In May 2023 the WHO stated that the acute phase of the Covid-19 (C-19)
pandemic had come to an end. But when and how will the chronic phase of this
pandemic end? Are we perhaps confusing chronicity with endemicity?
Many are likely wondering by now whether my theory regarding the further
evolution of the virus and the escalation toward a tsunami of C-19
hospitalizations and deaths will ever come to pass and whether such a
frightening outcome is indeed the only scientifically plausible scenario for
the chronic phase of this pandemic to end. I have asked myself that question
hundreds of times. Essentially, people are wondering whether there might be
another way to bring this SARS-CoV-2 (SC-2) pandemic to an end. That this
pandemic is still very much ongoing is beyond the slightest doubt. The virus
continues to systematically produce new variants, even though for quite some
time now, these have taken the form of quasispecies1. The viral
transmission rate is still relatively high, especially because of the high intrinsic
infectiousness of the circulating variants and since infections by the
currently circulating variants are often mild or asymptomatic.
Even though symptomatic infections now frequently have a milder or more
chronic course and viral concentrations in wastewater remain relatively low, it
is crystal clear that the currently circulating SC-2 variants still cause C-19
illness, hospitalizations and even deaths. The interpretation by our health authorities and, unfortunately, also by
many scientists and experts that this pandemic is gradually fading out to
transition into a seasonal infection—like the flu—is, therefore, pure nonsense.
It has long been evident that populations in highly C-19 vaccinated regions are
unable to develop sterilizing herd immunity. In other words, the SC-2
pandemic is far from over; at most, it has taken on a different course
(i.e., a more chronic progression) and has meanwhile caused many animal species
to now also serve as reservoirs for the virus.
In my view, the relatively ‘milder’ course, as
evidenced by the declining number of acute reinfections, can be attributed to a
buffering effect exerted by migratory dendritic cells (DCs) patrolling the
upper respiratory tract. Their lectin receptors strongly interact with viral
sugars on the surface of the highly infectious circulating variants (see fig. 1
appended below). Upon exposure, an increasing number of these highly infectious
variants are ‘parked’ on these DCs instead of being internalized into
susceptible epithelial cells. This likely explains the decline in the rate of
productive viral infection. This is the main reason why both laypeople
and scientists are under the mistaken impression that the pandemic is waning
and will soon transition into a seasonal epidemic that—according to our poorly
educated health authorities—could be managed in a flu-like manner through
annual vaccination of the most vulnerable in the population! However,
those among us who made just a bit more effort to understand these complex
biological phenomena realize that suboptimal, vaccine-induced immune pressure
on actively circulating respiratory viruses that easily mutate and/or tend to
recombine in animal reservoirs not only promotes viral immune escape but may
even be dangerous when the neutralizing capacity of vaccine-induced antibodies
(Abs) against new variants decreases significantly. This is because
such Abs markedly increase the risk of Ab-dependent enhancement (ADE) of
infection. Both suboptimal virus neutralization and ADE of infection promote
the further spread of the virus, respectively by facilitating natural selection
of viral immune escape variants and ‘enhancing’ viral infectiousness.
The evolutionary dynamics of the C-19 pandemic now increasingly rely on
viral replication and shedding in individuals with milder but prolonged
symptomatic infections (commonly referred to as 'long Covid'), the vast
majority of whom are C-19 vaccinees. This begs the question: If
vaccination is far from an effective method to curb the spread of currently
circulating SC-2 variants, what alternative options do we have to contain this
ongoing C-19 pandemic?
Given the current immune-epidemiological situation in highly C-19
vaccinated countries, I can only think of two scenarios that could contribute
to ending the pandemic -both, however, by triggering a hyperacute tsunami of
C-19 hospitalizations and deaths, as I have been predicting.
I recently discussed one of these scenarios in a previous contribution
that is available on the VSS website (https://www.voiceforscienceandsolidarity.org/scientific-blog/large-scale-flu-vaccination-could-facilitate-or-expedite-a-tsunami-of-case-fatalities).
It involves the reverse zoonosis of SC-2 in highly vaccinated
C-19 populations, initially leading to a higher prevalence of mild to
asymptomatic infections by avian influenza viruses in birds.
The fulminant expansion of highly pathogenic avian influenza virus (HPAI)
involving multiple genetic lineages (primarily belonging to the H5N1 subtype)
that have evolved through genetic drift and reassortment, is clearly increasing
the likelihood that a strain could emerge that is well adapted to humans and
capable of enabling human-to-human transmission upon zoonotic spill-over to
humans. Airborne avian influenza virus spread by birds could theoretically trigger
rapid global panzootics in several mammalian species or even a global pandemic
in humans, causing high morbidity and mortality rates, especially in
immunologically naïve populations. While this possibility cannot be fully ruled
out, I don’t believe HPAI will sufficiently adapt to mammalian populations that
have a high prevalence of species-specific anti-influenza Abs. Indeed, it is
reasonable to assume that the better newly emerging avian flu strains bind to
cell-surface receptors of susceptible mammalian cells, the more likely they are
to be recognized by pre-existing infection- or vaccine-induced Abs against
species-specific seasonal flu viruses. For example, it is estimated that about
50–60% of the human population in the United States has such Abs. However, this
recognition is non-functional (i.e., suboptimal), because these Abs
only cross-react with, but do not cross-neutralize,
avian flu strains due to some antigenic similarity between certain epitopes on
the hemagglutinin (HA) or neuraminidase (NA) proteins. Such cross-reactivity
may lead to ADE of disease (ADED) in populations with high levels of anti-flu
Abs.
Given the current surge in seasonal influenza cases—especially in C-19
vaccinated individuals—and the recommendations to vaccinate against seasonal
influenza, the proportion of the population with high anti-flu Ab titers is now
certainly increasing in many highly C-19 vaccinated countries. It is
therefore likely that, instead of witnessing a truly global avian flu pandemic,
we will see an increasing number of individual case fatalities due to ADED in
highly C-19 vaccinated populations. This will not only affect individuals
who developed high titers of infection-induced anti-flu Abs after suffering
from serious breakthrough infections with seasonal flu, but also those with
high vaccine-induced anti-flu Ab titers, regardless of their C-19 vaccination
status. For this reason, I strongly advise against vaccination
against the seasonal influenza virus, even in the context of current
multi-country flu surges. On the other hand, individuals with weak
innate immunity—such as those with underlying diseases or those whose
cell-mediated innate immunity (CMII) was not adequately trained during the
earlier phases of the pandemic (when their C-19 vaccination prevented
widespread acute SC-2 infections from training their CMII)—could also develop
high anti-flu antibody titers. These individuals might consider taking
antiviral medications at the early onset of symptoms.
However, the current surge in viral respiratory infections unrelated to
SC-2 (e.g., seasonal flu, Respiratory Syncytial Virus [RSV], and Human
Metapneumovirus [hMPV]) in highly C-19 vaccinated populations is much more
likely to trigger the end of the C-19 pandemic.
Because of the redirection of cellular immunity2 towards
dendritic cell (DC)-mediated inhibition of virulence (see Fig. 2 below), the
acute phase of C-19 disease increasingly transitioned into a more chronic form
(‘long Covid’). This transition induces a
shift in population-level immune pressure—from targeting viral
infectiousness to targeting viral trans infection and trans
fusion. As the prevalence of chronic infections is now increasing, the
occurrence of cryptic variants3 capable of intra-host transmission4 and shed by chronically infected individuals
also rises. Over time, this gradually increases the likelihood of a 'suitable5 cryptic variant emerging—one capable of
intra-host transmission while overcoming the suboptimal immune pressure on
viral trans infection and trans fusion (i.e.,
viral virulence) exerted by highly C-19-vaccinated populations exposed to
co-dominantly circulating variants.
As previously explained, circulating, highly
infectious SC-2 variants are increasingly being adsorbed onto migratory DCs
patrolling the upper respiratory tract (URT; see Fig. 1 below, including a
relevant reference from the literature). This not only dampens the rate of
productive viral infection but also prevents antiviral immunity from being
stimulated, as DCs cannot serve as antigen-presenting cells (APCs) unless the
virus or antigen is internalized into these cells—rather than merely adsorbed
onto them. As this diminishes viral production and shedding while failing to
abrogate transmission due to the lack of sterilizing immunity, the evolutionary
dynamics of this pandemic seem delayed. At this ‘metastable’ stage of the
pandemic, viral inter-host transmission largely relies on weak but prolonged
viral shedding by an increasing number of repetitively or ‘chronically’
SC-2-infected individuals. As this metastable equilibrium6 creates a sort of steady-state situation,
still enabling sufficient viral inter-host transmission for
the virus to survive, viral intra-host transmission is not yet
under sufficient cellular immune pressure for a new viral phenotype to be selected
that can overcome the virulence-inhibiting effect of viral attachment to
URT-patrolling DCs.
I have been wondering whether and how this
metastable equilibrium could suddenly transition to a more
stable, lower-energy state. In other words, the question remains as to when the
pressure currently exerted on viral trans infection and trans fusion
will become sufficiently high to trigger such a spectacular immune selection
event. Departing from the metastable equilibrium currently evidenced by
relatively low SC-2 wastewater levels, along with relatively low C-19
hospitalization and mortality rates, some external force would likely
be required to increase collective immune pressure on viral trans infection
while promoting the emergence of new variants with enhanced intra-host
transmissibility. Such a force could destabilize the current balance, leading
to a more stable state in which viral propagation in highly C-19 vaccinated
populations is no longer mitigated by population-level immunity.
Outbreaks of other viral respiratory diseases,
which are currently surging in several highly C-19 vaccinated countries, are
likely to expedite the emergence of a new coronavirus (CoV) lineage that may
prove highly virulent in highly C-19 vaccinated populations and could thereby
provide enough energy for the metastable state of this pandemic to transition
into a stable, low-energy state.
Why is this a scientifically plausible hypothesis,
and what is the mechanism by which these viral respiratory epidemics could soon
lead to the end of the C-19 pandemic?
During the acute phase of the pandemic, the overwhelming prevalence of
acute SC-2 infections inhibited training of CMII in C-19 vaccinees, as well as
in unvaccinated individuals who suffered severe C-19 disease. Deficient or
insufficient training of CMII in these individuals has now triggered outbreaks
of other respiratory viruses (e.g., seasonal flu, RSV, hMPV), which were
previously largely outcompeted by SC-2. Symptomatic infection by these viruses not only contributes to training
the CMII system of these individuals but also activates broadly functional
cytotoxic T lymphocytes (CTLs). These CTLs not only contribute to abrogating
viral infection and curb the spread of these other respiratory viruses but also
helps reduce the transmission of circulating SC-2 variants. However, instead of
enabling herd immunity7, this additional reduction in the overall SC-2 transmission rate is
likely to further increase the prevalence of more infectious circulating
variants, thereby increasing their adsorption on URT-patrolling DCs. This is
likely to further raise immune pressure on viral intra-host
transmission while augmenting the prevalence of chronic SC-2
infection and associated diseases (i.e., ‘long Covid’), thereby facilitating
natural selection of cryptic, intra-host transmissible CoV lineages
in chronically SC-2-infected individuals. Given the large-scale immune
selection pressure on intra-host transmission, a newly emerging
cryptic CoV lineage capable of trans infection and trans fusion of susceptible
cells in distant organs would suddenly gain a significant fitness advantage.
Its sudden and overwhelming dominance in prevalence would lead to the
large-scale abolishment of the immune pressure collectively exerted by highly
C-19 vaccinated populations on intra-host transmissibility.
This would inevitably provoke a rapid and massive surge in SC-2-associated
disseminated intravascular coagulation (SADIC) causing sudden death in
all parts of the population that are unable to eliminate this newly emerging
CoV lineage at an early stage of infection.
In other words, the current surge in non-SC-2
respiratory infections in highly C-19 vaccinated countries is expected to
expedite the emergence and natural selection of a CoV lineage that proves
highly virulent in individuals who failed to train their CMII, either during
the acute phase of the SC-2 immune escape pandemic or during the acute seasonal
epidemics currently occurring during this chronic phase of the C-19 immune
escape pandemic. Protection from virulence would require such
individuals to prophylactically take efficient antivirals.
Could training of the CMII by the ongoing other
respiratory infections enable protection of C-19 vaccinees
against a newly emerging virulent CoV lineage?
The emergence of a new, cryptic CoV lineage with
high virulence in highly C-19 vaccinated populations could lead to a hyperacute
C-19 tsunami of hospitalizations and deaths, rapidly reducing large parts of
the population and enable the remaining, largely unvaccinated population to end
this immune escape pandemic through a combination of sterilizing natural
immunity and diminished population density.
However, for others, this could present an
opportunity for innate immune system training. It is important to note,
though, that while this may enhance their immune protection, it will not enable
herd immunity. Why not? Achieving sterilizing immunity requires the synergistic
collaboration of the innate and adaptive immune systems unless cell-mediated
innate immunity (CMII) becomes exceptionally robust, capable of eliminating all
viral load independently of the adaptive immune system. This level of immune
competence has now been observed in unvaccinated individuals who were
repeatedly exposed to the virus during this immune escape pandemic. For C-19
vaccinated individuals, exposure to one or more of the other circulating
respiratory viruses may now enable their CMII to synergize with their adaptive
immune system, potentially sterilizing these new infections. However, they won’t
be able to strengthen their CMII strongly enough to sterilize the remaining
circulating SC-2 variants in the population such as to generate herd immunity.
There are two key reasons for this:
- Other respiratory infections will be
effectively contained, as sterilizing immunity prevents immune escape and
recurrent infection.
- The partial reduction—but not complete
sterilization—of SC-2 transmission will rapidly cause the population to
exert selective pressure on viral trans infection and trans fusion (see
text).
As SC-2's intrinsic infectiousness is already
nearing its upper limit (recent increases have only been marginal), the virus's
survival will now likely require all brakes on viral intra-host transmission to
be lifted. This, in turn, is expected to drive natural selection of a virulent
CoV lineage and trigger a tsunami of hyperacute fatalities. Tragically, this is
likely to affect a large part of C-19 vaccinees as only a minority of healthy C-19
vaccinees will have an opportunity to train their CMII following exposure to
other currently circulating respiratory viruses (e.g., seasonal Flu, RSV,
hMPV).
Indeed, there is a considerable chance that even
C-19 vaccinees who managed to train their CMII following exposure to the other,
currently circulating respiratory viruses may still contract a highly virulent
infection upon exposure to the newly emerging cryptic lineage (which I tend to
call ‘HIVICRON’).
This could particularly be the case in regions where
there is currently a high prevalence of seasonal flu infections. Exposure to
seasonal flu will provide large parts of C-19 vaccinated populations with high
titers of anti-flu Abs, even in the absence of vaccination against seasonal
flu! As mentioned above, these high titers could make them highly susceptible
to ADED when exposed to the rapidly spreading avian influenza strains.
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.
Fig. 2 below summarizes the virological and
immunological changes that occurred at the population level during the C-19
pandemic in highly C-19 vaccinated populations. The graph on the left-hand side
illustrates the corresponding changes in the pandemic's evolutionary dynamics.
However, no one knows when the collective
DC-mediated immune pressure on viral virulence will rise to a high enough level
to collectively trigger the natural selection of phenotypic variants capable of
dramatically reducing this pressure and thereby fully unleash viral virulence8.
As we cannot measure the level of pressure
collectively exerted on the viral infection or viral trans infection, and since
we do not know the level of immune pressure the virus can tolerate before it
gains a new function/ phenotype (i.e., either more infectious or more
virulent), it is impossible to predict when exactly the tsunami of CoV
hospitalizations and deaths will occur and how high mortality rates will arise.
No matter how much data is collected on the
evolution of circulating and cryptic variants, including details about their
sequences and prevalence, it will not change the uncertainty of any prediction.
The same applies to data collected on the evolution of viral wastewater activity,
hospitalization rates, and death rates.
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.
In other words, the transition from a
metastable pandemic state to a stable post-pandemic state will likely occur as
a short but spectacular surge in case fatalities, triggered once a CoV lineage
shed by a chronically SC-2-infected individual and capable of escaping DC-mediated
inhibition of viral trans infection is selected as the
dominantly circulating lineage in highly C-19 vaccinated populations. There
can be no doubt that the virulence of such a CoV lineage will primarily affect
C-19 vaccinees and unvaccinated individuals who previously suffered severe C-19
disease.
We’re in the final stretch now, just staring at the horizon, fully aware
that the tsunami could appear at any moment. What else or what more could I
say?
The laws of thermodynamics are increasingly making it clear to me that
no single model, no single method of surveillance, sequencing, or any other
tracking of viral mutants can exactly predict when Nature will proceed with
this hyperacute event to restore a sound, low-energy equilibrium.
As it has always been my goal to share scientific truth—not only to warn
people about the harmful outcomes of human intervention in this pandemic but
also to predict when Nature will retaliate—it is now time
for me to end my deductive research and communications on this disastrous yet
intriguing phenomenon, brought about by the largest gain-of-function
experiment ever conducted in the history of mankind, one that, however,
involved the human species itself.
I have never been interested in the molecular details revealed by either
virological or immunological analyses unless they could potentially help me
predict the type and timing of the end of this pandemic. I believe I have
largely succeeded in sharing substantial parts of the biological truth.
However, I eventually have to admit that I will not be able to predict
the exact moment when Nature will finally take back control over the health
chaos orchestrated by mankind. As I said, no single analysis can shed light
on that. This is the complete uncertainty in which we currently find ourselves,
despite living in an era of unprecedented technological revolution. We are
nothing compared to Nature. From now on, I intend to spend more of the precious
time that remains exploring and admiring its beauty, as well as that of the
people who respect it. I will continue to participate in the Immune Biology
Forum for as long as there is broad and genuine interest of those who want to
learn more about the unimaginably disastrous consequences of this insane and
unprecedented interference with the immune system of individuals and even with
the collective immune protection of entire populations.
Conclusion
Connecting the dots between the overwhelming occurrence of a diverse
spectrum of diseases, the ongoing evolution of the virus, the various
manifestations of collective immune dysregulation, and the emergence of other
viral panzootics (e.g., avian flu) and ongoing outbreaks of viral respiratory
infections (e.g., seasonal flu, RSV, hMPV) in highly C-19 vaccinated
populations, it becomes difficult to avoid the conclusion that these
unprecedented phenomena—particularly their temporal and spatial overlap—are indirectly
the result of reckless human intervention in the collective host immune
response to the SC-2 pandemic.
The more the prevalence of chronic
C-19 disease replaces that of acute C-19 disease, the closer we come to a
tsunami of C-19 hospitalizations and mortality. As long as cryptic SC-2 lineages emerging in chronically SC-2-infected
individuals do not overcome the collective immune pressure exerted by highly
C-19 vaccinated populations on viral virulence, the pandemic situation remains
'metastable,' giving society the impression that the pandemic is
subsiding. However, outbreaks of other respiratory illnesses in highly C-19
vaccinated countries are currently increasing the likelihood of the remaining
immune pressure collapsing. As the
sudden emergence of a new, ‘suitable’ SC-2 lineage is highly likely to result
in a hyperacute CoV pandemic in highly C-19 vaccinated countries, I keep
warning that society in these countries will be caught off guard.
Who will clean up
all the mess and restore order?
In my view, these unprecedented phenomena and their spatial and temporal
overlapping in highly C-19 vaccinated countries highlight the detrimental
consequences of interfering with natural immunity at both, the individual and
population level during a pandemic caused by an acute, self-limiting viral
infection. When attempting to connect all these dots, I believe we must acknowledge that only Nature can ultimately bring an
end to this immune escape pandemic, and its course will not be positively
influenced by any of the vaccines that our public health authorities or
so-called ‘experts’, who have shown incompetence and ignorance all along,
continue advising as the holy grail of public health interventions.
Figures
Figure 1
Figure 2
Footnotes
1 A quasispecies is a well-defined distribution of highly similar
but genetically distinct variants that is generated by a mutation-selection
process. The composition of a quasispecies is dynamic, with
certain variants becoming dominant under selective pressures from environmental
changes such as the immune response or antiviral treatments. The diversity
within a quasispecies gives the virus a survival advantage by allowing rapid
adaptation to such environmental changes.
2 The
redirection of cellular immunity occurs following the refocusing of humoral
immunity and involves a shift from cytotoxic T lymphocyte (CTL)-mediated
killing/ elimination of virus-infected host cells at an early stage of
infection to dendritic cell (DC)-mediated adsorption/ elimination of infectious
virions (see Figs. 1 and 2).
3 Cryptic
SARS-CoV-2 (SC-2) variants may harbor novel mutations that are selected during
chronic SC-2 infections and are not commonly seen in acute infections. Although
they may eventually be shed into the population, they do not spread widely in
populations that either do not exert immune pressure or exert a type of immune
pressure that fails to provide these variants with a fitness advantage. These
variants are, therefore, not regularly identified in wastewater analyses or
through standard viral surveillance and tracking methods, which is why they are
referred to as 'cryptic’. However, under specific collective immune pressure,
such as that exerted by highly C-19 vaccinated populations*, a specific
emerging cryptic variant could, however, gain a competitive advantage.
* but not in previously SC-2 infected populations,
as the latter do not exhibit a high prevalence of subneutralizing anti-Spike
protein antibodies
4 Chronic
infections provide a prolonged environment for viral replication and evolution,
enabling the virus to acquire mutations that improve its fitness within the
specific host. These adaptations may make the virus better suited for
intra-host transmission between cell types or tissues.
5 For the
purpose of this article, ‘suitable’ means ‘being well adapted to overcome the
suboptimal population-level
immune pressure on viral trans infection and trans fusion.’
6 ‘Metastable’
refers to a state where the equilibrium is only temporarily stable. This can be
visualized by the position of a golf ball in a small hole on a steep slope. It
is stable under small disturbances (e.g., in the case of weak selection
pressure) as those will only make it roll around inside the small hole but then
leave it to return to its resting position. However, if perturbed strongly
enough (i.e., in the case of strong selection pressure), it can transition to a
much lower and stable energy state as a strong push will provide it with enough
energy to escape the confines of the hole (i.e., to overcome the energy barrier
preventing its transition to a lower energy state) and roll down the steep
slope to a much lower position, which represents a more stable equilibrium.
7 To
explain why additional acquisition of CMII training in vaccinees at this late
stage cannot longer contribute to herd immunity, I’d like to refer to my answer
to a Q raised on the Immune Biology Forum (https://lnkd.in/e9ZRVsFQ): “You seem to be suggesting that C-19 vaccinees could benefit
from exposure (to other currently circulating cold viruses). If so, then
wouldn't that create counter pressure to the imminent tsunami? And if an
inflection point is reached, herd immunity is then possible?”
Answer: As the pandemic has transitioned into
a chronic phase, other "cold" viruses are no longer being largely
outcompeted by SC-2 variants (see more accurate explanation above in the text).
This allows these viruses to cause illness, particularly in poorly trained C-19
vaccinees and those recovering from severe Covid-19. This situation is especially concerning for vaccinated individuals with
underlying immunosuppressive conditions, as they are at higher risk of severe
illness and may, therefore, require antiviral treatment.
8 For the purpose of this article, ‘virulence’ refers to the
capacity of the virus to trans infect and trans fuse host cells in susceptible
individuals. Virulence, therefore, greatly depends on the immune status of the
exposed individual.
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
