It's unlikely to _completely_ escape immunity - humans will raise antibodies against different regions of the spike protein, but it does seem to confer a pretty significant average resistance to patient sera. There's another study looking specifically at several different monoclonal antibodies against this mutation at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7723407/
No idea why the downvotes here (at initial time of writing), that’s literally how the immune system functions, it’s a random process and everybody’s antibody DNA will be different to someone else’s antibody sequence against the same antigen.
No vaccine is training the body on the exact antibody to raise, it’s training it to (hopefully, because sometimes the stochastic process missed) recognise particular epitopes.
Important to also note that generally (and particularly during early infection) there will be many antibodies that recognise parts of an antigen.
Affinity Maturation through somatic hypermutation is one of the most amazing processes the body does - look it up or for a very brief summary look at my notes on page 32 (or the whole mechanism of adaptive immunity from 27) with a little diagram on page 28
It truly is. In early medschool we had a group student session on the adaptive immune system where we had to brainstorm on antibody generation and nobody in the group even came up with an idea remotely close to how it actually works. Robust and amazing. Talk about brute-force searching.
Still, at this day my hope is that we'll be able to do the body's work even better at some point using computer designed antibodies (or similar) at least for therapies. There are some notable bottlenecks in the adaptive system where antigen fragments have to be broken down and shown to potential antibodies and this is a bit different between humans etc. The human antibody molecule is also very large and it's particular design doesn't fit some epitopes you'd want to hit (not an expert on it but I remember one of the HIV proteins having an area you'd want to train on but that can't accommodate the antibody variable fragments well).
When you say average here, is that in the sense of average resistance over time for a given patient or average resistance across a population? The paper seemed to imply a great deal of heterogeneity in individual responses to the variant, so significant average would just be something like part of the population affected very badly, another part not at all, vs everyone affected mildly?
Averaged over a population - some people will have resistant sera and others not depending on the parts of sars-cov-2 targeted by their polyvalent antibody response. Note that this is only looking at antibodies, not T-cell responses... so the clinical consequences are harder to predict, but it's certainly a bit concerning.
