Lizzy schreef: ↑ma 28 dec 2020, 09:34
En in een weer andere krant lees ik inderdaad dat er nog nul bewijs voor is. Weet je, ik geloof dat ik qua nieuws lezen maar onder een steen ga zitten
Ik heb vandaag eea uitgezocht voor collega’s maar dat is in het Engels, ik ben alleen beetje moe nu, dus doe even copy paste en als niet duidelijk is, vraag maar. Dit gaat alleen over de Britse variant.
There is a publication about this variant (
https://virological.org/t/preliminary-g ... ations/563 ) which shows that there are variations in the spike protein. That is not new (there have been several mutations in that area of the virus) and also not unexpected. A virus that goes from one animal to another will try to adjust itself. What was seen in GB was a shift from several strains of COVID19 to a new dominant strain, the B.1.1.7, this strain had an unusual high number of mutations in the spike protein. Usually they see 1-2 mutations/month in the clones from the original virus, but this one has more than average and that suggests genetic adaptation/evolution and not just accidental variation. Or so to say: in order to be so different from the original, there ‘must’ be some advantage for the virus.
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. (this is the same mutation as seen in the mink strains in Denmark)
· Mutation P681H is immediately adjacent to the furin cleavage site. This mutation has been shown to promote entry into respiratory epithelial cells and transmission in animal models.
So in this strain three previously described mutations come together. This might have the effect that this strain binds easier to the ACE2 receptor in human cells, perhaps has the potential to evaded the immune system and might get easier into human lung cells (these are the hypothesis).
Modelling data on the increase of the number of strains with these mutations, suggest that it might spread more easily. Note: these are epidemiological data and not transmission studies. The number op 70% increase in transmissibility is mentioned in a presentation by Dr Erik Volz, from Imperial College London but it is still uncertain (other modellers suggest other numbers). (I did not look at the presentation, the whole event takes more than 3 hrs..) There could also have been other factors that increased the spread of this variant, for example human behavious, superspreading events etc.
So what we have is a virus variant that very quickly (september – december) became the dominant clone and has mutations that suggest it is more adapted to infecting humans. This could mean that a lower number of viral particles could cause an infection.
For those who are interested , there is a website where you can see some of the research done on the worldwide genetic evolution of SARS CoV2 :
https://nextstrain.org/ncov/global
An article from the BBC:
https://www.bbc.com/news/health-55388846
So I guess there is still a lot of uncertainty about how this variant is going to behave.