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Interviewer: Professor Klenerman, thank you for taking the time
today to do this newest update to what is
currently known in the immune system response to the SARS-CoV-2 virus.
What are some of the main changes which have
occurred since your last interview in December?
Prof. Klenerman: I think when we last talked
the spectre of the Kent variant was just emerging, and the vaccines were just licensed.
Since that time it's changed quite substantially, in terms of our understanding of
the significance of those variants and the deployment of the vaccines.
If I start with the variant,
when it first emerged it was clear there was a cluster in Kent of
a variant which was genetically distinct, and spreading apparently quite fast.
Indeed, as was predicted at the time,
it did spread substantially.
There was (of course), pre-Christmas,
an enormous amount of spread in the community anyway,
but the variant does appear to have some kind of advantage.
In terms of the biology and the immunology,
the impact of the individual mutations in the spike are a bit clearer now.
The virus is making mutations in that spike protein which do a couple of things.
One is to improve its ability to bind its receptor, which is ACE2.
In doing so, because that region of the spike is also a target for antibodies,
it can also evade a fraction of the antibody response.
It's not a very sharp peak so
that one mutation would knock out all the antibody responses, it's more of a surface.
That is evident when you look at