Probably not. B cells can return to germinal centers and undergo further affinity maturation.
Hoskins effect does not block this process, but may slow it down. If the original antibody is still effective, no problem.
Now, if the virus mutates to completely escape existing antibodies, we might have a different story. But in that story, the vaccinated are probably better off than the natural infection crowd.
The vaccine targets a highly conserved region of the RBD; it is largely essential to bind to ACE2. Mutation there is likely to reduce binding affinity and thus become less infectious / virulent.
Natural immunity however suffers from the problem that the body builds antibodies against other regions that are more prone to mutation. Some of those mutations have been shown to enhance infectiousness. So you could end up with a scenario where non RBD targeted antibodies enhance infectiousness while simultaneously you have slowed affinity maturation.
Hoskins effect does not block this process, but may slow it down. If the original antibody is still effective, no problem.
Now, if the virus mutates to completely escape existing antibodies, we might have a different story. But in that story, the vaccinated are probably better off than the natural infection crowd.
The vaccine targets a highly conserved region of the RBD; it is largely essential to bind to ACE2. Mutation there is likely to reduce binding affinity and thus become less infectious / virulent.
Natural immunity however suffers from the problem that the body builds antibodies against other regions that are more prone to mutation. Some of those mutations have been shown to enhance infectiousness. So you could end up with a scenario where non RBD targeted antibodies enhance infectiousness while simultaneously you have slowed affinity maturation.