It looks like this VUI – 202012/01 has several spike protein mutations, but atm it isn't known to evade the current vaccines. If you want to pour gas on your freak out fire, he's a Japanese preprint that suggests that antibodies from previous infection can enhance severity. Take it with a grain of salt, though. Personally, I wouldn't be surprised if the UK variant evades the vaccine. These single-strand RNA viruses are known for antigenic drift, and as am_Unition says, with the sheer numbers of people harboring the virus, and the opportunity to select for reinfections, well... BTW, found this while searching: https://systembio.com/shop/ppack-spike-n501y-sars-cov-2-s-pseudotype-n501y-mutant-lentivector-packaging-mix/
I'm not going to worry about it until some data exists. It all seems so speculative right now. Even in that preprint, a small minority of antibodies seem to enhance the binding. Maybe that explains why some small subset of people are vulnerable to reinfection while most people appear to have robust immunity. Anyway it won't matter once a sufficiently large number of people are vaccinated or recovered, because those vulnerable people shouldn't encounter the virus anymore. Personally, I think that the vaccine trials missed a really good opportunity in their trials. I think they should have been 3 arm trials where you have placebo, 2 doses, and 1 dose followed by a placebo. Would have been really instructive to learn how much immunity a single dose gives. If it's, say, 60%, then it's probably far better mathematically to give twice as many people a single dose than half the people the 95% immunity that a double dose confers. After all, we don't have to worry about mutations if the virus is defeated before a potentially catastrophic one arises (if it hasn't already). Not sure how or why that decision was made, but I guess when thigs are done hastily, it's easy to be a Monday morning quarterback. As an aside, antigenic drift probably wouldn't destroy the effectiveness of the vaccine, but rather reduce it marginally, because the domain that the vaccine are produced against is too important to the virus to change that radically. The Ab's that are produced by the vaccine will be effective to a certain extent. (And anyway there's even evidence that a recent dose of MMR vaccine reduces severe disease just by ramping up innate immunity.) So even if we can't achieve 95% immunity, it's still worth taking as soon as possible. This isn't a doom scenario, as far as I can tell.
Yeah. We'll just have to wait and see. Even so, if it's a 10% chance that the vaccine doesn't protect against this strain, that's a 10% chance of a global bummer. Global bummers ought to be like 0.01%. They don't call me depressing preprint guy for nothing. This one hot off the presses from Harvard and University of Pittsburg.Since coronaviruses have alower substitution rate than other RNA viruses this gave hope that spike glycoprotein is an antigenically stable vaccine target. However, we describe an evolutionary pattern of recurrent deletions at four antigenic sites in the spike glycoprotein. Deletions abolish binding of a reported neutralizing antibody. Circulating SARS-CoV-2 variants are continually exploring genetic and antigenic space via deletion in individual patients and at global scales. In viruses where substitutions are relatively infrequent, deletions represent a mechanism to drive rapid evolution, potentially promoting antigenic drift.
But be careful how you read things. Escaping a mAb treatment isn't the same as escaping a vaccine. Your body doesn't produce mAb's. It produces a mutifactorial response that involves IgM and IgG, probably with Ab's against multiple epitopes for any given antigen. Escaping a lab-made mAb presents a much lower bar than adaptive immunity. Again, you may not be wrong, but there are a lot of reasons not to despair.
Just trying to read what's out there, and there isn't much. It's difficult to say if Boris Johnson was a moron or a pragmatist by saying what the worst case scenario is (70% more infective). It turns out that that number isn't based on experimental data, but rather pure modeling. The scientist who helped derive the model says herself in that article that there's no data on whether the heightened transmissibility is entirely due to human behavior. Apparently, the same mutation has been seen in up to 90% of South African samples for some time now, so it isn't exactly novel.