Viruses do not exist. Viruses are computer simulations that fit observations. They are nothing more than models we create ourselves. No virus has ever been physically isolated, and a definition for 'virus' has been devised that is still not met. Thus the repeated complaints from virus deniers against virus variants. (Those 'postulates' themselves are partly outdated - but that is also another discussion).
All in all a challenging and therefore amusing controversy, but this site is about an infectious respiratory disease - from viruses or something else - and the response to it. The question is how proportionate and substantiated the response was and is, especially in the Netherlands. Call it a virus, an exosome, a replicon, or a self-replicating pathogen - the name does not change the reality: contamination between individuals exists, is experimentally reproducible, and the discussion about what to call it only distracts from pandemic handling: how do we deal with infections: can we prevent or moderate them and at what cost? We still have to learn to deal with infections; viruses or not.
Are there studies on this?
Especially in the initial investigations, forcing infections was not always easy.1November 2020 article: Hard evidence of infectious aerosols Het druppeldogma zat in de weg. Men heeft het vaak geprobeerd met neusdruppels: vrij kansloos, want dat is alsof je een schuimblusser probeert aan te steken met een lucifer en als dat niet lukt concludeert "er bestaat geen vuur" of "overslaande brand is onmogelijk". De neus, slijmvliezen en bovenste luchtwegen (aka mucosale bescherming) vormen immers de belangrijkste firewall tegen pathogenen, die binnen minuten worden afgevoerd richting slokdarm, weg van de ontvankelijke longen. In latere studies gaat dat een stuk beter. Er staan er hieronder enkele genoemd.
Another basis of evidence is the fact that - in other types of research - serial passage is used: how a pathogen adapts to a new host. This is studied by transferring infections from animals to other animals. So that works without any problems. Also a number of links to studies.
Finally, a few studies with ferrets that infect each other, in different setups. Poor animals...
Contact or air
1. The Poker Experiment (Dick et al., 1987) 2Dick EC, Jennings LC, Mink KA, Wartgow CD, Inhorn SL. Aerosol transmission of rhinovirus colds. J Infect Dis. 1987;156(3):442-448. PubMed: https://pubmed.ncbi.nlm.nih.gov/3039011/ JSTOR (full text): https://www.jstor.org/stable/30134751
Already treated in 20233Playing poker with infections https://virusvaria.nl/pokeren-met-besmettingen/:
What happened:
- 8 sick Donors played 12 hours of poker with 12 healthy Recipients
- Half of the Recipients were physically prevented from touching their faces
- A separate experiment tested only contaminated objects (cards, tokens, furniture — zero Donors in the room)
The outcome:
- Aerosol-only: 56% contaminated, all routes: 67% contaminated (difference not statistically significant)
- Fomites-only: 0% besmet
There is something transmissible that goes from person to person through the air. Fomites do nothing. The discussion about what exactly it is, virus or not, is irrelevant to the outcome.
2. EMIT-1 proof-of-concept (2012) 4Killingley B, Enstone JE, Greatorex J, et al. Use of a human influenza challenge model to assess person-to-person transmission: proof-of-concept study. J Infect Dis. 2012;205(1):35-43. PubMed: https://pubmed.ncbi.nlm.nih.gov/22131338/ DOI: https://doi.org/10.1093/infdis/jir701
Donors en Recipients in quarantaine without mechanical ventilation.
Secondary attack rate: 16%. Transfer takes place.
3. EMIT-1 follow-on (Killingley et al., 2020) 5Nguyen-Van-Tam JS, Killingley B, Enstone J, et al. Minimal transmission in an influenza A (H3N2) human challenge-transmission model within a controlled exposure environment. PLOS Pathog. 2020;16(7):e1008704. Full text (open access): https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1008704 DOI: https://doi.org/10.1371/journal.ppat.1008704
Same setup, but now with mechanical ventilation. Secondary attack rate: 1.3%. Turn on the ventilation, and the transmission disappears. Ventilation only dilutes things floating through the air. The agent appears to be transmissible through the air.
"The main difference between these studies was mechanical building ventilation, suggesting a possible role for aerosols."
4. EMIT-2 — naturally infected Donors, still ventilation dependent6Coleman KK, Bischoff W, Tellier R, et al. Evaluating modes of influenza transmission (EMIT-2): Insights from lack of transmission in a controlled transmission trial with naturally infected donors. PLOS Pathog. 2026;22(1):e1013153. https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1013153
Naturally infected Donors (no lab inoculation, mild symptoms, possible cross-immunity in recipients, 8 people 2-4 hours in a room with one donor), limited ventilation but high air recirculation, regulated climate (temp, humidity). Zero transmission. Mild symptoms and cross-immunity probably played a role.
Conclusion: without concentrated respiratory plumes - no transmission.
(Note: they made the donor cough several times. However, they would have been better off letting him sing some carnival songs, as evidenced by this piece in Nature, February 20197Nature, februari 2019 https://www.nature.com/articles/s41598-019-38808-z)
Serial passaging
Serial passage involves infecting a healthy animal with tissue from a sick animal. That healthy animal becomes sick. A healthy animal is then 'infected' with that new lung tissue, etc. → repeat 10-20 times. At the end, the mutations of the tissue are mapped.
5. Serial passaging: A/Kansas/14/2017 H3N2 — 17 passages8Dynamic adaptation mutations and pathogenic characterization of a mouse-adapted seasonal human H3N2 influenza virus. Virol J. 2025.
Full text: https://virologyj.biomedcentral.com/articles/10.1186/s12985-025-02793-9
17 passages in mice. Wild type: zero detectable RNA in lungs. Passage 17: 1010 copies/mL, lethal. Fourteen specific mutations accumulated (Virology Journal, 2025).
6. Serial passaging: A/Switzerland/9715293/2013 H3N29Synergistic PA and HA mutations confer mouse adaptation of a contemporary A/H3N2 influenza virus. Sci Rep. 2019;9:16616. Full text: https://www.nature.com/articles/s41598-019-51877-4 DOI: https://doi.org/10.1038/s41598-019-51877-4
Serial passages, polymerase activity increased >300%. Synergistic mutations in HA and PA caused lethal pneumonitis where the wild type did nothing (Scientific Reports, 2019).
7. Serial passaging: A/HK/1/68 H3N2 — genomische analyse10Ping J, Keleta L, Forbes NE, et al. Genomic and protein structural maps of adaptive evolution of human influenza A virus to increased virulence in the mouse. PLOS One. 2011;6(6):e21740. Full text: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0021740
39 variants from 10 independent passages. 51 of 115 mutations under positive selection, 27 parallel mutations. Virulence increased by factor >105.
8. Serial passage: SARS-CoV-2 Beta — IFITM3 as a barrier11IFITM3 deficiency drives SARS-CoV-2 adaptation while preserving variant-specific traits. Nat Commun. 2026. Full text: https://www.nature.com/articles/s41467-026-68485-2
20 passages in IFITM3-deficient mice. Virus replicated more efficiently in mice, but at the same time lost fitness in human cells. A classic host-adaptation trade-off (Nature Communications, 2026).
9. Serial passing: SARS-CoV-2 Beta and Delta — parallel evolution12SARS-CoV-2 rapidly evolves lineage-specific phenotypic changes during serial passage in hACE2 transgenic mice. Commun Biol. 2024;7:248. Full text: https://www.nature.com/articles/s42003-024-05878-3
20 passages. Early passage virus (P2) versus late (P21): dramatic difference in virulence, weight loss, and mortality. TNF-deficient mice were spared — the mechanism has been causally demonstrated (PNAS, 2023).
10. Serial passaging: SARS-CoV-2 N501Y VIC2089 — 21 passages13SARS-CoV-2 mouse adaptation selects virulence mutations that cause TNF-driven age-dependent severe disease with human correlates. PNAS. 2023. PubMed: https://pubmed.ncbi.nlm.nih.gov/37523564/
21 passages. Early passage virus (P2) versus late (P21): dramatic difference in virulence, weight loss, and mortality. TNF-deficient mice were spared — the mechanism has been causally demonstrated (PNAS, 2023)
11. Natural serial passage on an industrial scale: Danish mink14Emergence and spread of SARS-CoV-2 variants from farmed mink to humans and back during the epidemic in Denmark, June-November 2020. PLOS Pathog. 2024;20(7):e1012039. Full text: https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1012039
Large-scale natural serial passage. ~136 human-to-mink transmissions, ~59 mink-to-human transmissions, mink-to-mink transmission between farms. The Y453F Spike mutation emerged early and dominated — population-scale adaptive evolution (PLOS Pathogens, 2024).
12. H5N1 — transmission between mammals15Eisfeld AJ, Biswas A, Guan L, et al. Pathogenicity and transmissibility of bovine H5N1 influenza virus. Nature. 2024. https://www.nature.com/articles/s41586-024-07766-6
Bovine H5N1 transmission from mother to pup in mice. Inefficient but real respiratory droplet transmission in ferrets. The authors: "a paradigm shift."
13. Bonus: systematic review confirms aerosol as dominant route16Transmission route of rhinovirus — the causative agent for common cold. A systematic review. Am J Infect Control. 2023;51(4):438-445. https://www.ajicjournal.org/article/S0196-6553(22)00866-5/fulltext
Conclusion after 25 studies: "Moderate evidence that airborne transmission is the major transmission route of rhinovirus in real-life indoor settings."
Physically separated ferrets
These are perhaps the strongest experiments yet.
14. Zhou et al. (2018) — from impactor-studie17Zhou J, Wei J, Choy KT, et al. Defining the sizes of airborne particles that mediate influenza transmission in ferrets. PNAS. 2018;115(10):E2386-E2392. PubMed: https://pubmed.ncbi.nlm.nih.gov/29463703/ Full text: https://www.pnas.org/doi/10.1073/pnas.1716771115
The setup:
- Two stainless steel chambers, one for Donor frets, one for Recipient frets
- Connected by a impactor — a plate with holes that separates particles by size
- Four different impactors tested: 50% capture efficiency at 9.9μm, 5.3μm, 2.5μm, en 1.0μm
- Air flow exclusively from donor to recipient chamber via a vacuum pump
- HEPA filters on inlet and outlet
Large droplets (>10μm) are struck against the impaction plate due to their mass and inertia. Only small aerosols make the turn and reach the receiver.
Results:
- Transmission via particles >1.5μm was successful
- With the 9.9μm and 5.3μm impactors: transmission occurred
- With the 2.5μm impactor: reduced transmission
- With the 1.0μm impactor: no transmission via natural exhalation - but there is with artificial aerosolization of the virus
- Donors were the most contagious for fever, and remained contagious for up to 5 days
- Viral load in the air correlated with transmission success
The implication: the infectious particles are in the fine aerosol fraction (1.5-10μm), not in the large droplets that settle within a meter. This explains why ventilation has such a dramatic effect in the EMIT studies — it dilutes precisely these particle sizes.
15. Kutter et al. (2012) — pandemic vs seasonal influenza in ferrets18Kutter JS, Spronken MI, Fraaij PL, Fouchier RA, Herfst S. Exhaled aerosol transmission of pandemic and seasonal H1N1 influenza viruses in the ferret. PLOS One. 2012;7(4):e33118. Full text: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0033118
The setup:
- Two rooms connected by one 7×7×15cm tunnel with mesh at both ends
- Air flow 12 L/min from donor to recipient
- No direct contact possible — only what floats through the tunnel
- Exposure: 3 hours (to approximate real human exposure time) and continuous (>24 hours)
Results:
- Continuous exposure: robust transmission
- 3-hour exposure: viral RNA in the throat, but below the infection threshold
- Seasonal flu produced lake virus in exhaled air, but pandemic strains were more efficient in transmission, i.e. more transmission per exhaled virus particle
- This shows that transmission efficiency depends not only on the amount of exhaled virus, but also on intrinsic properties of the strain
16. Turgeon et al. (2019) — the three-chamber setup with particle separator19Turgeon N, Hamelin MÈ, Verreault D, et al. Design and validation with influenza A virus of an aerosol transmission chamber for ferrets. Int J Environ Res Public Health. 2019;16(4):609. Full text: https://www.mdpi.com/1660-4601/16/4/609
The setup:
- Three airtight chambers in series — index ferret in cage 1, two naive ferrets in cages 2 and 3
- Air flows from cage 1 → cage 2 → cage 3
- Between cage 2 and 3: a particle separator with adjustable cut-off size (5-8μm aerodynamic diameter)
- Cage 2 receives drops + aerosols; cage 3 receives only aerosols
- Ferrets stayed in the setup for 10-12 days — long-term natural exposure
Results:
- Influenza transmission via aerosols-only (cage 3): 2 out of 3 experiments
- Influenza transmission via aerosols + droplets (cage 2): 3 out of 3 experiments
The inescapable conclusion
The first few studies mentioned speak for themselves.
With serial passage, if it were a static toxin, each passage would greatly dilute it. You should see no more disease after 3-4 passes. It must therefore multiply in a host to regain a pathogenic effect ('viral' aspect).
You even see the reverse of weakening: the contagiousness of the disease becomes stronger, the agent adapts, the same mutations appear in independent experiments, and it develops resistance to antibodies.
The ferret experiments prove robust contamination (via aerosols).
Either way: something is replicating. Something mutates. Something evolves. A disease is transmissible from individual to individual. So again:
"Noem het een virus, een exosoom, een replicon, of een zichzelf vermenigvuldigend pathogeen agens - de naam verandert niets aan de realiteit: besmetting van een ziek naar een (vatbaar) gezond individu bestaat, is experimenteel reproduceerbaar, en de discussie over hoe we het moeten noemen leidt alleen maar af van de pandemie-handling: hoe kunnen we besmettingen voorkomen, matigen en behandelen."
Again: it's the aerosols
The public health implications are far-reaching, especially as current recommended measures to limit the spread of COVID-19 focus on social distancing, wearing face masks when around others and washing hands. As for aerosol transmission, measures such as physical distancing of one and a half meters indoors does not helpone false sense of security give and lead to exposure and outbreaks. Given the current rise in cases, clear guidance on control measures against SARS-CoV-2 aerosols is essential to help contain the COVID-19 pandemic…
The public health implications are broad, especially as current best practices for limiting the spread of COVID-19 center on social distancing, wearing of face-coverings while in proximity to others and hand-washing. For aerosol-based transmission, measures such asphysical distancingby 6 feet wouldnot be helpful in an indoorsetting,provide a false-sense of securityand lead toexposuresandoutbreaks. With the current surges of cases, to help stem the COVID-19 pandemic, clear guidance on control measures against SARS-CoV-2 aerosols are needed
International Journal of Infectious Diseases, November 202020IJID,November 2020:-Viable SARS-CoV-2 in the air of a hospital room with COVID-19 patients
The cover-up committee sits there and stares impassively when the one and a half meter rule is discussed. The drip dogma has brought an incredible amount of misery.
The dogma that infections of respiratory diseases occur via droplets and/or fomites creates more room for research in which an error - such as a lab accident - can have epidemic consequences. Thanks to the drip dogma, this danger is not recognized and experiments become easier and cheaper to carry out.
The basic assumption for any infectious respiratory disease should be that transmission occurs through the air unless proven otherwise. However uncomfortable that may be for virologists and pharmaceutical companies.

Footnotes
- 1November 2020 article: Hard evidence of infectious aerosols
- 2Dick EC, Jennings LC, Mink KA, Wartgow CD, Inhorn SL. Aerosol transmission of rhinovirus colds. J Infect Dis. 1987;156(3):442-448. PubMed:
https://pubmed.ncbi.nlm.nih.gov/3039011/JSTOR (full text):https://www.jstor.org/stable/30134751 - 3Playing poker with infections https://virusvaria.nl/pokeren-met-besmettingen/
- 4Killingley B, Enstone JE, Greatorex J, et al. Use of a human influenza challenge model to assess person-to-person transmission: proof-of-concept study. J Infect Dis. 2012;205(1):35-43. PubMed:
https://pubmed.ncbi.nlm.nih.gov/22131338/DOI:https://doi.org/10.1093/infdis/jir701 - 5Nguyen-Van-Tam JS, Killingley B, Enstone J, et al. Minimal transmission in an influenza A (H3N2) human challenge-transmission model within a controlled exposure environment. PLOS Pathog. 2020;16(7):e1008704. Full text (open access):
https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1008704DOI:https://doi.org/10.1371/journal.ppat.1008704 - 6Coleman KK, Bischoff W, Tellier R, et al. Evaluating modes of influenza transmission (EMIT-2): Insights from lack of transmission in a controlled transmission trial with naturally infected donors. PLOS Pathog. 2026;22(1):e1013153.
https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1013153 - 7Nature, februari 2019 https://www.nature.com/articles/s41598-019-38808-z
- 8Dynamic adaptation mutations and pathogenic characterization of a mouse-adapted seasonal human H3N2 influenza virus. Virol J. 2025.
Full text:https://virologyj.biomedcentral.com/articles/10.1186/s12985-025-02793-9 - 9Synergistic PA and HA mutations confer mouse adaptation of a contemporary A/H3N2 influenza virus. Sci Rep. 2019;9:16616. Full text:
https://www.nature.com/articles/s41598-019-51877-4DOI:https://doi.org/10.1038/s41598-019-51877-4 - 10Ping J, Keleta L, Forbes NE, et al. Genomic and protein structural maps of adaptive evolution of human influenza A virus to increased virulence in the mouse. PLOS One. 2011;6(6):e21740. Full text:
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0021740 - 11IFITM3 deficiency drives SARS-CoV-2 adaptation while preserving variant-specific traits. Nat Commun. 2026. Full text:
https://www.nature.com/articles/s41467-026-68485-2 - 12SARS-CoV-2 rapidly evolves lineage-specific phenotypic changes during serial passage in hACE2 transgenic mice. Commun Biol. 2024;7:248. Full text:
https://www.nature.com/articles/s42003-024-05878-3 - 13SARS-CoV-2 mouse adaptation selects virulence mutations that cause TNF-driven age-dependent severe disease with human correlates. PNAS. 2023. PubMed:
https://pubmed.ncbi.nlm.nih.gov/37523564/ - 14Emergence and spread of SARS-CoV-2 variants from farmed mink to humans and back during the epidemic in Denmark, June-November 2020. PLOS Pathog. 2024;20(7):e1012039. Full text:
https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1012039 - 15Eisfeld AJ, Biswas A, Guan L, et al. Pathogenicity and transmissibility of bovine H5N1 influenza virus. Nature. 2024.
https://www.nature.com/articles/s41586-024-07766-6 - 16Transmission route of rhinovirus — the causative agent for common cold. A systematic review. Am J Infect Control. 2023;51(4):438-445.
https://www.ajicjournal.org/article/S0196-6553(22)00866-5/fulltext - 17Zhou J, Wei J, Choy KT, et al. Defining the sizes of airborne particles that mediate influenza transmission in ferrets. PNAS. 2018;115(10):E2386-E2392. PubMed:
https://pubmed.ncbi.nlm.nih.gov/29463703/Full text:https://www.pnas.org/doi/10.1073/pnas.1716771115 - 18Kutter JS, Spronken MI, Fraaij PL, Fouchier RA, Herfst S. Exhaled aerosol transmission of pandemic and seasonal H1N1 influenza viruses in the ferret. PLOS One. 2012;7(4):e33118. Full text:
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0033118 - 19Turgeon N, Hamelin MÈ, Verreault D, et al. Design and validation with influenza A virus of an aerosol transmission chamber for ferrets. Int J Environ Res Public Health. 2019;16(4):609. Full text:
https://www.mdpi.com/1660-4601/16/4/609 - 20IJID,November 2020:-Viable SARS-CoV-2 in the air of a hospital room with COVID-19 patients
10 kleine druppels hebben een hogere besmettelijke load dan 1 grote druppel met hetzelfde totale volume omdat de load niet IN maar OP de druppel zit.
Kleine druppels raken dieper in de longen.
Een grote druppel die wel blijft zweven en deels verdampt word een kleine druppel met meer virale load dan een fijne druppel die als fijne druppel ontstaan is.
Hoe kun je nou niet in het bestaan van virussen geloven als virologen en celbiologen in labs, zoals in Wuhan, er in kunnen knutselen, ze meer of minder via mensen overdraagbaar kunnen maken, en ze precies kunnen aangeven welke rijtjes aminozuren/nucleotiden in genomen e.d. bepaalde eigenschappen representeren? Er is ook nog veel onbekend, bijvoorbeeld hoe de eerste ooit is ontstaan. Maar dat ze niet bestaan?
Misschien vinden sommigen mijn kritische beschouwing hier over de PEC ook nog leuk….
Margrite Kalverboer, kinderombudsman, 24 juni 2026
Ik ben kennelijk een “Über-Wappie”.
Ik kan het positieve oordeel over Margrite Kalverboer namelijk absoluut niet delen. Ik zal mijn kritische beschouwing puntsgewijs weergeven.
1. Ze voert absoluut een gepassioneerd, maar zeker voor een hoogleraar, veel te emotioneel, betoog over de belangen van kinderen. En bevestigt dat kinderen zeker geen prioriteit hadden; noch bij het Kabinet, noch bij de tweede Kamer, noch in de media. Noch bij de adviseurs zoals OMT, PO/VO-raad, RIVM etc. etc.
En je voelt haar machteloze woede, dat ze eigenlijk nergens wat in de melk te brokkelen heeft en geen echte toegang heeft tot “de macht”.
2. Vervolgens blijkt haar betoog geheel gebaseerd te zijn casuïstiek; weliswaar ca. 2.000 per jaar, maar nog steeds casuïstiek. Op de (herhaalde) vraag over cijfers, c.q. extrapolatie en/of generalisatie c.q. impact naar de hele Nederlandse bevolking geeft ze totaal niet thuis. Van een hoogleraar mag je toch echt wat anders verwachten….
3. Niettemin had het gesprek meerwaarde, maar anders dan wat Marianne en Maurice betoogden:
a. ze legde duidelijk bloot dat de meeste kinderen eigenlijk helemaal niet zo veel last hadden van de lockdown; integendeel: ze kregen eindelijk aandacht van papa en mama.
b. ze maakte wel duidelijk dat kwetsbare kinderen uit “lelijke milieus” met geweld e.d. wel echt heel veel slechter af waren; dat zijn er volgens haar schatting ca. 100.000. Dat is natuurlijk zeer ernstig.
c. ze maakte duidelijk dat het “praktisch onderwijs” (MBO) zeer zwaar was getroffen.
d. ze maakte ook duidelijk dat niet eens de cognitieve achterstand, maar vooral de sociaal-emotionele ontwikkeling van de middelbare scholieren een enorme knauw/achterstand had gekregen.
e. het meest interessante en relevante was wellicht dat bij het afschalen van zorg, kinderen en ouders meldden dat ze beter af waren! Weer een indicatie van het failliet van de jeugdzorg. Alleen de afschaling van de GGZ jeugdzorg was wel heel problematisch
4. Met haar betoog ondergraafde ze in feite zelf voor een groot deel de urgentie van “nooit meer lockdown” voor kinderen. Haar betoog impliceert dat je alleen voor enkele categorieën nooit een lockdown moet afkondigen.
5. Ze zag het hele vaccinatie gebeuren als “gewoon”. Geen verwijten over, of vraagtekens bij kinderen die gedwongen/gedrongen werden tot vaccinaties, terwijl ze een praktisch 0-risico liepen voor gevolgen van Corona.
Paul Rosenmoller, voorzitter VO-raad, 24 juni 2026
Het oordeel over deze man van Marianne en Maurice kan ik volgen. Een zeer welbespraakte ex-politicus die zich overal handig uit redde, m.u.v. enkele passage waar hij duidelijk aarzelde (en ik vermoed gewoon niet de waarheid vertelde [of hij {nog meer} contact had gehad met ministers en tweede kamer leden].
Zijn uitspraak dat de sluiting op 15 maart 2020 “onhoudbaar” was, getuigt van zeer slappe knieën. Als hij later vertelt dat als je het goed uitlegt, je mensen best mee krijgt, staat daar haaks op. Het feit dat de FMS intervenieerde over het OMT-standpunt heen, waardoor ook de vakbonden de angst onder leraren als argument hanteerden, had zeker door Rosenmoller gepareerd moeten worden als hij het belang van kinderen zo hoog acht(te). Desnoods door OMT en FSM in één hok te zetten. Zeker omdat FMS later ook nog excuses heeft aangeboden, had dat soelaas geboden.
Zijn uitspraken, met de kennis van nu, over “nooit meer scholen” sluiten getuigt ook van inconsistentie. De mega-schade was echt al in mei/juni 2020 bekend. Toch ging hij met de volgende 2 sluitingen tamelijk geruisloos akkoord! Hij had, i.t.t. Kalverboer, wel makkelijk toegang tot alle media en politici [hij appte zelfs Rutte en De Jonge]. En hij beschikt(e) over een ijzersterke en scherpe retoriek Maar hij deed het niet. Verschool zich achter Arie Slob, minister voor onderwijs en achter de “eenzijdige virologische en medische wetenschappers”.
Ook zijn uitspraken over 1,5 meter en vaccinaties getuigen dat hij nog steeds niet door heeft hoe ongehoord onwetenschappelijk de totale aanpak van het Corona-beleid was. terwijl hij zich herhaaldelijk achter “de wetenschap” verschool.
En de commissie liet hem herhaaldelijk met dit soort inconsistenties wegkomen.