediated innate immunity and/or innate immune sensing without compromising intrinsic viral infectiousness. When combined with failing adaptive immunity, this would inevitably result in immune tolerance and consequently trigger unchecked viral replication and dissemination of the virus within the host — and even on a large scale due to the associated increase in inter-host transmission of the virus.
However, a variant with such properties will not only lead to immune tolerance in many C-19 vaccinated individuals—due to the failing efficacy of the combined immune responses (adaptive and innate)—but will also inevitably outcompete other variants because of its indirect (i.e., context-driven) fitness advantage. The enhanced diversity of highly infectious SC-2 variants therefore increases the likelihood that a variant will suddenly emerge somewhere with the ability to sufficiently suppress the innate immune system to completely overwhelm the infected host. Severe innate immune suppression is particularly likely in individuals whose cell-mediated innate immunity remains untrained—such as many C-19 vaccine recipients. In these individuals, additional weakening of the innate immune system could fully dismantle the last remaining frontline of immune defense—already the sole residual barrier in many C-19 vaccinated individuals.

In earlier writings, as well as in my book (‘The Inescapable Immune Escape Pandemic’), I have repeatedly explained why and how, in many C-19 vaccinated individuals—unlike in the unvaccinated—the cell-mediated innate immunity was bypassed as a result of the mRNA vaccines and/or VBTIs, and therefore could never be sufficiently trained to subsequently avoid new VBTIs.

While the attention of public health experts and authorities remains focused on rising cases of severe disease and death, these increases must be interpreted as the result of the growing spread of certain variants such as NB.1.8.1, XFG, and LP.8.1.1, rather than a consequence of increased virulence. The real concern, though, should lie in curbing viral transmission. This is essential to drastically reduce, or ideally minimize to near-zero, the stochastic probability of further chronic infections occurring, and thereby the risk of harmful tolerogenic mutations or recombinations.

Now more than ever, safe and effective antiviral treatments should be deployed on a large scale in highly C-19 vaccinated populations.

I have previously stated that the apparent steady state of relatively low symptomatic SC-2 infections and hospitalizations was the result of a kind of metastable equilibrium—a fragile balance between the virus’s infectious potential and the residual strength of combined immune mechanisms. As such, even a small perturbation could suffice to knock the ‘golf ball’ out of the shallow cup and send it hurtling uncontrollably down the steep slope. That perturbation—however unlikely in the context of a purely natural SC-2 evolutionary trajectory—has now become increasingly probable as the final outcome of a mass vaccination–induced immune escape pandemic. It is no longer a question of if such a variant will emerge, but when.
In my humble opinion, we are now very close.
The summer season in many countries will only amplify the competitive advantage of variants with higher intrinsic replicative capacity (e.g., NB.1.8.1, XFG, LP.8.1.1), thereby increasing their prevalence in chronic infections and potentially triggering the tsunami sooner than expected. Such a tsunami would be unambiguously marked by a sharp rise in viral activity levels in wastewater, accompanied by an equally dramatic increase in cases of hyperacute disease and death.

For over three years, I have warned that society will be caught off guard, yet my message continues to be met with ridicule and derision. But as Norman Mailer once wrote:
“There is no greater impotence in all the world like knowing you are right and that the wave of the world is wrong, yet the wave crashes upon you.”

Lastly, it’s crucial to understand that irrational infection-prevention policies, followed by mass C-19 vaccination, have transformed a natural, acute, self-limiting pandemic into an artificial, chronic, self-perpetuating (immune escape) pandemic, thereby altering the drivers, dynamics, and clinical manifestations of SC-2 evolution, which has continued to shift in unprecedented ways.
How is it possible that this doesn’t set off massive alarm bells among epidemiologists and other so-called health experts?

The table below summarizes the key shifts during the evolution of the C-19 immune escape pandemic:

‘

Viral gain-of-function is associated with immunological pain-of-function as mass C-19 vaccination turned an acute, self-limiting pandemic into a chronic, self-perpetuating immune escape epidemic

___

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