SSI - BOLETTE SØBORG: CORONA-SMITTE I KRAFTIG STIGNING

OG FEIGDARBOÐ DR. GEERT VANDEN BOSSCHE

Skrivið niðanfyri er í dag 29.06.2024 sent til Landslæknan, Heilsumálaráðið, Heilsustýrið, Landsapotekarin og Heilsutrygd

Avrit er sent til

javnadarflokkurin@logting.fo, loysing@olivant.fo, MAIL@framsokn.fo, samband@olivant.fo, folkaflokkurin@folkaflokkurin.fo, midflokkurin@midflokkurin.fo, VP.fo, katrinp@kvf.fo, politi@politi.fo

Avrit er tann 30.06.2024 sent til

lms@lms.fo, bjorts@logting.fo, bardurn@logting.fo, beinirj@logting.fo, jenisr@logting.fo, bot@ssi.dk

Verður sent eftir almennari áheitan frá fremstu óheftu serfrøðini Dr. Geert Vanden Bossche

GREIÐ OG ÁLVARSOM CORONA FEIGDARBOÐ HAR KJARNAN Í BOÐNUM ER HENDAN

"ØLL COVID KOPPSETT HAVA TØRV Á AT TAKA ANTIVIRALA HEILIVÁGIN IVERMECTIN NÚ NÝTT SARS-CoV-2 VIRUSFYRIBRYGDIÐ NB. 1.8.1 ER ÁVEGIS SUM VIL GERAST SERA VANDAMIKIÐ FYRI ÁVÍS COVID KOPPSETT"!

SUBSTACK - VOICE FOR SCIENCE AND SOLIDARITY

GEERT VANDEN BOSSCHE

Large-scale antiviral treatment - a strategy proven effective even against HIV - is not even considered - because its implementation would threaten the most profitable strongholds of

the Vaccine Industry!

SUBSTACK 29. mai 2025 Nobody seems to see the drama unfolding right before our eyes 

I’m sure some of you have become aware of new COVID-19 (C-19) outbreaks in several Asian countries (Thailand, Taiwan, Singapore, China, Japan). But even in Australia, NB. 1.8.1 is now spreading, and it has already made landfall in the US as well. These outbreaks are continuing to rise rapidly and at least Taiwan has been reporting a sustained increase in severe and fatal cases too.

While critics are rightfully concerned about the many direct side effects of the C-19 vaccines, few are aware of the threat posed by the large-Scale and out-of-control gain-of-function experiment that has been triggered by irrational human intervention in highly C-19 vaccinated populations. After psychotic infection-prevention measures and insane C-19 mass vaccination drove viral escape from anti-SARS-CoV-2 (SC-2) immunity, making the virus more infectious, ongoing vaccine breakthrough infections now appear to be evolving in a way that facilitates immune deficiency against SC-2 altogether, thereby facilitating increased viral virulence of newly emerging, highly transmissible SC-2 lineages. As I always said:

This is not going to have a happy ending (in highly C-19 vaccinated populations).

SUBSTACK 1. juni 2025 From Consensus to Censorship: The Tabooing of Generally Accepted Scientific Knowledge

Let me reiterate, once and for all, that the claim that viruses ‘naturally’ evolve to become milder—because supposedly it's not in their interest to kill us—is sheer nonsense! The origin of such primitive statements lies in a blatant lack of knowledge—not necessarily in virology, but in immunology, especially population-level immunity. Viruses that spread extracellularly, like coronaviruses, will eventually face transmission dead-ends when the majority of the population develops high titers of neutralizing antibodies (Abs). These Abs have the capacity to neutralize the virus before it can infect susceptible cells, thus mitigating disease symptoms and eventually terminating the infection. The more the virus spreads, the more people will be infected and re-infected, driving their Ab titers higher—until transmission collapses entirely.

This basic immunological mechanism leaves immunologically illiterate scientists with the absurd impression that a virus somehow possesses a brain, capable of strategically deciding not to kill its hosts in order to ensure its own survival! The stupidity of this reasoning is exposed by the observation that even mild pandemics—those with low mortality rates—can still lead quite quickly to a decline in cases and disease severity, even though such viral behavior does not require the virus to evolve into something particularly ‘gentle’.

As outline in the referenced article (New HIV variant discovered in the Netherlands | Financial Times), viruses like HIV can combine high virulence with high transmissibility. If that is the case, there is absolutely no scientific basis to assume that a highly transmissible SARS-CoV-2 (SC-2) variant couldn't also become more virulent!

Given the high level of immune resistance exhibited by the currently circulating SC-2 variants, any further evolution toward greater virulence would culminate in a catastrophic triad: high immune escape, high transmissibility, and high virulence. Ominously, the ongoing erosion of innate immunity (cfr. NB. 1.8.1) by currently circulating variants suggests we are already heading in that direction.

Yet, public health authorities remain willfully blind, arrogantly issuing insane recommendations to continue mass Covid-19 (C-19) vaccination—directly fueling the disastrous immune escape this virus is exploiting. Anyone with even a basic biological education will recognize the grave warning presented in the attached publication: “The HIV and SARS-CoV-2 pandemics demonstrate that viruses can—and will—evolve higher virulence when such traits are favored by natural selection.” This report also confirms that under high, suboptimal intra-host immune pressure, extensive genetic changes can occur—resulting in significant phenotypic differences—without intermediate steps in the viral evolutionary pathway, a process known as ‘saltational’ evolution. Yet, when it comes to taking these principles into account in the formulation of policy recommendations for managing SC-2 in highly C-19–vaccinated populations, heads that once nodded in agreement suddenly begin to shake in denial!

Large-scale antiviral treatment—a strategy proven effective even against HIV—is not even considered, because its implementation would threaten the most profitable strongholds of the Vaccine Industry!

This level of reckless, willful blindness is unprecedented—a direct, arrogant assault on science itself. And tragically, it is one that will come with enormous public health consequences.

SUBSTACK 29. mai 2025 I THINK IT'S ABOUT TIME WE COME UP WITH AN EMERGENCY PLAN!

I may be wrong, but I now feel that we are finally approaching the end phase of this pandemic!
Until recently, highly COVID-19 (C-19)–vaccinated populations have primarily exertedadaptive immune pressureonviral infectiousness, leading to the emergence of variants capable of evading virus-neutralizing antibodies (Abs) targetingspecificspike (S) proteinpeptide epitopes. However, highly C-19-vaccinated populations now appear to be shifting toward exertinginnate immune pressureon viraltrans infectiousness1,resulting in the emergence of variants (e.g., NB.1.8.1) that can–at least to some extent– evadevirus-inhibitinginteractions with dendritic cell-expressed lectins, whichnonspecificallyrecognize S-associatedglycan motifs. While earlier (adaptive) immune escape variants primarily causedvaccine breakthrough infectionsresulting inenhanced viral infection rates, these newer (innate) immune escape variants are more likely to cause ‘high-viral-load’breakthrough infectionsin individuals with poorly trained cell-mediated innate immunity, potentially leading toincreased rates of highly virulent infections—associated with severe disease and death—in highly C-19-vaccinated populations.

So I wouldn’t be surprised if we start the summer with a nasty surprise…

1 Viraltransinfectiousness refers to the ability of a virus to infect new host cells indirectly via interactions with host immune cells, such as dendritic cells, rather than through direct infection of target cells. It typically implies a process where:
Antigen-presenting cells (especially dendritic cells or macrophages) capture viral particles at mucosal surfaces via lectin receptors (e.g., DC-SIGN), not to become productively infected themselves, but rather to transfer the virus to permissive target host cells. This lectin-mediated transfer mechanism is often referred to as viraltransinfection.Transinfection facilitates intra-host transmission of SARS-CoV-2 and promotes cell-to-cell fusion (so-calledtransfusion), leading to the formation of syncytia—structures that are considered pathognomonic of viral virulence. In the context of SARS-CoV-2, migratory dendritic cells (DCs) patrolling the upper respiratory tract can bind spike protein–associated glycans via cell surface-expressed, nonspecific pattern recognition receptors (e.g., C-type lectins), facilitating indirect viral transmission to ACE2-expressing host cells.
This mechanism would bypass traditional neutralization by anti-spike antibodies targetingpeptide epitopes, contributing toinnate immune escape.
The distinction fromviral infectiousnessis important when discussing immune escape, as the current evolution of SARS-CoV-2 appears to reflect a shift fromadaptive immune evasion(antibody/epitope specificity) towardinnate immune evasion. In the case of SARS-CoV-2, innate immune evasion is thought to be due to the diminished capacity of circulating escape mutants to induce inflammatory cytokines and/or interferons (particularly type I interferons such as IFN-α and IFN-β), which are known to upregulate the expression of C-type lectins on the surface of migratory DCs (pattern recognition receptor evasion).

SUBSTACK 29. mai 2025 Even setting aside conflicts of interest, a lack of thorough analysis of complex biological phenomena may lead to polarization in science and undermine consensus on what constitutes scientific truth.

Most of us tend to view science as a discipline capable of revealing objective truth. However, this perception seems less straightforward when it comes to complex biological phenomena or processes, as even leading scientists sometimes hold fundamentally different viewpoints regarding the ‘truthful’ outcomes of certain human interventions in complex biological ecosystems. This conundrum prompted me to pose the following question to ChatGPT:

How is it possible that world-class experts or scientists sometimes hold opposing views on the impact of human intervention in complex biological phenomena, such as the effects of mass vaccination on pandemics or human behavior and consumption on climate change? I believe this divergence is not because one side is right and the other wrong, but because whenever we perturb a complex ecosystem that has been in balance for millions of years, a multitude of mutually interacting chain reactions and feedback loops are triggered—effects that can be interpreted in different ways. These interactions often partially compensate for each other, thereby enabling the system to gradually establish a ‘best-case’ equilibrium, which I often refer to as ‘metastable.’ To smooth this transition, some effects may be interpreted as beneficial outcomes of the intervention, while others seem detrimental—depending on which aspects a scientist focuses on. Would this be a correct interpretation?

Here comes Chat-GPT’s reply:

“Yes, your interpretation aligns well with current scientific understanding of complex systems and explains why experts may hold differing views.

To elaborate: 

Complexity and Feedback
Biological and ecological systems are highly complex, characterized by numerous interacting components and nonlinear feedback loops. Human interventions can trigger cascades of effects that propagate through these networks, sometimes reinforcing and sometimes counteracting each other.

Metastable Equilibria
The concept of a ‘metastable’ state is apt—it describes a condition where the system settles into a relatively stable but not permanent equilibrium. Such states can persist for long periods but may shift if disturbed again, reflecting the dynamic balance in ecosystems.

Perspective and Focus
Different scientists may emphasize different variables or scales—molecular, individual, population, or ecosystem level—leading to varying interpretations of the same intervention’s impact. For example, mass vaccination may reduce disease burden (a clear positive) but may also exert selective pressures on pathogens (a more complex, potentially negative effect).

Time Scale and Measurement
Effects observed in the short term can differ from those manifesting over longer time frames, complicating consensus on outcomes.

Therefore, opposing expert views are often a reflection of the multifaceted nature of the systems studied, rather than simple right-versus-wrong dichotomies. Your framing captures this nuance well.”

Geert: Please don’t think I am obsessed with ChatGPT, but I must admit that in many cases I find its answers more balanced and refreshing than the stereotypical feedback I often receive from those who seem to prefer adhering to entrenched, polarized viewpoints on complex questions rather than engaging in open-minded debate.

SUBSTACK 21. apríl 2025 T.A.C.T.: The threat of the currently circulating variants doesn’t lie in its virulence....OMG!!!

Here comes my take on their interpretation:
I find it difficult to understand how some scientists fail to grasp that ongoing immune pressure on the virus still holds tremendous potential to further acceleratethe already remarkable accumulation and diversification of selected viral mutations!These mutations are already changing SC-2’s infectious behavior quite dramatically by enhancing the virus’s intrinsic infectivity—through stronger binding to the ACE2 receptor—diminishing its susceptibility to neutralizing Abs and increasing its replication capacity. Collectively, these changes enable continued viral transmission.

What they seem to ignore is that sustained immune pressure has not yet driven extensive exploitation of potential mutations in the virus’s surface-expressed glycan structures—an evolutionary space that could allow it to evade both humoral and cellular immune responses even more spectacularly!

[AI/Vitlíki: In summary, mutations in the virus’s surface-expressed glycan structures significantly impact its ability to infect host cells, evade immune responses, and maintain stability during replication, ultimately influencing public health strategies for managing viral infections.]

It is, therefore, hard to understand how some researchers can downplay the threat posed by the ongoing viral evolution (‘the threat of the currently circulating variants doesn’t lie in its virulence’) by focusing only one the type of phenotypic changes observed to date, without modeling the potentially dramatic impact of even modest alterations in the viral glycosylation profile on pathogenicity.

SUBSTACK 25. jan. 2025 (Er sent við telduposti 26.01.2025 til hmr@hmr.fo, hst@hst.fo, heilsutrygd@heilsutrygd.fo, Landslæknin/foe@stps.dk, landsapotekarin@apotek.fo, dkma@dkma.dk, sst@sst.dk, serum@ssi.dk, bjorts@logting.fo, kvf@kvf.fo, vp@vp.fo): In May 2023 the WHO stated that the acute phase of the Covid-19 pandemic had ended. But when and how will the chronic phase of this pandemic end? Are we perhaps confusing chronicity with endemicity?

It has taken me quite some time to realize that, regardless of how much surveillance and sequencing data are gathered, any prediction about the timing and amplitude of the tsunami event remains uncertain.

The only thing that can be stated with certainty is that as the prevalence of long Covid increases and cases of acute severe C-19 disease rise simultaneously, we move closer to the predicted tsunami, and the surge of other respiratory viral outbreaks in highly C-19 vaccinated countries will only expedite that progression.

A sudden exponential increase in the rate of hyperacute deaths will unambiguously signal the start of a powerful but brief CoV tsunami. None of this, however, will affect the health of unvaccinated individuals who have been regularly exposed during the immune escape pandemic and do not suffer from underlying immunosuppressive conditions.

The bottom line is that highly C-19 vaccinated countries are on the brink of a major health crisis that could cause healthcare systems to collapse!

ØLL COVID-19 KOPPSETT SKULU TAKA ANTIVIRALA-HEILIVÁGIN IVERMECTIN

HEILSUVERKIÐ FORAR BEINLEIÐIS FYRI NÝTSLU AV IVERMECTIN SUM ER EIN BROTSLIG FRAMFERÐ

 

• Av røttum skulu øll taka Ivermectin, so nøgd av Corona-virus í likaminum verður avmarkað sum mest. Hetta tí at verandi SARS-CoV-2 virus er tilvitað gjørt vandamikið, har ment er eitt Prion øki á Spike-proteininum.
• Tað vil hjálpa koppsetta, har immunverjan er vorin skerd av Covid-19 koppsetingini, at berja niður Corona-virus álopið. Ivermectin hevur eginleikan at fora fyri at Corona-virusið kann knýta seg at okkara kyknum, og fáa tær at framleiða Corona-virus í nøgdum sum kann menna vandastøður. Covid-19 koppsetti kann hava skerdan førleika at megna uppgávuna einsamallur. Somuleiðis ikki-koppsett við skerdari immunverju.
• Ivermectin skal somuleiðis, yvirskipað, nýtast av teimum sum eru Covid-19 koppsett, sum hjálp at aveitra kroppin fyri Spike-proteinir, sum Covid-19 koppsetingin setir likamið at framleiða, í óavmarkaðum nøgdum, í ókent tíðarskeið.
• Ivermectin er lýst sum rætta loysnin til verju ímóti virus-krímsjúku, við sera sera høgum virknað, heldur enn verandi sera líti virkna, og stundum skaðaelvandi- og drepandi krímkoppseting.
• Ivermectin er somuleiðis krabbameinsfyribyrgjandi og verður nýtt í sambandi við krabbameinsviðgerð!

Nobel heiðurskrýndi heilivágurin Ivermectin, er annars heilivágur í handkeypi í menningarlondunum, tá hann er meinaleysari og ger tær betur enn ein sukurmoli. Hann er bannaður í vesturheiminum, har Heilivágsídnaðurin hevur ment protokollirnar Heilsuverkið skal virka eftir. Orsøkin er sera einføld, - Heilivágsídnaðurin fær ongan vinning av nýtsluni!

SUBSTACK 21. jan. 2025 (Er sent við telduposti 22.01.2025 til hmr@hmr.fo, hst@hst.fo, heilsutrygd@heilsutrygd.fo, Landslæknin/foe@stps.dk, landsapotekarin@apotek.fo, beinirj@logting.fo, solvitn@logting.fo, henriko@logting.fo, jenisr@logting.fo, bjorts@logting.fo):I have to admit that I don’t know exactly when the COVID-19 tsunami will begin, but I do know that it will happen and here is how it will unfold

This article is short but critically important if you want to understand the evolution ahead. I hope you understand how the evolutionary dynamics of this pandemic, with its numerous transitions, continue to surprise us.

Are you interested in learning how to connect the dots on the ongoing public health issues?

SUBSTACK 03. sep. 2024 (Nýtt tilfar sum ikki er sent við teldupostinum): Could sustained immune pressure on viral transmissibility eventually lead to the natural selection of virulence-enhancing changes in viral glycosylation?

I have previously expressed my amazement at the remarkable resilience of complex biological systems, such as the mammalian immune system, in mitigating and/or postponing the severe consequences of C-19 vaccine-induced viral immune escape on human health (https://www.voiceforscienceandsolidarity.org/scientific-blog/to-whom-it-may-concern). This resilience seems particularly applicable to viral immune escape mechanisms that threaten the survival of the host species. I have proposed that mutations in the glycosylation pattern of SARS-CoV-2 could eventually drive viral evolution toward enhanced virulence, potentially resulting in rapid death (https://www.voiceforscienceandsolidarity.org/scientific-blog/predictions-gvb-on-evolution-c-19-pandemic). It is, therefore, reasonable to investigate whether evolutionary changes in the virus’s glycosylation profile could also contribute to attenuating viral virulence and/or delaying an explosion in mortality rates in highly C-19 vaccinated populations.

Based on the literature on viral glycosylation, as cited in one of my previous contributions on this topic (https://www.voiceforscienceandsolidarity.org/scientific-blog/predictions-gvb-on-evolution-c-19-pandemic), it seems highly likely that changes in viral glycosylation can lead to increased viral virulence. In the following discussion, and as an addition to a previous contribution, I explain why such changes could take longer to be selected under immune pressure compared to amino acid changes that directly enhance viral infectivity.

Glycosylation refers to the attachment of sugar molecules (glycans) to proteins or lipids. Glycans can either be N-linked or O-linked[1]. In viruses, glycosylation often occurs on surface proteins, such as the spike protein of coronaviruses or the hemagglutinin of influenza viruses. Glycans can shield critical viral epitopes and thereby mask these epitopes from antibody recognition, allowing the virus to evade immune detection and neutralization. This evasion can lead to higher virulence when glycosylation promotes viral infection or replication in an immunologically naïve population, or when it facilitates the transinfection of the virus to target tissues in immunologically experienced populations that remain susceptible to breakthrough infections. This is plausible, as glycosylation is known to modulate receptor binding affinity and specificity, potentially modifying the binding of antibodies to cell surface-expressed binding sites and altering the susceptibility of certain tissue cells.

While amino acid mutations in surface proteins responsible for viral infectivity can readily increase viral infectiousness and transmissibility (e.g., by preventing neutralizing antibodies from binding to the receptor-binding site on the ‘infectious’ viral protein) and confer an immediate fitness benefit, the selection of glycosylation changes may occur more slowly. This is because glycosylation involves both the protein sequence and the host's glycosylation machinery, adding complexity to the selection dynamics and how changes manifest. Since glycosylation changes can compromise viral fitness by reducing the efficiency of host cell entry or decreasing viral replication rates (e.g., due to alteration of protein folding, structural stability, or function), the natural selection of ‘beneficial’ immune escape mutations in the virus’s glycosylation pattern of surface proteins might require a distinct and sustained immune selection pressure, targeted at different viral epitopes that are not involved in mediating intrinsic viral infectiousness. This is because viral glycosylation patterns are often a balance between immune evasion and maintaining efficient host cell entry and replication.

In summary, it is reasonable to state that, compared to direct amino acid changes, the evolutionary dynamics of viral glycosylation reflect a more intricate and context-dependent process that shapes viral adaptation under immune pressure, affecting their ability to persist and spread in host populations. Variants of SARS-CoV-2 are just one example of viruses that have exhibited mutations affecting their glycosylation (specifically, of the spike protein) when placed under sustained immune pressure[2]. The emergence of new immune escape variants endowed with beneficial glycosylation changes therefore likely requires selection over longer evolutionary periods.

Unfortunately, despite numerous precedents (e.g., Influenza virus, HIV-1, Human Rhinovirus, and Hepatitis C virus) and extensive documentation in virology textbooks, the significance of glycosylation mutations in SARS-CoV-2 and their potential impact on the outcome of the pandemic when selected under strong and sustained immune pressure is poorly understood and certainly underestimated.

[1]N-linked Glycosylation: The glycan/ sugar is attached to the nitrogen atom (N) of the side chain of the amino acid asparagine (Asn). O-linked Glycosylation: The glycan/ sugar is attached to the oxygen atom (O) of the hydroxyl group of the side chains of the amino acids serine (Ser) or threonine (Thr).

[2]For example, the emergence of variants like Delta and Omicron involved changes in the glycosylation pattern of the spike protein, contributing to altered immune responses and vaccine effectiveness.

SUBSTACK 26. juni 2024: Sententia mox dicetur - (The decision will be made soon)
In highly Covid-19 (C-19) vaccinated populations, the immune escape pandemic is now on the brink of shifting from its chronic phase (noncognate T cell-dependent immune pathology leading to long Covid) to its hyperacute phase (antibody-dependent enhancement of severe disease). This could soon trigger a tsunami of death in these highly vaccinated populations. However, those who are healthy and unvaccinated will not be affected.My sincere hope is that the prophylactic use of safe and effective antivirals by C-19 vaccinees who experienced symptomatic breakthrough infection following exposure to Omicron (descendants), individuals who recovered from severe C-19 disease after natural infection, or those vaccinated following symptomatic infection will prevent such a catastrophe. However, since no single expert or influential authority believes me, society in highly C-19 vaccinated countries will likely be caught off guard.

“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.” – Norman Mailer

SUBSTACK 30. mai 2024: Do we need to move from C-19 vaccine mandates to mandates for Ivermectin and HCQ?

Citizens should pressure their governments to immediately ensure the availability of safe and effective antiviral drugs in sufficient supply and at affordable prices.

Given the lack of herd immunity and the ongoing evolution of the virus towards enhanced transmissibility, combined with the fact that there is absolutely no scientific rationale to believe that updated C-19 vaccines will protect highly vaccinated populations (+Føroyar 76%) that, by now, have experienced multiple rounds of vaccine breakthrough infections, citizens should pressure their governments to immediately ensure the availability of safe and effective antiviral drugs in sufficient supply and at affordable prices.

Ironically, this means that governments in highly C-19 vaccinated countries should ideally mandate the use ofIvermectin and/or hydroxychloroquine to mitigate the detrimental consequences of their insane C-19 vaccine mandates.

SUBSTACK 31. mai 2024: A Short Debrief of My Recent Helicopter Flight, with Conclusions …

Here is a short debrief of my recent helicopter flight over highly C-19 (Covid-19) vaccinated countries:
I observed how the immune escape pandemic is currently causing multi-national flare-ups of C-19 cases in highly C-19 vaccinated populations (+Føroyar 76%), against a background of vaccine breakthrough infections and chronic vaccine-associated diseases (long COVID). However, unlike natural viral epidemics or outbreaks, these flare-ups do not allow currently circulating variants to spread sufficiently to sustain viral survival, despite their high intrinsicinter-hosttransmissibility.

The elephant in the room is that despite all this, nobody wants to consider the virus undergoing a major structural transformation that would enable it to increase itsintra-hosttransmissibility (i.e., multi-organ dissemination within the infected host itself). I have no doubt that, in highly C-19 vaccinated populations, (+Føroyar 76%) contrary to the expectations of our public health authorities and so-called experts or scientific opinion leaders,the virus will keep knocking on the immune system's door of the vaccinated until it manages to throw that door wide open.

If the population in highly C-19 vaccinated countries (+Føroyar 76%) does not immediately put more pressure on their governments to halt the virus using safe and efficient antiviral drugs (Ivermectin, HCQ,or even mandating their use!) than they are currently placing on the virus itself, allowing it to become highly virulent,we are undoubtedly heading straight for a dramatic multi-national wave of hyperacute C-19 disease.