Thread by @ewanbirney

New SARS_CoV_2 virus strain update. TL;DR - there is something to understand more, and it looks like the virus has tweaked its biology at least on transmissibility; Public health, scientists + surveillance systems are on it.

(Context: I am expert on human genetics/genomics + computational biology; I know experts in viral evolution - including @arambaut, @Nick_Goldman, @firefoxx66 and @EvolveDotZoo , and testing @The_Soup_Dragon + sequencing @jcbarret)

What do we know? Like all viruses SARS_CoV_2 changes - like typos in a manuscript that is endlessly retyped - and in fact this virus has a pretty pedestrian rate of typos. One version ("variant" or "strain") found in the south east England has a number of interesting properties

1. It has, at some time in relatively recent past, accumulated many more changes (typos). This means something in its history is interesting but also that it potentially has fallen "further from the tree" in terms of potential to change biology

2. It is growing in frequency, but as important than growing in frequency, which might be the "by chance" growth for other reasons like some regional quirk in restrictions, it looks like it is displacing other lineages.

(Editorial - it is super tricky to sort out "growth for other reasons" vs "growth due to inherent properties of the virus"
- in particular in real world data - this is called phylodynamics and phylogeography. Tune into @arambaut and @EvolveDotZoo here)

3. One of the changes interact with the testing system in some tests - to stress, in a way that is pretty well understood, and has been seen elsewhere. Mainly this means we can see this strain's growth in close to real time.

(Another editorial; SARS_CoV_2 is being so intensively studied and tracked that this "recurrent but real" mutation property now is present a fair bit; it gives the classic phylogeneticists like @Nick_Goldman plenty to think about)

Despite the complexity of working out if growth is just being "the right virus strain at the right time" vs "actually about the virus" the people I trust most on this (@arambaut and colleagues) think it is the case.

What don't we know yet?

We don't (yet) know if this change in biology changes other aspects, in particular disease progression. Given the numbers in the South East and that at some level hospitalisation rates are not massively above or below the case reports it can't be huge differences ...but...

It certainly could be quite different in a host of details and could have different impact from how it transmits (eg, age ranges) or aspects of the clinical progression of disease. Clinical researchers will have to look v. carefully at this

The other big question is whether this will be different for the vaccines. It's worth stressing this one of thousands of variants of the virus; it has more changes, but overall the changes are small.

The fact that all 3 successful vaccines are against mixtures of many different strains and they have high efficacy rates is a reassuring point to start; but it deserves more attention and looking at beyond this broad statement.

It's also worth stressing that although the "business" of the immune system are B-cell antibody production - sort of guided missiles that latch onto viruses, prevent viral action and trigger engulfing by macrophage (pac-man like immune cells) there are also T-cells.

T-cells come in two types. One is a sort of "public health of cells" check which regularly knocks on the doors of cells, check there is nothing dodgy in them; if they find anything dodgy they hit the "please commit suicide button" of the cell. The other is a command-and-control>>

<<these T-cells knock on the door of B-cells and effectively say "please show me what you've caught using your antibodies" using a similar mechanism to the "public health" T-cells, but if they find anything rather than hitting the "please commit suicide" button they hit >>

<< "permission granted to replicate like crazy and get those b*stards". The good thing about T-cell immunity is in both cases they work off *fragments* of viral proteins, not the entire thing. As such any one mutation can at most impact one fragment.

When we assay immune response it is easier to assay the B-cell response (the antibodies - presence of these guided missiles) but in fact the T-cell response is just as important (both arms), and less "sensitive" to the precise overall configuration of the virus.

(Yup - the mammalian immune system is super-smart and real one of the jewels of mammalian evolution).

So - there are good, principled reasons to think that the vaccines - that stimulate both B and T cell immunity - will give us protection to a variety of strains, this one included. But ... we should definitely check!

In terms of NPIs ("Teir Restrictions + TTI") this means the English - but likely most - governments will have to up their game - more NPIs and more efficient TTI needed to reduce transmission. Such ... is this reality.

(Editorial: the UK's surveillance system in particular @CovidGenomicsUK but also the broad testing is good and linked - so this can be seen and tracked across England and all 4 nations. Broadly many other European countries have good surveillance but it will need to be good>>

<<with the sheer number of cases worldwide, I suspect this is not the first shift to higher transmissibility - rather it is the first we've clearly detected - of course super, super hard to tell.)

This story is going to move fast I suspect over this week - I would stay tuned to @arambaut, @Nick_Goldman @firefoxx66, @EvolveDotZoo, @The_Soup_Dragon and @jcbarret amongst others.