If you were to ask me based on the knowledge I currently have, what I think is really happening, it’s as following: People move towards an IgG4 antibody response against SARS-COV-2, as their body’s response becomes IgG dominated after the first two vaccines. With IgA and IgM taking an abnormal backseat and IgG being forced to fight the virus on its own, inflammation becomes severe and antigen exposure becomes chronic, so that isotype class switching begins towards IgG4.
Once IgG4 emerges, it triggers a positive feedback loop whereby over time IgG4 becomes the dominant antibody response, as illustrated in the link above. It seems to me, that vast droves of people are in the process of having their immune response tipped towards an IgG4 tolerance response.
If people are then eventually reinfected, the antibody response is effectively entirely IgG4 dominated, which doesn’t trigger inflammation and so the infection becomes effectively silent, you don’t really notice common cold-like symptoms. IgG4, as an anti-inflammatory antibody that doesn’t activate complement and poorly binds to the Fcr receptor fails to bring the viral load down to zero. The virus eventually damages the cardiovascular system, resulting in a sudden unexpected death.
You would prevent this, with a strong IgM antibody response. When IgM class switches, it first switches to IgG3. IgG3 then switches to IgG1 and 2. Finally, these switch to IgG4. If you immediately start out without IgM and IgA dominating the immune response, you end up at IgG4 more rapidly. This of course would be especially the case in the context of chronic antigen stimulation, that is, the unprecedented mRNA/adenovirus experiment. Instead of injecting dead virus material (temporary antigen stimulation), we’re reprogramming cells to keep producing viral material (chronic antigen stimulation).
