The quieter it gets around the acute cases of Covid-19, the more worried I become…
A couple of months ago, a colleague was publicly attacking me and ridiculing me for predicting a major storm of severe Covid-19 (C-19) disease in highly C-19 vaccinated populations. While calling himself a vaccinologist, this person clearly doesn’t understand the interplay between the immune system and the evolutionary dynamics of SARS-CoV-2 (SC-2). Although eager to learn from me at the outset of the mass vaccination campaign, this colleague now derogatorily refers to me as the veterinarian who, in support of his arguments, cites the effect of mass vaccination against Marek’s disease. Nevertheless, that colleague knows all too well that I have always maintained that the example of Marek’s disease vaccination is anything but applicable to the effect of mass vaccination during the current SC-2 pandemic. Instead of learning from my online course (https://www.voiceforscienceandsolidarity.org/geerts-books-and-lectures), this individual prefers to take the easy way out and simply dismisses my predictions as irresponsible.
Because I attach no importance to the prattle of those who deny vaccination-associated viral immune escape, I want to reiterate my predictions for the last time here. They remain unchanged despite the fact that the timeline has drastically changed compared to the initially projected timeline. As I have repeatedly indicated, this change occurred because I did not take into account a hitherto unknown phenomenon at the time, namely that of vaccination-associated immune refocusing. This phenomenon is directly caused by the mechanism of action of mRNA vaccines (see my book: “The inescapable immune escape pandemic”, https://www.voiceforscienceandsolidarity.org/geerts-books-and-lectures), or indirectly as a result of breakthrough infections of individuals immunized with any C-19 vaccine.
My most recent insights into the immune response in vaccinated individuals are shared weekly with my online students. They are among the few who understand why I am rightly very concerned. I do not wish to overwhelm the many who, due to a lack of understanding of this complex matter, lose credibility in my predictions this time. Instead, I simply invite them to verify the following predictions. These are predictions of what will precede the predicted tsunami in highly C-19 vaccinated countries:
– SC-2) infection will increasingly be transformed into a chronic illness. The latter will increasingly constitute the bulk of the so-called ‘long Covid’ cases and predominantly occur in C-19 vaccinated people.
More isolated cases of severe C-19 disease will contribute to the vaccine-associated excess deaths while hospitalization and death rates will remain relatively low.
The concentration of SARS-CoV-2 virus in wastewater (comprising all circulating variants) will also remain low.
The JN.1. clade will remain the dominant circulating lineage in highly C-19 vaccinated countries while other subvariants of Omicron are co-circulating (including BA.2.86, XBB.1.5, EG.5.1 and JN.1, JD.1.1, GE.1. etc.).
More subdominant variants can emerge but they won’t displace the JN.1 clade due to lack of higher transmissibility.
- The incidence of long Covid will steadily increase during this spring to then usher in a tsunami of ‘antibody-independent enhancement of severe C-19 disease. This mega-wave will thus occur even further outside the winter season.
- C-19 disease and mortality are not only no longer seasonal, they are also no longer age-dependent but mainly bound to C-19 vaccination (2 doses).
- Tsunamis of severe C-19 disease will occur independently of each other, first in countries that used mRNA vaccines for mass vaccination.
- The unvaccinated are already becoming less frequently significantly ill, and this situation will only improve as the immune escape pandemic peaks.
In Africa, little of this nefarious evolution will be noticeable because the vast majority of African countries did not have the ‘privilege’ of undergoing mass vaccination.
The increasing decline of acute, symptomatic infections leaves our public health authroities and experts with the false impression that we have the worst part of the C-19 pandemic behind us and that the virus is now transitioned into endemicity thanks to herd immunity! They seem to ignore that the virus is still highly transmissible and evolving. As infections are no longer typically acute self-limiting but have become more subclinical or even chronic, much of the noise that surrounded acute cases of C-19 disease has now make way for other noises, which, however loud, are still less threatening than this insidious immune escape pandemic.
Those who are interested in understanding the immunology behind the increasing shift of acute symptomatic infection to subclinical and chronic C-19 disease, may want to read the following reasoning:
Lack of herd immunity enables repeated VBTI due to variants with a steadily increasing level of infectiousness to raise the incidence of asymptomatic/ subclinical shedding or chronic disease (‘long Covid’). This is now contributing to sustained viral transmission and continuing evolution of the virus. However, as viral infectiousness increases, interactions between the virus and APCs (including peripherally patrolling DCs) shift from rapid virus internalization into those cells to virus adsorption onto these cells. This shift underlies the shift from acute self-limiting infection to chronic disease! Why? The more highly infectious virus adsorbs to URT-resident DCs, the higher the concentration of PNNAbs required to suppress viral virulence. I am explaining in my online course how complexation of viral particles by low-affinity Abs following VBTIs leads to virus-Ab complexes that promote viral uptake into APCs rather than triggering recall of PNNAbs. Consequently, the concentration of the latter falls to suboptimal levels and thereby put viral virulence under immune selection pressure, paving the way to the emergence of new variant that broadly escapes virulence-inhibiting PNNAbs in highly C-19-vaccinated populations.
Those interested in comprehending the immunological factors contributing to the shift from acute symptomatic infection to subclinical and chronic COVID-19 disease may find the following explanation informative:
The absence of herd immunity facilitates recurrent viral breakthrough infections (VBTIs) driven by variants with escalating infectiousness, leading to the formation of large virus-Ab complexes that are readily taken up by APCs to activate CTLs. Enhanced clearance of virus-infected host cells promotes asymptomatic/subclinical shedding. This phenomenon is currently fueling sustained viral transmission and immune selection pressure on viral reproduction (as manifested by mutations in other viral proteins).
However, as JN.1 and its descendants change the interaction between the virus and antigen-presenting cells (APCs), including upper respiratory tract (URT)-resident dendritic cells (DCs) from virus internalization to virus adsorption, there is an increased demand for polyclonal non-neutralizing antibodies (PNNAbs) to effectively neutralize viral virulence. While the formation of large viral-Ab complexes following VBTIs, facilitated by low-affinity antibodies, enhances viral uptake by APCs rather than prompting the recall of PNNAbs, the concentration of the latter declines to suboptimal levels, exerting immune selection pressure on viral virulence.
This process sets the stage for the emergence of new variants that can broadly evade the inhibitory effects of PNNAbs, particularly within highly C-19 vaccinated populations.
Understanding the evolutionary dynamics of virus-Ab interaction during an immune escape pandemic is key to understand the pivotal transition from acute self-limiting URT infection to subacute self-limiting pulmonary disease to chronic disease symptoms in distal organs (commonly referred to as ‘long Covid’).
All of the above explains why I have continuously been using the following one-liners:
“Societies in highly C-19-vaccinated countries will be caught off guard.”
“Africa will win”
“We are currently witnessing the calm before the storm (tsunami).”
“When two dogs fight over a bone” (alluding to the conflict between stakeholders and opponents of the mass vaccination program), “the third” (referring to the virus) “will run away with it” or “parties are vying for control, but no one can master the virus.”
” Scientists and public health authorities are no longer seeing the forest for the trees”
“It was highly predictable that the C-19 mass vaccination program would lead to catastrophic consequences.”
“Only Nature has the ability to restore the disrupted balance between the virus and immunity
While that colleague prefers not to engage in the more rigorous work but rather to ‘check back in a couple of months’, I reiterate that such a casual approach will undoubtedly fail to mitigate the crisis, as it will not provide ample time for any actions to be implemented aside from severe lockdowns. Consequently, someone must undertake the unpleasant task of informing highly C-19 vaccinated societies about the projected timeline for SC-2 to release a new variant capable of circumventing the virulence-inhibiting effect of non-neutralizing antibodies:
The likelihood for this to occur before the end of April 2024: 50%
The likelihood for this to occur before the end of July 2024: 99%
Back in 2015, I designed a simple, safe, and pure neopeptide construct capable of training NK cells to recognize pathologically altered host cells upon intradermal administration. In my humble opinion, it could be used – among many other prophylactic and therapeutic applications – for training NK cell-mediated innate immunity in C-19 vaccinees and thereby provide them with the same ‘training’ status as the unvaccinated. To acquire such training status, the unvaccinated had to endure symptoms and discomfort. The pure, unadjuvanted construct would generate this targeted training without causing symptoms of C-19 disease or side effects. However, even if I manage to find a group of scientists willing to collaborate on further development of this NK cell enhancer, clinical studies will come too late to enable licensing in due time. Just that people know that I am not trying to take commercial advantage of this invention (beyond the fact that I have always been willing to make this technology accessible to all those who benefit from it not financially but in terms of their health).
The sole alternative, not reliant on immunity, for fully vaccinated individuals to significantly decrease the risk of experiencing severe C-19 disease enhancement is the prophylactic (!) utilization of antivirals. These antivirals must be safe, broadly effective (i.e., against all circulating SC-2 variants), and accessible in ample quantities at an affordable cost.
I expect that this communication will likely prompt another call from my colleague, urging the broader public once again to ‘stop listening to my predictions of doom and gloom that keep getting recycled and updated every six months’. He blames the mass vaccination lobby for not listening to him. Sometimes, when I hear his criticism, I cannot help but think of the saying: ‘The pot calling the kettle black…’
About Geert Vanden Bossche
Geert Vanden Bossche received his DVM from the University of Ghent, Belgium, and his PhD degree in Virology from the University of Hohenheim, Germany. He held adjunct faculty appointments at universities in Belgium and Germany. After his career in Academia, Geert joined several vaccine companies (GSK Biologicals, Novartis Vaccines, Solvay Biologicals) to serve various roles in vaccine R&D as well as in late vaccine development.
Geert then moved on to join the Bill & Melinda Gates Foundation’s Global Health Discovery team in Seattle (USA) as Senior Program Officer; he then worked with the Global Alliance for Vaccines and Immunization (GAVI) in Geneva as Senior Ebola Program Manager. At GAVI he tracked efforts to develop an Ebola vaccine. He also represented GAVI in fora with other partners, including WHO, to review progress on the fight against Ebola and to build plans for global pandemic preparedness.
Back in 2015, Geert scrutinized and questioned the safety of the Ebola vaccine that was used in ring vaccination trials conducted by WHO in Guinea. His critical scientific analysis and report on the data published by WHO in the Lancet in 2015 was sent to all international health and regulatory authorities involved in the Ebola vaccination program. After working for GAVI, Geert joined the German Center for Infection Research in Cologne as Head of the Vaccine Development Office. He is at present primarily serving as a Biotech / Vaccine consultant while also conducting his own research on Natural Killer cell-based vaccines.
Email: info@voiceforscienceandsolidarity.org
Questions And Answers
What happens if June 2024 comes and goes without incident?
This is the wrong Q.The right Q would be:What if this new variant hits highly C-19 vaccinated populations any time soon and you ignored every single informed warning?The A to your Q is simple:GVB gets blamed and forever discredited for scaring the hell out of people for no reason.
Since the quieting down can be a prelude to a tsunami as you put it, what would “good news” look like, in a crudely observable way? Besides waiting for July, what could be some indicators to look out for, which, if observed, would tilt your hypotheses towards being less likely?
Easy: Evidence of herd immunity! i.e., virus spread diminished and the virus stops to evolve, followed by decrease in long Covid cases and in C-19 mortality rate. Covid reverting to one lineage causing acute self-limiting infection and becoming endemic. It won’t happen, though!
Robert Malone lost faith in Geert’s prediction because his timing was currently wrong and has ceased to exercise caution.
Malone blames the immune suppressed for being a breeding ground for new emerging variants.That’s is wrong as I extensively documented.He called Omicron a ‘blessing’; that was wrong too. Now he claims the pandemic is over,which again will be proven wrong. What’s he up to nex
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