Please, find below my rebuttal to Mikolaj Raszek’s latest video (Jan 16th, 2024): Vagus nerve thrills: 4 exciting insights including challenging Dr. Geert v Bossche pandemic outcomes (youtube.com)
We have been wrong in thinking that the immune system has a role to play in determining whether or not a person develops symptoms upon exposure to SARS-CoV-2 (SC-2) or its descendants. The occurrence of symptomatic infection exclusively depends on the interaction between the spike (S) protein of the circulating SC-2 lineage and the acetylcholine receptors of the vagus nerve. Since SC-2 can infect the vagus nerve, and considering its innervating branches in various organs, including the lower respiratory tract, circulating SC-2 (sub)lineages binding to the vagus nerve's acetylcholine receptors could readily trigger Covid-19 symptoms whereas lineages unable to do so, such as Omicron and its derivatives, could not. That is at least what Mikolaj Raszek (M.R.) believes. With the current evolutionary trajectory of the virus exclusively spawning Omicron descendants, he anticipates, or at least hopes, that this marks the beginning of the end of the C-19 pandemic!
If I understand M.R. correctly, it doesn't really matter whether you have developed natural immunity or have been vaccinated against C-19 as far as the clinical outcome of SC-2 infection is concerned. If you extend that line of reasoning, one could even conclude that depleting antibodies in subjects, whether immunologically naive or not, prior to (re-)exposure would not change the outcome of a challenge experiment using Omicron or a descendant thereof, i.e., no harm would be inflicted. I am not sure if M.R. has been asking himself the question of how a highly infectious virus known to destroy living host cells upon infection can be prevented from provoking disease other than by a functional immune system..... unless the host cells are not receptive to the virus, but that's definitely not the case with SC-2.
M.R. continues his plea, arguing that the succession of different circulating SC-2 variants results from their introduction into the human population through an external source, which could either be the lab (!) or an animal reservoir. Hence, we should be thankful for the introduction of Omicron into the human population. This variant is currently propagating efficiently and is antigenically so distant from the previously circulating SC-2 lineages that there is no way to revert to the pre-Omicron situation! As M.R. is focusing solely on C-19 symptoms, Omicron has, in alignment with the WHO's stance, effectively concluded the acute phase of this pandemic. Consequently, he is filled with excitement, anticipating that the descendants of Omicron will soon bring an end to the C-19 pandemic.
I can only conclude that M.R. doesn't appear to keep himself updated on the current evolution of Omicron's variants and how their biological properties (including such related to disease severity!) are already changing in a less ‘exciting’ direction. It seems he doesn't read peer-reviewed publications that report data clearly illustrating that immune pressure in highly C-19 vaccinated populations is shaping the evolutionary trajectory and dynamics of SC-2 and ‘that the global pandemic indeed has greatly promoted the efficiencyof the virus to evolve immune escape mutations’ (https://www.nature.com/articles/s41586-022-05644-7; https://pubmed.ncbi.nlm.nih.gov/37169744/).
How does he reconcile his new insights with his previous video, in which he entirely dedicated his excitement to scientists confirming that immune responses in highly C-19 vaccinated populations (e.g., induced by serial vaccinations or vaccine breakthrough infections) can trigger immune refocusing to novel S-associated epitopes? Wouldn't this indicate that the targeted epitopes and, consequently, the evolutionary trajectory of the virus are largely determined by the host immune response? Thus, mutations could accumulate rapidly, even in the Omicron clan. For instance, the Omicron BA.2.86 variant quickly incorporated over 30 mutations in the S protein alone, compared to the original Omicron BA.1 version. Claiming that gain-of-function experiments, coupled with lab leaks or spectacular jumps from animal reservoirs, can explain all of this is an insult to science, as such postulates completely ignore the dynamics of pathogen-host immune interactions.
To bring M.R. back down to earth, I sent him my most recent article:
https://www.trialsitenews.com/a/immunocompromised-patients-are-not-a-potential-breeding-ground-for-highly-mutated-sars-cov-2-variants-e81b1c11. I can only hope it will make him think twice about disregarding the immune system when predicting the outcome of complex interactions between the pathogen and the host.
Lastly, I haven't delved into the likely involvement of the vagus nerve in long Covid. However, it seems to me that the symptomatology of long Covid is more complex than simply resulting from interactions of the S protein with acetylcholine receptors on the vagus nerve. I tend to believe that the vagus nerve may be involved through other, potentially additional, pathways, for example such that rely on autoreactivity towards myelin basic protein—a component of the myelin sheet surrounding nerves. It is well known and documented that chronicity or prolonged viral infection can lead to neurological disorders, even causing multiple sclerosis in certain cases of chronic or prolonged viral infection (https://pubmed.ncbi.nlm.nih.gov/9759852/; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7133435/; https://pubmed.ncbi.nlm.nih.gov/7691962/; https://pubmed.ncbi.nlm.nih.gov/10352259/).
I am always open to criticism, alternative viewpoints, and new insights, but I am never super-excited about overlooking the essential role of the immune system when it comes to studying pathogen-host interactions. What I would be excited about is M.R. going back to the drawing board of the pandemic and revisiting the fundamentals of these interactions.
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.