Seeing that B1.1.7 now acquired the E484K mutation in the UK, could we, at least for now, stop the narrative that this double mutation occurs by high immune pressure, please?
because I'd assume you have a seroprevalence of <20% (???)

2 Thoughts: https://twitter.com/_b_meyer/status/1356342110115475466

you DO have 2 effects that are at play here:
1) affinity to the Ace2 entry receptor. This seems to be regulated by mutations in the RBD. it seems to make the virus (at least partially) more transmissible. It would appear that N501Y is followed by E484K & they act synergistically

yes, fully agreed both mutations cause a certain level of resistance to neutralising antibodies. However, currently I do see this almost as a byproduct of the mutation as you simply change the footprint, surface electrostatics and overall twist the protein slightly. I would

describe the receptor affinity, which might be accompanied by higher transmissibility, as the main reason and dominant cause of the RBD mutations.
2) Then we have a mutation hotspot in a 2nd part of the protein, the NTD. There mutations, which include small deletions or

point mutations in close proximity to the signal peptide seem to be more directly involved in immune escape and affect the folding of the protein, which overall affect antibody binding to more classes of antibodies.
Together, I do think we do see a more functional change

change to the spike protein, that helps it to bind and transmit better.
As quick afterthought, the N501Y mutation was also seen in mink as it increased mink-Ace2 binding there as well. I suspect a potential immune pressure there would differ, assuming different mutations to form

And one last point why I don't think antibody pressure is the main driver here: in the lab one can readily generate the N501Y/E484K double mutation. The selection for this occurs without immune or antibody pressure being present.
/fin