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Exposure of a highly C-19 vaccinated population to monkeypox virus (MPV) spilling over from an animal reservoir promotes asymptomatic human-to-human transmission in susceptible sexual minority communities (SMCs). MPV infection in SMCs could therefore evolve more infectious viral variants that spread to all parts of a highly C-19 vaccinated population and thereby prevent establishment of herd immunity
Increasing numbers of outbreaks of human monkeypox have been reported from across central and west Africa over the last 3-4 decades. Zoonotic infection with MPV in the current setting of limited smallpox vaccination and little orthopoxvirus immunity[1]in several parts of the world renders human populations more susceptible to contracting monkeypox disease. MPV has therefore been considered a well-suited candidate for a global epidemic.
As productive poxvirus infection is mostly symptomatic and viral transmission almost exclusively occurs through close contact with an infected animal or person or via virus-contaminated objects, such as bedding or clothing, it has been generally acknowledged that naturalepidemic outbreaks in humans can largely be contained through basic infection-prevention measures (including good hygiene practices). Unless the viral infection rate is high (e.g., in densely populated areas and poor [environmental] hygiene conditions), it is difficult to imagine how MPV could evolve to adapt to the human population, let alone how it could ignite a multi-country epidemic or even a pandemic in countries where MPV is not an endemic zoonosis. Pandemics typically occur with pathogens that cause so-called acute self-limiting infection, meaning that they have the potential to spread asymptomatically before inducing a type of natural immunity that prevents productive infection upon subsequent exposure and, therefore, generates herd immunity. Whereas until recently many still tended to believe that the threat of a globally spread MPV was a myth, cases are now being reported globally (at least in all highly C-19 vaccinated parts of the world) to the extent that WHO has now declared MPV a health emergency of international concern—all of this has happened within just a few months. This does not provide enough time for population-level innate immunity to become sufficiently trained to turn MPV infection, which is typically symptomatic (so-called ‘acute self-limiting viral disease’, ASLVD) into an infection that is predominantly asymptomatic (so-called ‘acute self-limiting viral infection’, ASLVI) and can therefore much more easily spread between people. On the other hand, adaptation of a virus to a new host population never implies natural selection of less infectious viral variants, on the contrary. If neither viral evolution nor immune training is responsible for shifting symptomatic into asymptomatic viral transmission (thereby allowing MPV to spread more efficiently from person-to-person and eventually become a pandemic), other non-evolutionary disease-mitigating influences must be considered. As spread of MPV is now particularly expanding in countries with high C-19 vaccine coverage rate and as ASLVD-enabling viruses that are predominantly transmitted through close contact do not spread rapidly, there must be a link between the type of population-level immunity in highly C-19 vaccinated populations and the rapid expansion in prevalence of MPV cases. It’s also important to note that—so far— MPV disease symptoms in these populations have been rather ‘mild’ and predominantly manifest in individuals from the gay and bisexual male community. This already suggests that sexual contact, especially when the latter is at risk of traumatizing the skin or mucosa (e.g., in case of anogenital intercourses), facilitates symptomatic MPV infection.
While I cannot unambiguously prove this, I strongly believe that the sudden emergence of a significant number of (mild) cases of MPV in highly C-19 vaccinated countries is not purely coincidental but related to enhanced activation of broadly reactive, MHC-unrestricted CD8+ T cells in vaccinees. I have previously reported on how a universal CTL (cytotoxic T lymphocyte) epitope can facilitate elimination of host cells infected with ASLVI- or ASLVD-enabling glycosylated viruses and thereby allow recovery from disease, however without inducing immunologic memory (https://www.voiceforscienceandsolidarity.org/scientific-blog/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment). More specifically, MHC-unrestricted CD8+ T cells that now increasingly prevent C-19 disease in healthy vaccinees are the same as those required to abrogate productive infection with other glycosylated viruses that have evolved reduced susceptibility to our innate immune system[2], including poxviruses (https://www.frontiersin.org/articles/10.3389/fimmu.2021.740223/full).
Given the enhanced immune activation of pathogen-nonspecific CTLs[2] in C-19 vaccinees, MPV infection in C-19 vaccinees is likely to become abrogated at an early stage of productive infection, thereby dampening productive MPV infection and potentially causing asymptomatic/ mild infection in sexual minority communities (SMCs) of a highly C-19 vaccinated population. Consequently, MPV infection may even fail to induce MPV-neutralizing antibodies (Abs) in vulnerable[3], C-19-vaccinated individuals that are immunologically naïve to MPV (i.e., today persons younger than 45 to 55 years of age, depending on the country). However, it is reasonable to assume that asymptomatic MPV infection may elicit short-lived, low affinity anti-MPV Abs in these individuals (as has, for example, been reported in case of asymptomatic infection with SARS-CoV-2 (SC-2; https://www.medrxiv.org/content/10.1101/2020.06.22.20137141v2.full.pdf). As asymptomatic infections promote viral transmission within these minority communities, the infection rate of MPV in this vulnerable subpopulation is likely to grow over time. This rise in viral infection rate will subsequently increase the likelihood for recently asymptomatically infected persons from SMCs to become re-infected while titers of their short-lived, low-affinity anti-MPV antibodies are still relatively high. Binding of such low-affinity, non-neutralizing Abs to the virus is thought to enhance viral infectiousness and could thereby cause a disease outbreak in these communities. It is, therefore, reasonable to expect that the proportion of vulnerable individuals who develop virus-neutralizing Abs (i.e., upon their recovery from MPV disease[1]) in the C-19 vaccinated part of the population will increase over time. However, in vulnerable, non-C-19-vaccinated individuals, trained innate immune cells (i.e., NK cells) are likely to prevent MPV from breaking through this first line of immune defense and would therefore largely prevent priming of virus-neutralizing Abs. For the time being, symptomatic manifestations in highly C-19 vaccinated populations are predominantly mild and mostly occurring in SMCs. This suggests that even in cases of symptomatic infection, viral clearance via innate or adaptive cytolytic immune cells (in the case of non-C-19 vaccinated or C-19 vaccinated, respectively) is still effective enough to prevent more problematic symptomatology in most cases.
Rising virus-neutralizing Ab titers can only prevent monkey disease but not viral infection. Hence, re-exposure to MPV of C-19 vaccinated individuals who are in the process of seroconverting promotes natural selection of more infectious MPV immune escape variants while fostering asymptomatic transmission and thereby contributing to a further rise in viral infectious pressure. Due to the steadily growing infection rate in SMCs of highly C-19 vaccinated populations, the overall MPV-neutralizing Ab response in these communities is likely to exert suboptimal immune pressure on viral infectiousness and can therefore be expected to drive dominant circulation of naturally selected, more infectious MPV immune escape variants. Based on all the above, the enhanced infection rate mediated by asymptomatic transmission of MPV in SMCs of highly C-19 vaccinated populations is likely to increase the probability of adaptive evolution of MPV in these communities. It is, therefore, critical to monitor the selective landscape of MPV as unfolded in SMCs of highly C-19 vaccinated populations in order to verify whether the evolutionary trajectory is shifting towards promoting natural selection and expansion of immune escape variants that are more infectious (as is smallpox virus, for example).
Several countries are now about to start vaccination campaigns targeted at people who are at risk of contracting monkeypox disease using live attenuated, replication-incompetent smallpox vaccine. Both, individuals from SMCs engaging in high-risk sexual behaviors for MPV infection and close contacts of monkeypox cases (including very young children, pregnant women, elderly or immunocompromised individuals) are eligible for MPV vaccination (https://www.ecdc.europa.eu/sites/default/files/documents/Monkeypox-multi-country-outbreak.pdf).Live attenuated, replication-incompetent orthopox (e.g., smallpox) vaccines prime virus-neutralizing Abs in the vast majority of both vaccinated and non-vaccinated individuals (i.e., individuals < 50y). However, unlike live attenuated replication-competentorthopox vaccines[1], they do not train cell-based innate immunity. There can be no doubt that vaccination in the context of more infectious circulating MPV variants will further promote natural selection and dominant propagation of even more infectious immune escape variants and thereby allow MPV to evolve into a human pathogen exhibiting an even higher level of infectiousness (comparable to smallpox?). This situation is reminiscent of that which has been responsible for driving adaptative evolution of more infectious SC-2 (SARS-CoV-2) variants following C-19 mass vaccination campaigns. The evolutionary dynamics of MPV will only be expedited when vaccine coverage rates grow; they could eventually modify the current mode[2] and course of chain of MPV transmission such as to asymptomatically spread to all parts of a homogenously mixed, highly C-19 vaccinated population. This would increase the risk for C-19 unvaccinated subjects to contract MPV disease, especially for those who are particularly vulnerable to MPV disease because of Ab-mediated enhancement of viral infectiousness or enhanced susceptibility to MPV infection due to risky (sexual) behavior (see further below). Because of asymptomatic transmission, highly C-19 vaccinated populations would serve as a human reservoir of more infectious MPV immune escape variants.
It is reasonable to assume that populations which do not ‘benefit’ from hyperactivation of cytotoxic CD8+ T cells will become more susceptible to productive infection with new, more infectious MPV variants (https://www.voiceforscienceandsolidarity.org/scientific-blog/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment). This applies, for example, to several different animal populations as well as to human populations in poorly C-19 vaccinated countries (e.g., in Africa). Asymptomatic infections in highly vaccinated C-19 countries are likely to promote spill-over events involving transmission of more infectious MPV variants from these highly C-19 vaccinated human reservoirs to vertebrate animals (possibly even including livestock) and poorly C-19 vaccinated human populations that are immunologically naïve to orthopoxvirus.
Asymptomatic transmission of more infectious MPV variants can also become problematic for the C-19 unvaccinated in highly C-19 vaccinated countries, particularly for C-19 unvaccinated children and vulnerable people (e.g., part of SMCs) who are immunologically naïve to orthopoxvirus.
In young children, rapid re-infection subsequent to previous asymptomatic MPV infection by more infectious MPV variants is likely to entail a rise in cases of Ab-dependent enhancement of MP disease[1] whereas risky sexual behavior renders individuals from SMCs more susceptible to viral infection. One can therefore expect the incidence rate of monkeypox disease to increase in both, non-C19-vaccinated children and SMC members.
While recall of Abs induced by vaccination against smallpox virus in the past will provide an additional layer of natural immunity in the unvaccinated, repetitive recall of Spike (S)-specific infection-enhancing Abs[2] in C-19 vaccinated individuals by circulating SC-2 variants will allow the latter to outcompete other glycosylated pathogens for internalization into mucosa-resident dendritic cells, thereby reducing or potentially even preventing recall of previously smallpox vaccine-induced Abs. This would imply that older (> 45-50y) C-19 unvaccinated individuals are likely to benefit from their smallpox-vaccination in the past whereas their C-19 vaccinated peers may not. However, as already mentioned, the infection can be expected to be largely asymptomatic/ mild in the vast majority[3] of vaccinated and unvaccinated individuals in highly C-19 vaccinated populations, even in the absence of previous smallpox vaccination.
Vaccination with replication-incompetent orthopoxvirus-based vaccines of highly C-19 vaccinated (sub)populations is not only going to drive the expansion of more infectious MPV variants but will also have the same detrimental effect as C-19 vaccines in children: the continuous recall of vaccinal anti-MPV Abs (by circulating, more infectious MPV variants) will keep the innate Abs on the sideline and could thereby predispose the child to immunopathologies[4](https://www.voiceforscienceandsolidarity.org/scientific-blog/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment).
But even replication-competent smallpox vaccines can put the child’s health at risk. Akin to all other live attenuated & replication-competent vaccines (e.g., childhood vaccines), these vaccines are known to come with a risk of side-effects:
“Health complications can occur after receiving the vaccine, and the risk of experiencing serious side effects must be weighed against the risk of experiencing a potentially fatal smallpox infection. The vaccine may cause myocarditis and pericarditis, which are inflammation and swelling of the heart and surrounding tissues and can be very serious. Based on clinical studies, myocarditis and/or pericarditis occur in 1 in 175 adults who get the vaccine for the first time” (https://www.fda.gov/vaccines-blood-biologics/vaccines/acam2000-smallpox-vaccine-questions-and-answers).
“Potentially life-threatening reactions could occur in 14-52 cases out of every million. According to CDC it is estimated that 1 to 2 people out of every 1 million people vaccinated could die” https://www.cdc.gov/smallpox/vaccine-basics/vaccination-effects.html).
The risk of severe disease may significantly increase when these live attenuated, replication competent orthopoxvirus-based vaccines are administered to C-19-vaccinated children. S-directed Abs are thought to sideline the child’s innate immune Abs and thereby prevent NK cell-mediated innate immune recognition of host cells infected by glycosylated viruses (including pox viruses) [https://www.voiceforscienceandsolidarity.org/scientific-blog/intra-pandemic-vaccination-of-toddlers-with-non-replicating-antibody-based-vaccines-targeted-at-aslvi1-or-aslvd2-enabling-glycosylated-viruses-prevents-education-of-innate-immune-effector-cells-nk-cells]. This may enable live attenuated, replication competent orthopoxvirus (e.g., vaccinia virus) comprised within the vaccine to blow through the child’s first line of immune defense and cause (severe) monkeypox disease.
The vast majority of C-19 vaccinees and C-19 unvaccinated individuals in highly C-19 vaccinated populations develop asymptomatic (or very mild) infection upon exposure to MPV. However, close and disruptive physical contact may promote viral entry through broken skin/ mucosa and is therefore more likely to cause symptomatic infection. Whereas strong training of cell-based innate immunity is likely to prevent productive infection of C-19 unvaccinated persons in highly C-19 vaccinated populations and contributes to herd immunity, hyperactivated cytolytic CD8+ T cells in C-19 vaccinated individuals can only enhance abrogation of productive infection, resulting in substantial mitigation of disease symptoms.
Due to the current advanced stage of the evolutionary trajectory of the C-19 pandemic in highly C-19 vaccinated SMCs, MPV is likely to evolve more infectious/ pathogenic variants. Public health authorities in several highly C-19 vaccinated countries have now started rolling out MPV vaccination campaigns targeted at SMCs. MPV vaccination in the ‘at risk’ groups typically use live attenuated, non-replicating smallpox vaccines. Although these vaccines are much less problematic in terms of vaccine-induced side effects (they have even been approved for use in immunocompromised or immunodeficient people), they can only prevent orthopox (including smallpox) disease—not productive infection. As the type of protection conferred by these vaccines is solely based on the induction of antigen-specific, virus-neutralizing Abs, MPV vaccination programs using this type of vaccines will inevitably expedite adaptive evolution of MPV and hence, further promote dominant circulation of more infectious immune escape variants. Consequently, even small-scale deployment of live attenuated, non-replicating orthopox vaccines targeted at preventing disease in vulnerable individuals are highly problematic in that they have the potential to rapidly turn highly C-19 vaccinated populations into a human reservoir for asymptomatic transmission of more infectious MPV variants to poorly C-19 vaccinated populations that are immunologically naïve to orthopoxvirus. Viral transmission from these reservoirs is therefore at risk of igniting multi-country epidemics in poorly C-19 vaccinated countries while increasing the risk of Ab-dependent enhancement of disease in young C-19 unvaccinated children and individuals at high risk of exposure to MPV (due to risky behavior) living in highly C-19 vaccinated countries.
Given the current epidemiologic situation, mandatory vaccination against monkeypox cannot be justified, regardless of C-19 vaccination status. In C-19 vaccinated populations, current vaccination campaigns will only promote further expansion of more infectious MPV variants. But even in non-C19-vaccinated countries, vaccination is not a reasonable option. This is because poxvirus epidemics do not generate herd immunity sensu stricto[1] and prevention, therefore, of world-wide poxvirus epidemics is only possible when the virus can be eradicated. However, eradication is only feasible provided there are no asymptomatic reservoirs and a global mass vaccination program is conducted with vaccines that are capable of preventing productive infection. The first condition is obviously not fulfilled since highly vaccinated countries now serve as asymptomatic reservoirs for MPV. The second condition cannot be fulfilled either since this would require usage of replication-competent vaccines, ideally in a pre-exposure prophylactic setting (or at least within a few days after suspected exposure). However, even replication-competent smallpox vaccines would not enable protection from productive infection by more infectious MPV immune escape variants for the latter will not be a good match for the vaccinal Abs and could, therefore, expedite propagation of more infectious variants in non-C-19 vaccinated populations too. Furthermore, side-effects caused by the existing replication-competent smallpox vaccines may raise additional concerns in regard of vaccine safety.
Finally, no child should be vaccinated with any of the current C-19 vaccines (https://www.voiceforscienceandsolidarity.org/scientific-blog/intra-pandemic-vaccination-of-toddlers-with-non-replicating-antibody-based-vaccines-targeted-at-aslvi1-or-aslvd2-enabling-glycosylated-viruses-prevents-education-of-innate-immune-effector-cells-nk-cells) and no non-C-19-vaccinated young child should be vaccinated with any type of smallpox vaccines. This is because the replication-competent vaccines may cause (severe) MPV disease in these young children whereas the replication-incompetent vaccines put them at risk of contracting immunopathologies.
In conclusion, no C-19 unvaccinated person should engage in sexual behavior that is at risk of enhancing MPV infectiousness (e.g., anogenital intercourses) or be vaccinated with zoonotic orthopoxvirus types once human-to-human transmission of antigenically shifted (i.e., more infectious) MPV variants is occurring!
The current MPV pandemic is to be considered an indirect consequence of the unfortunate C-19 mass vaccination program and does not yet constitute a public health emergency of international concern. However, each vaccination program that uses non-replicating vaccines targeted at immunologically naïve ‘at risk’ communities to fight ASLVI-enabling glycosylated viruses[1]will expedite the expansion in prevalence of more infectious immune escape viral variants. This is why the MPV vaccination campaigns that are currently kicked off are not only likely to have a detrimental impact on individual health (particularly in C-19 unvaccinated children and vulnerable people) but should also be considered at risk of provoking a true public health emergency of international concern.
However, as far as highly C-19 vaccinated countries are concerned, the evolution of MPV towards establishing an asymptomatic reservoir of more infectious MPV variants is merely a ‘side-effect’ of the ongoing evolutionary trajectory of SC-2 in these countries. I therefore predict that the imminent detrimental health consequences of the C-19 mass vaccination program will soon obviate the need for further speculation on how the MPV pandemic/ multi-country epidemic is going to evolve in industrialized countries and, therefore, in third-world countries.
The immunological mechanisms underlying asymptomatic transmission of MPV from highly C-19 vaccinated populations to immunologically orthopoxvirus-naïve, C-19 unvaccinated individuals or poorly C-19 unvaccinated populations also largely apply to a zoonotic influenza virus. This is to say that vaccination (with a non-replicating zoonotic flu vaccine) of a C-19 vaccinated subpopulation that is at high risk of contracting zoonotic influenza infection is prone to further promoting the expansion of zoonotic flu virus and causing (severe) influenza disease in vulnerable people from the C-19 unvaccinated part of the population.
Which individuals are to be considered vulnerable to zoonotic influenza virus?
Whereas orthopoxviruses originating from various animal species induce cross-neutralizing Abs, influenza viruses from animal species do not induce broadly cross-neutralizing Abs. Individuals who received smallpox (i.e., cowpox-based) vaccines in the past are therefore not prone to developing Ab-dependent enhancement of viral infectiousness upon subsequent exposure to MPV. However, asymptomatic human-to-human transmission of an antigenically shifted influenza variant spilling over from an animal reservoir (e.g., birds) may become particularly problematic in individuals who have recently recovered from productive infection with a common seasonal influenza virus type or who have recently been vaccinated against predominantly circulating influenza virus types (i.e., primarily the elderly and people with co-morbidities are who are otherwise immune suppressed). Zoonotic infection of these individuals with an antigenically shifted viral variant (most likely avian influenza) will likely lead to more and more cases of Ab-dependent enhancement of influenza disease[1] in humans. However, severe disease is unlikely to occur due to trained cell-based innate immunity (in C-19 unvaccinated persons) or cell-based adaptive immunity (in C-19 vaccinated persons). Should public health authorities recommend vaccination of the elderly and people with co-morbidities against the zoonotic influenza virus (most like, avian influenza virus), we will undoubtedly witness circulation of more infectious variants in highly vaccinated populations, resulting in enhanced rates of disease predominantly in C-19 unvaccinated children (because of a higher chance of re-infection shortly after previous exposure) and individuals who have recently been primed with common (seasonal) influenza virus types.
Similar to the epidemic predictions made for MPV, asymptomatic transmission of zoonotic influenza (most likely avian influenza) from highly C-19 vaccinated populations will likely give rise to multi-country epidemics of zoonotic influenza in poorly C-19 vaccinated populations and several animal species (livestock?) that are immunologically naïve to the transmitted zoonotic influenza virus.
Similar also to the risks associated with MPV vaccination of young children, immunization of young children with any type of zoonotic influenza vaccine is at risk of causing (severe) zoonotic influenza disease (i.e., in the case of replication-competent vaccines) or immunopathologies (i.e., in the case of replication-incompetent vaccines).
In conclusion, no C-19 unvaccinated person should be vaccinated with common (seasonal) or zoonotic influenza virus types once human-to-human transmission of antigenically shifted (i.e., more infectious) influenza variants is occurring!
[1] Populations aged < 50y have not been vaccinated in the past against smallpox. The smallpox vaccine uses live attenuated, replication-competent cowpox (vaccinia) virus and largely protects against monkeypox disease.
[2] Infections with these viruses typically cause acute self-limiting viral disease
[3] As the current SC-2 variants are further strengthening their infectiousness, presumably as a result of stronger binding to the infection-enhancing Abs (https://www.voiceforscienceandsolidarity.org/scientific-blog/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment), more SC-2 virions are internalized into migrating dendritic cells and thereby contribute to activation of cytolytic CD8+ T cells
[4] For the purpose of this manuscript, ‘vulnerable’ refers to individuals from sexual minority communities (SMCs), wherein SMCs refer to gay and bisexual male communities engaging in high-risk sexual behaviors for MPV infection (e.g., anogenital intercourses)
[5] Disease in vulnerable, C-19 vaccinated individuals occurs when the virus breaks through the cytolytic immune defense provided by the hyperactivated CTLs
[6] Regardless of safety concerns about potential side-effects, live attenuated, replication-competent orthopox vaccines will not be effective when used in highly C-19 vaccinated populations. This is because elimination of MPV-infected cells by cytotoxic innate or adaptive immune cells (i.e., trained innate NK cells or CTLs in the non-C19-vaccinated or C-19 vaccinated, respectively) will largely prevent ‘vaccine take’.
[7] Enhanced intrinsic infectiousness could even enable airborne transmission (e.g., via particle/ droplet aerosol) as in the case of smallpox
[8] Re-infection with MPV in the presence of non-neutralizing, low-affinity anti-MPV Abs enhances viral infectiousness and, therefore, disease in young, C-19 unvaccinated children
[9] These Abs are currently making C-19 vaccinees more and more susceptible to productive re-infection with SC-2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8351274/
[10] The additional protective effect of past vaccination with smallpox vaccines might predominantly benefit the elderly (> 65 y) and vulnerable people.
[11] Because of deficient or insufficient education of NK cells to sense virus-associated self-mimicking peptides expressed on the surface of host cells infected by said ASLVI- or ASLVD-enabling glycosylated viruses (https://www.voiceforscienceandsolidarity.org/scientific-blog/intra-pandemic-vaccination-of-toddlers-with-non-replicating-antibody-based-vaccines-targeted-at-aslvi1-or-aslvd2-enabling-glycosylated-viruses-prevents-education-of-innate-immune-effector-cells-nk-cells).
[12] Herd immunity sensu stricto relates to a level of naturally induced, protective immunity that has been established in the majority of the population and is high enough to protect the remainder of that population by virtue of diminished infectious transmission.
[13] Although monkey pox is an ASLVD, it can be considered an ASLVI when spreading in a highly C-19 vaccinated population at this stage of the C-19 pandemic (i.e., due to hyperactivation of cytolytic CD8+ T-cells)
[14] This is because the antigenically shifted immune escape variant from the animal reservoir will not properly match the vaccine-induced Abs.
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
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