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by edh649 2003 days ago
For those (like me) who are looking for some more details of this new strain, I found 2 papers from the `COVID-19 Genomics Consortium UK (CoG-UK)` of great interest. It seems like the prime reasons for concern are increased frequency of mutations, increased proportion of cases, and possible change in immune response

> Several aspects of this cluster are noteworthy for epidemiological and biological reasons and we report preliminary findings below. In summary: The B.1.1.7 lineage accounts for an increasing proportion of cases in parts of England. The number of B.1.1.7 cases, and the number of regions reporting B.1.1.7 infections, are growing. B.1.1.7 has an unusually large number of genetic changes, particularly in the spike protein. Three of these mutations have potential biological effects that have been described previously to varying extents:

> - Mutation N501Y is one of six key contact residues within the receptor-binding domain (RBD) and has been identified as increasing binding affinity to human and murine ACE2.

> - The spike deletion 69-70del has been described in the context of evasion to the human immune response but has also occurred a number of times in association with other RBD changes.

> - Mutation P681H is immediately adjacent to the furin cleavage site, a known location of biological significance.

> The rapid growth of this lineage indicates the need for enhanced genomic and epidemiological surveillance worldwide and laboratory investigations of antigenicity and infectivity.

https://www.cogconsortium.uk/wp-content/uploads/2020/12/Repo...

https://virological.org/t/preliminary-genomic-characterisati...

4 comments

Anecdotally I know a family where every member tested positive for COVID in the spring with severe symptoms at the time. They recovered, then over thanksgiving they started experiencing very mild symptoms (some none at all, others loss of taste and smell to more typical cold like symptoms), and all tested positive once again.

It might be that after you contracted COVID once, or a particular strain of COVID once, that you have a heightened immune response and less severe symptoms when you do catch the disease again. It is hard to say for sure what is going on from an isolated case, but this certainly doesn't bode well.

>but this certainly doesn't bode well

How doesn't it bode well? If you get one strain of covid, get over it, then catch another strain and your symptoms are much less than the first time due to your body having the proper defenses against covid, then that's your immune system working as intended.

It doesn't bode well that you can get it twice to begin with.
Is it impossible to get a cold twice in one season? If so, why is catching covid twice a bad thing, especially if the second time is a lot milder than the first time, even for people who experience mild symptoms the first time?
Do you not understand that this means you can spread it twice?
Seemingly not at same rate tho. I guess some specialist can explain it better, but afaik there are some viruses and vaccines where you can spread and some you don’t.

For covid there’s no data yet, but my hunch says it reduces spread only slightly.

It doesn't bode well for people who have lung scarring and neurological damage.
Does anyone have insight on how much / specific changes in the spike protein would be needed to render the mRNA vaccines - which to my understanding create only those spikes - would be render less effective or not effective?

Is that a concern here?

Page 8 of https://www.cogconsortium.uk/wp-content/uploads/2020/12/Repo... hints towards this.

The short answer is that 'The extent to which SARS-CoV-2 may evolve to escape immunity induced by infection or vaccination is not currently known'. However analysis has been carried out to work out how far from the receptor-binding site the mutations are, and how 'antibody-accessible' these are, with a few such as . No conclusions are drawn from this analysis.

Earlier on in the report (towards the end of page 1), this statement is given `One of these (the N501Y mutation) occurs in the region of the Spike protein, the receptor binding domain (RBD), that the virus uses to bind to the human ACE2 receptor. Changes in this region of the Spike protein can result in the virus changing its ACE2 binding specificity and alter antibody recognition`.

Saying all this, vaccines are designed to create a range of antibody responses, in order to stop this very fear of a single mutation rendering a whole vaccine useless. [https://www.nature.com/articles/d41586-020-02544-6] I also recall reading somewhere that adapting the vaccine to account for a mutation (much like is done yearly with the flue vaccine) is relatively easy, though I haven't managed to find that article again yet.

Thanks for all this detail.

That's my laymen's guess at the end - even if spike changes too much we can just fire up a new yearly vaccine, maybe bundle with the flu.

Wasn’t Moderna’s vaccine started in January - like a few days after first genome sequence was published...
Thank you, that's a nice detailed read, but still relatively readable by a non-bio person like myself.
I've read that COVID-19 can sometimes be found inside the body even after testing negative for some time. This being a reason for continued weakness and impairment after infection.

Could this possibly continued infection lead to faster mutation, or is the amount of people infected the cause for the rapid mutations, or something else?

It's suspected that this mutation arose from a single patient who had a long case of COVID-19. Here's an interesting pre-print study on an individual (not the one from this mutation) who harboured many mutations over a 101-day period. [https://www.cogconsortium.uk/news_item/persistent-sars-cov-2...]

In terms of this strain, the actual rate of mutation is higher (5.6E-4 nucleotide changes/site/year vs 5.3E-4) [https://virological.org/t/preliminary-genomic-characterisati...]