The science behind the catastrophic consequences of thoughtless human interventon in the Covid-19 pandemic

– Geert Vanden Bossche (DVM, PhD, March 13 2021)

I am herewith postng a list of a series of publicatons that have been instrumental in providing enlightening insights on the interplay between Covid-19 and the host immune system. They provide so to speak critcal pieces of the puzzle that I have been putng together. Entre puzzles are rarely published. That’s why publicatons rarely bring solutons to complex problems. For your convenience, I have allocated the publicatons I consulted to diferent categories. As you will appreciate, I have been tapping into several disciplines. To ‘solve’ a problem as complex as a viral pandemic, one has to draw from several diferent felds, including epidemiology, (molecular) biology, virology, immunology, genetcs, vaccinology and even biophysics. Again, this is why ‘fnished’ puzzles cannot be found in science journals specifcally dedicated to a specifc feld of interest.

The publicatons atached support my scientfc interpretaton of how a natural pandemic develops and how its natural course can be profoundly disturbed by human interventon. For your convenience, I atach a synopsis of my science-based postulate below. I invite scientsts from all over the world to read it and refect on how we could shif gears and possibly intervene in ways that prevent the emergence of additonal highly infectous Covid-19 variants and eventually enable eradicaton of variants that are circulatng already.


I cannot emphasize enough how passionate I am about vaccines, but I cannot accept that we use vaccines which, instead of mitgatng the Covid-19 pandemic, are now at risk of dramatcally aggravatng it.

The original Covid-19 strain was only causing mild symptoms, or even no symptoms at all, in the vast majority of healthy individuals. So, before recommending administraton of any type of current Covid-19 vaccines to everyone, one should frst make sure that the vaccine will reduce the rate of morbidity and mortality below the rates one could reasonably expect when letng the pandemic run its natural course. It’s even more simple than that: if one analyses the dynamics of a pandemic caused by a natural, self- limitng viral infecton (e.g., Infuenza pandemic during World War One), it becomes obvious that the toll taken on human lives is no higher than what is strictly required for the virus to perpetuate. Without human interventon, a pandemic ultmately results in herd immunity. This potentally leaves the door open for the virus to become endemic with interspersed seasonal fare-ups (as we usually see, for example, with the infuenza virus). No pandemic has lasted longer than two years, not even Spanish fu or Swine fu and, once herd immunity is established, resurgence of the virus is controlled by our immune systems thanks to their memory of previous encounters with the virus.

Author: Geert Vanden Bossche, DVM, PhD (March 13 2021) – htps://

Hence, in order for a vaccine to do beter than the natural pandemic, it would need to expedite herd immunity. However, it’s exactly the opposite what we are seeing right now: the vaccines are not able to prevent viral spread by vaccine recipients exposed to the emerging highly infectous strains. This is preventng herd immunity from developing. Whereas at the outset of the Covid-19 pandemic, innate immunity in healthy people provided for a solid frst line of immune defense to Covid-19, this is no longer the case when highly infectous strains are increasingly dominatng the scene. Healthy subjects, including children, are now increasingly exposed to circulatng highly infectous strains while the quality or quantty of their antbodies is insufcient.

Why are the Covid-19 vaccines likely to enhance viral infectousness? It is because they are prophylactc vaccines – designed to build immunity in individuals before they get exposed to the pathogen/virus. They are not suitable at all for administraton to people during a pandemic because the likelihood that a vaccine recipient already comes under atack while not yet being endowed with a full-fedged immune response increases as the infectous pressure augments. This partcularly applies in case of highly infectous circulatng variants.

What happens when you get a vaccine? For an individual who has just received the frst dose of vaccine, his or her body will be in the process of building an immune response. It could take several weeks for the immune response to be fully developed and if you are exposed to the virus during this tme, your immune response may be too weak to efectvely fght the virus. Even though the frst dose may protect you from developing symptoms, the virus may stll be able to replicate and transmit. Exertng high immune pressure without preventng viral replicaton and transmission is a recipe for selectve viral immune escape. However, what we are now more and more observing is even more worrisome: even those who got fully vaccinated before exposure to Covid-19 are no longer controlling virus replicaton and transmission. This is because they’re now increasingly infected by more infectous variants, the spike protein of which is diferent from the one comprised in the vaccine. Hence, the virus increasingly evades the vaccinal antbody response. We have already seen this in many care homes where highly infectous variants have been spreading within no tme despite large vaccine coverage rates (i.e., up to 80-90%). The only beneft of these vaccines is that they may temporarily protect from severe disease and mortality (depending on the antgenic features of the infectng variant).

Selectve immune evasion also favors further disseminaton of highly infectous strains as mass vaccinaton is now increasingly turning vaccine recipients into asymptomatc spreaders. The later transmit highly infectous virus to the unprotected or not yet infected subjects. This is exactly the opposite of what the vaccines were supposed to do. Indeed, there is now a general consensus that the vaccines will, indeed, fail to generate herd immunity. In additon, they will also fail to eliminate the steadily increasing number of highly infectous strains because the vaccinal antbodies do no longer match with the variant spike protein of the circulatng strains whereas they’re stll hampering binding of natural antbodies to the virusi.

Author: Geert Vanden Bossche, DVM, PhD (March 13 2021) – htps://

The combinaton of immune escape and dominant circulaton of highly infectous variants is a recipe for expeditng viral resistance to the vaccine and long-lived suppression of our innate immune response against Coronaviruses in general. It is impossible to scientfcally understand how this could have a happy end. Humanity, therefore, is at crossroads. Contnuing mass vaccinaton with these ‘leaky’ vaccines (see ‘leaky’ vaccines under references from the literature) in the course of a full-blown pandemic inevitably implies that we will witness the emergence of more, more infectous variants putng people at a higher risk of severe disease.

In conclusion: while vaccinaton may help to momentarily protect an individual, mass vaccinaton of individuals during the height of a pandemic is going to worsen the global situaton by encouraging the virus to select specifc mutatons enabling it to overcome ‘suboptmal’ immunologic hurdles. As a consequence, the global populaton will likely have to deal with a worse version of the virus and a worse health-care situaton than earlier in the pandemic. We should stop using conventonal prophylactc vaccines in the ongoing Covid-19 mass vaccinaton campaigns.

Author: Geert Vanden Bossche, DVM, PhD (March 13 2021) – htps://

i Neutralizing ant-Covid-19 IgGs have high AFFINITY for S, whereas IgM have high AVIDITY for the virus; ant-S Abs may stll weakly bind to S, even though they cannot prevent binding of the virus to ACE2 (as AFFINTY of S for ACE2 is much higher than for S-specifc Abs). On the other hand, even weak binding of highly specifc IgGs to S can prevent binding of multmeric IgMs as binding of the later is not S- specifc. Indeed, multmeric IgMs don’t interact with individual antgens but bind through multvalent interactons with repettve paterns on the surface of the virus (‘ensemble efect’). So, despite their high AVIDITY for the virus, IgMs cannot outcompete S-specifc IgGs for binding to S.

Supportve references from the literature

Topic 1: Natural antbodies (B-1A cells, sIgM, natural Abs & innate immunity to CoV and Covid-19)

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doi: https://10.1097/SHK.0000000000001610 htps://

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doi: htps://doi:10.1111/nyas.12137 htps://

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Topic 2 :

– Role of natural Abs and NK cells in asymptomatc carriers

– Substantal transmission by asymptomatcally infected subjects ; protecton of asymptomatc carriers not due to Abs

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topic 3 :
– Natural Abs facilitate MHC class I-restricted antgen presentatonpage5image41559616page5image41559808page5image41560192page5image41560768page5image41560960page5image41560384page5image41560576page5image41561152page5image41561344page5image41561536page5image41561728page5image41561920page5image41562112page5image41562304page5image41562496

– Conserved, CoV-associated cell surface-expressed MHC cl. I peptdes htps://

doi: htps://10.1038/nm933 htps://

doi : htps://10.1128/JVI.00079-09 topic 4 :

– Abs may bind to Sars-CoV-2 without neutralizing the virus/ preventng infectonhtps://


Topic 5 :
– Natural and vaccine-induced immune escape

htps:// doi : htps://

htps:// doi: htps://10.1126/science.371.6527.329

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topic 6 :
– Mechanism of viral shedding and clearance

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topic 7 :
– Dynamics of humoral ant-Covid-19 immune response and potental for reinfecton

htps:// doi : htps://

topic 8 :
Lessons learned from Smallpox vaccines and Infuenza pandemic 1918

htps:// doi: htps://10.2217/fmb.10.98


htps:// 180975040/


About abyssum

I am a retired Roman Catholic Bishop, Bishop Emeritus of Corpus Christi, Texas
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