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

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Avrit er tann 30.06.2024 sent til

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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 KP.3+ ER ÁVEGIS SUM VIL GERAST SERA VANDAMIKIÐ FYRI ÁVÍS COVID KOPPSETT"!

Top Virologist Dr Geert Vanden Bossche warns ‘Massive Tsunami’of ‘Death’ among Vaccinated is ‘Imminent’! (Time 20:44)

https://substack.com/@geertvandenbossche

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.