Regarding ADE and SARS-CoV-2 IMO;
1) ADE is historically a major risk for coronavirus vax development
2) Clear ADE signal has not been previously detected with the genetic SARS-CoV-2 vax to date
3) highest risk for ADE occurs during waning phase of vax immune responses
4) The reports of equivalent (or perhaps higher in vax recip?) levels of virus in vaccinated and unvaccinated is odd.
5) Viral infection/replication is necessary but not sufficient for disease – disease is the patient hyperinflamm response
6) The clinical trials were not designed to detect ADE, despite it being a major risk for corona vax development
7) FDA specifically acknowledged that ADE was a risk, and suggested focused trials were warranted – but did not require them.
8) I find no trials to rule in/out ADE
For some reason, junior academics feel the need to act like Trolls rather than discuss hypotheses and ideas. I see this all the time as a NIH study section member or charperson. I think that this is partially a consequence of the pyramid system that they are subjected to.
And finally, ADE has many mechanisms. The easiest to explain and understand is facilitation of monocyte infection. So that is the example I use. The mechanism of ADE observed in prior coronavirus vax efforts is not very clear.