I Took the Test and Answered the Questions─Still Naively Hoping That Those Asking Them Might Actually Think About the Answers...
Recently, I noticed on X that Stefan Pöhlmann, who regularly comments on the currently circulating variants and apparently follows my work, while seemingly paying little attention to what I actually write, posed the following questions (
):
1. How should public health respond, if at all, to SARS-CoV-2 variants disproportionately affecting children?
2. To what extent does immunity from COVID-19 protect against emerging coronaviruses, including MERS-CoV?
3. What is the zoonotic and pathogenic potential of animal coronaviruses such as PDCoV and SADS-CoV, and what countermeasures are needed?
4. Can we develop broadly active antiviral drugs against coronaviruses?
5. Can we develop broadly protective coronavirus vaccines? A major scientific challenge - not yet in sight, but an important goal.
6. More general and perhaps the most important question: how can societies fully recover from the impact of the pandemic?
I answered them in an unusually kind and moderated manner, which is probably not what most people have come to expect from me. Perhaps that will encourage Pöhlmann and others to take a closer look at my arguments and give them some serious thought. One can always hope. After all, hope springs eternal...
1. How should public health respond, if at all, to SARS-CoV-2 variants disproportionately affecting children?
Before recommending additional interventions, public health authorities should first establish whether children are genuinely more susceptible to a particular variant or whether they merely represent one of the few demographic groups that have largely escaped the immune conditioning experienced by highly C-19-vaccinated adult populations.
From my perspective, the current tendency to interpret higher infection rates in children as evidence of ‘child-adapted variants’ risks confusing cause and effect. I have already addressed this issue in a previous substack article (https://voiceforscienceandsolidarity.substack.com/p/ba322-and-the-imaginary-child-reservoir). Young children rely heavily on broadly reactive innate immune mechanisms and natural antibodies (Abs). They therefore occupy a different immunological landscape than adults repeatedly exposed to vaccine-induced and breakthrough infection-driven adaptive immune stimulation.
The key question is not whether a variant infects more children, but why.
If children are simply serving as a window into what a less immune-conditioned host response looks like nowadays, then vaccination strategies designed to mimic adult immune profiles may prove counterproductive rather than protective. In other words, public health should refrain from vaccinating children against SARS-CoV-2 (SC-2) infection. Time will show that unvaccinated children rapidly train their innate immune system to cope even with SC-2 variants that challenge their natural Abs (https://voiceforscienceandsolidarity.substack.com/p/ba322-and-the-imaginary-child-reservoir).
2. To what extent does immunity from COVID-19 protect against emerging coronaviruses, including MERS-CoV?
This depends entirely on what one means by ‘immunity’.
Ab-mediated cross-protection between highly divergent coronaviruses is generally limited. However, broader cell-mediated innate immune responses may provide varying degrees of heterologous protection.
My concern is that excessive focus on highly antigen (Ag)-specific immune responses will obscure the critical role played by such broadly reactive innate cell-mediated immune defenses. These are often the first and most important barriers against newly emerging pathogens.
The assumption that repeated exposure to SC-2 or repeated vaccination necessarily broadens protection against future coronaviruses remains largely unproven. Indeed, one of the central observations made during the still ongoing immune escape pandemic is that repeated immune focusing (i.e., ‘immune refocusing’) on a continuously evolving target actually reduces the flexibility of future responses rather than enhancing it.
3. What is the zoonotic and pathogenic potential of animal coronaviruses such as PDCoV[1] and SADS-CoV[2], and what countermeasures are needed?
The current zoonotic and pathogenic potential of animal coronaviruses such as PDCoV1 and SADS-CoV2 in humans appears to be very limited. However, the greatest mistake would be to assess these viruses solely through the lens of their current intrinsic characteristics or pathogenicity at the time of spillover.
History repeatedly demonstrates that the most important question is not how dangerous a virus is today, but how it may adapt and evolve after entering a susceptible host population.
The likelihood that a spillover virus establishes sustained productive infection and transmission in a new host species depends not only on its capacity to replicate and generate sufficient infectious pressure, but also on the nature and intensity of the immune selection pressure exerted by the newly infected population.
It is precisely this interaction between viral replication and host immunity that drives adaptation of the virus to its new host.
Countermeasures should therefore focus primarily on reducing opportunities for zoonotic emergence, particularly by limiting industrial high-density animal farming practices that facilitate viral amplification, recombination, and cross-species transmission. At the same time, efforts should aim at strengthening the overall innate immune resilience of susceptible populations, including the preservation of robust cell-based innate immunity.
By contrast, reactive large-scale vaccination of human populations deployed during widespread circulation of newly emerging variants of animal viruses should be avoided.
As vaccines fail to kill virus-infected host cells, they favor evolutionary opportunities for continued viral adaptation under immune pressure, thereby increasing the likelihood of immune escape and the emergence of variants better adapted to transmission within the vaccinated human population.
The lesson of SC-2 is not merely that viruses evolve.
It is that mass deployment of non-sterilizing vaccines during active exposure of a potentially susceptible human population to a multitude of newly generated variants may fundamentally alter the evolutionary interaction between the circulating virus and host immunity.
Under such circumstances, the virus and the adaptive immune system can enter a process of continuous mutual adaptation, creating sustained selective pressure that may ultimately favor viral phenotypes with enhanced transmissibility and virulence (a phenomenon I refer to as in vivo gain-of-function).
For this reason, preparedness strategies should focus not only on preventing spillover events, but also on refraining from population-level immune interventions that intensify and prolong the evolutionary trajectory of emerging immune escape variants.
4. Can we develop broadly active antiviral drugs against coronaviruses?
Probably yes.
Unlike vaccines that depend on recognition of specific Ags, antiviral drugs can target highly conserved aspects of viral replication.
Broadly active antivirals may therefore prove less vulnerable to immune escape-driven evolutionary dynamics.
However, large-scale antiviral deployment should be approached carefully. Any intervention capable of exerting strong selective pressure on viral populations can potentially drive adaptation if used improperly!
The challenge is to use antivirals in ways that suppress viral replication sufficiently while minimizing the risk of selecting resistant variants.
5. Can we develop broadly protective coronavirus vaccines?
This remains one of the greatest scientific challenges.
The difficulty is that coronaviruses possess extraordinary evolutionary flexibility, particularly under strong immune pressure.
From my perspective, the key question is not whether broadly protective vaccines can be developed but whether they can induce the type of immunity required to interrupt transmission without simultaneously generating selective pressures that promote further adaptation.
Currently, there are no vaccines that can broadly induce cytolytic immune responses, i.e., responses capable of eliminating virus-infected cells.
Any such non-sterilizing vaccine will merely promote large-scale viral immune escape when administered during a viral epidemic or pandemic.
Future vaccine strategies may need to place far greater emphasis on:
Innate cell-mediated immunity and training thereof
Immune interventions that are not Ag-specific, but rather ‘pathogenicity-specific’ (e.g., via NK cell-based immunization).
rather than relying predominantly on narrowly focused neutralizing Ab responses or MHC-restricted Tc responses.
At present, such a solution remains largely aspirational.
6. Perhaps the most important question: How can societies fully recover from the impact of the pandemic?
The C-19 pandemic can only end when viral transmission and concomitant evolution stop. From a scientific perspective, this would only be possible if only those survive who effectively contribute to the development of sterilizing herd immunity. That requires a combinatorial effect of innate and infection-primed adaptive immunity.
C-19 vaccine-primed immunity, even if subsequently boosted by natural infection, cannot contribute to protective herd immunity.
But true recovery will also require intellectual honesty. Even if SC-2 is ultimately eliminated from the human population, societies cannot fully recover if fundamental questions remain unexamined. Such ‘mental’ recovery does not require universal agreement; it requires open scientific debate, critical reassessment of assumptions, and a willingness to learn from mistakes.
In my view, one of the most damaging consequences of the pandemic has been the widespread belief that complex biological phenomena can be managed through simplistic narratives and linear thinking.
Whether one agrees with my analysis or not, the pandemic has demonstrated the dangers of scientific groupthink, disciplinary silos and suppression of dissenting perspectives.
In conclusion, ultimate recovery will therefore require both the elimination of SC-2 from the human population and the creation of a new culture that values scientific curiosity over scientific certainty, multidimensional analysis over reductionism, and open debate over consensus-driven dogma.
Only then can societies become truly resilient against the next global crisis─whatever form it may take.
[1],[2] PDCoV and SADS-CoV are porcine coronaviruses that infect pigs and cause severe diarrheal disease, especially in newborn piglets. PDCoV stands for porcine deltacoronavirus, and SADS-CoV stands for swine acute diarrhea syndrome coronavirus; both are recognized as emerging/reemerging swine enteric coronaviruses that can lead to dehydration and high piglet mortality.
I’m really glad to see this post Dr Geert. I really hope you will change your mind about the announcement you made on your latest interview with Dr Phillip McMillan. Your input on Covid is valuable and unmatched and we need it. Many of us believe in your expertise
“In my view, one of the most damaging consequences of the pandemic has been the widespread belief that complex biological phenomena can be managed through simplistic narratives and linear thinking.”
You have said this before and this is really where the problem lies. You were cordial, but very direct. As you should be. It’s amazing to me that they’re currently focusing on children. I guess their reasons for the ongoing Covid variant evolution is on a dartboard where they periodically throw darts to come up with a next reason for the viruses continued evolution. It’s sad that scientific professionalism seems to have left the building.