Your idealized description does not happen in the real world. The lipid carrier is observed in all organs of the body within 15 minutes of injection. The engineered mRNA uses redundant codons with GC substitutes for the wildcard positions. This causes more aggressive synthesis on the ribosomes. There are two prolines inserted on the engineered spike protein that prevent the geometry snap to cell fusion after attachment to ACE2. The consequence is significantly more antigenic surface exposure. The spike proteins appear in the brain having been generated after the lipid envelope permitted passing the blood-brain barrier. The S1 subunit is easily cleaved and misfolds into a prion. It’s a $#!+ show writ large with millions of victims.
Do you have a source for the 15 min timeframe?
The other thing, which you left out, is that without the modified spike protein entering the cells with the ACE2 receptors, is that those cells in response to the binding with the receptors, release a cascade of inflammatory cytokines; that, and contact of the spike protein with platelets can induce clotting even without whole coof virus present.
Please supply a link to the S1 folding into a prion; IIRC there are certain primary geometrical features which are common with those of prions; I haven’t yet seen a cogent mechanism by which the presence of the cleaved/folded S1 *causes* prions to form from other proteins.