It's fair to say that the vaccine is less effective against Delta than previous strains. So why? If it's not antibody attenuation then reduced affinity seems a likely explanation.
I don't understand why this would be a tough mystery to crack. I'd think antibody levels would be awfully easy to measure, and there'd be no shortage of volunteers for a study, but whatever.
Does the vax target solely the s2 membrane binding protein subunit? If they chose a hyperspecific portion, and that turns out to be mutable, reduced antibody affinity wouldn't be that surprising.
It's complicated and I haven't put in the time to understand. Still, in light of Delta, I'm questioning whether mutable region targeting was the way to go.
Reduced antibody levels and poor binding are both pathways for ADE, and I've yet to hear how we're not playing with fire. The best explanation I've yet heard is that although it's a possibility, refusing a solution to an existing threat on the basis of a speulative one is wrongheaded. Confess I remained unconvinced by that reasoning since the existing solution looks increasingly lame and the possibility of ADE seems not unlikely.
I think the vaccine's benefit against Delta, which I believe in, is the tail end of the vax honeymoon phase. Imo boosters will have to be tuned for variants. This shit is going to go on and on.
