Compiled for your reading convenience from this long Twitter thread:

I’ve been in touch with five U.K. university professors in departments which means they’re knowledgeable about immunology. All of us agree that the variants will not meaningfully alter immune recognition by our bodies of the virus. If you’ve been infected by the Wuhan sequence, you’re immune, not only to this original sequence but to all variants. The reason is that the number of point changes (17 is the most in one variant) is irrelevantly small compared with the size of the entire virus, which is 10,000 amino acids long. The most mutated virus is 99.8% identical to the Wuhan sequence.

It is possible that much smaller changes in spike protein could alter infectiousness. But that’s not what I’m talking about here, which is immune recognition. That’s not going to change overall, because we don’t only recognise the part which has changed, but dozens, perhaps scores of parts of the virus. The vast majority of these parts are unchanged. As a practical example, the original SARS virus from 2003 is around 80% identical to SARS-COV-2. Research has looked at immune recognition of various parts of SARS & found vigorous responses to multiple parts of SARS 17y later. What’s also amazing is that these same people showed strong & unequivocal responses to SARS-COV-2, even though they’d never seen this new virus.

In other words, a virus which is as different as 20% from SARS was easily recognised as already known by an immune system which had memorised common sequences in a earlier virus to which it’d been exposed. The 0.2% difference between the Wuhan sequence & any of the recent variants isn’t any kind of issue for our immune systems. No question, if you choose to focus upon just one (of very many different) antibodies which are raised to the virus, then if the sequence that one type of antibody binds to has changed, that antibody may no longer bind well.

But that’s not what protects you from illness: it’s the multi-locus nature of the immune response that does that. And most of those loci have not changed. Recognising & defending a person against those variants will not be problematic. And this sole focus on the profile of antibodies also completely ignores the panoply of T-cell responses, which are also created against dozens or scores of parts of the virus.

It’s worth noting that variants arise normally by error-prone replication by viruses. It’s how they evolve. Apparently around 40,000 different variants have already been identified, each a tiny amount different from the original sequence. Why we’ve decided to get over excited about a small subset of variants is inexplicable. As argued above, it’s not necessary to “keep foreign mutants out of the county”. In any case, a negative PCR test eliminates people bringing in a copy of the virus (whatever it’s sequence).

It’s a head scratcher why the idea has arisen that it’s necessary to keep out foreign mutants and why what amounts to a brief period of imprisonment is an appropriate method for doing it. More important still, as mentioned already, variants are arising right now, within U.K. Even with reduced daily cases, there’s a lot of replication going on in U.K. & requiring inbound travellers to have a negative test would almost completely eliminate any possibility of importing an irrelevantly tiny number of imports compared with those forming spontaneously in the country anyway. Variants are not only inevitable (& have occurred in great profusion already) but are “way points” as the virus comes into equilibrium with its human host.

As respiratory viruses move through a population, there is selection pressure favouring variants which are more easily transmitted from the person to person (they out compete less transmissible variants). They’re especially favoured if they’ve less harmful to the infected host (because an ill person or a dead person is far worse at spreading the virus). Over time it’s therefore entirely normal & predictable that variants get selected for which are easier to transmit but less dangerous.

That’s how this virus is highly likely to finish up being added to the existing four endemic coronaviruses which are causative agents in around a quarter of common colds. Indeed, it’s probably how those four got to their current status. There are probably other coronaviruses we’ve yet to characterise. SARS-COV-2 mutates very slowly compared with influenza & so it’s highly unlikely that we’d need a new vaccine annually, as we do with ‘flu.

These university professors with deep knowledge of immunology are fearful these days even of talking about basic viral immunology. Apparently they’re concerned they might end up in the bad books of the Wellcome Trust, which is one of the top sources of research funding in U.K. So I’m telling you instead. If you want, you can contort the science such that what you’re being told fits the narrative. But you’ll notice lots of things that are being said simply don’t fit & that’s because the tale they’re telling isn’t true. There’s a pattern. Lots of things that don’t make any sense. Why, I’ve no idea.