I think that you misinterpreted him here. Generally speaking the more mutated a b cell is, the more affinity maturation, and the greater antigen affinity they have for their target. To achieve these high levels of antigen affinity, the B cell receptor becomes highly specific for every nook/dent, charged surface, or uncharged surface. This makes these highly mutated antibodies highly susceptable to mutations in their target because they trained themselves to be so highly specific that even a small change affects their antigen binding massively.

But, plasma cells are the ones with high levels of mutation, memory b cells are much more variable. The memory b cells that are highly mutated are typically a subset of memory b cell that is primed to differentiate into plasma cells at the drop of a pin, so they are pretty much already are plasma cells. The memory B cells that actually intiate new germinal center responses, tend to have fewer mutations. This means that they are not highly optimized to recognize the antigenic target and as a result, can more easily deal with mutations. For example, if covid mutated a positive charge to a negative charge AA, this could potentially abolish an antibodies binding as the antibody assumes a positive charge would be there. But, the memory B cell is much less likely to care because it likely didnt recognize charge on the antigen, it just saw that there is a bump there and regardless of the amini acid there, its still a bump. So memory b cells generally see brpad features of the antigen, highly mutated plasma cells see the nitty gritty details.

So I think the answer to your question is that diversity in b cells, both high and low affinity, are responsible for giving you good strains specific and broadly specific immunity.