[RcouF1uZ4gsC]

There are two important things to temper how worried you should be:

1. Many times there is an inverse relationship between ease of transmission, and severity of symptoms. There is a good chance that this new more transmissible mutant is likely to make people less sick.

2. So far all the available evidence seems to indicate that the vaccines will be effects against this strain as well.

[saberdancer]

You shouldn't speculate about 1. especially as this is a virus that is new. It didn't have wave after wave where the "deadly" strains would lose out in evolution.

Death rate in London and Kent didn't seem very different to other affected areas which would imply that the virus has same severity of symptoms but it is easier to transmit/contract.

[irq11]

It’s not remotely clear that this strain is easier to transmit. It’s entirely hypothesis and speculation.

We have seen strains quickly accelerate because of founder effect several times in 2020, and particular strains dominate in particular regions. The experimental studies that are needed to confirm a claim of evolutionary advantage have not been done, and the observational evidence is weak.

Those who would panic about this should be just as circumspect in their their claims as those who would dismiss it.

[Jabbles]

It is a hypothesis with a small prior, yes.

But when considering the data - that the strain has grown faster than all others in the UK at the time - the likelihood becomes significant. Not certain, but not worthy of your casual dismissal.

You dismiss their observational evidence as weak, but offer no further analysis. Please do so.

[irq11]

“Hypothesis with a small prior” is a fancy way of saying “speculation”.

There are literally dozens of strains on nextstrain that have rapidly grown to be the predominant strain in a region. That alone is not a strong indication of anything other than founder effect.

[jibbit]

I'm guessing you're not living in Kent right now?

[jonny_eh]

Isn't this what happened with the 1918 flu? It mutated to be less deadly add became the seasonal flu.

https://www.history.com/news/1918-flu-pandemic-never-ended

[rolph]

yes this is a property of influenza virus, however the influenza virus is very different from corona virus, in particular the cryptic incubation period of coronavirus that occurs before symptoms can alter the hosts ability to interact with other prospecific hosts.

it is worthy of note that one single point mutation in the influenza virus corresponded to high lethality.

https://journals.plos.org/plospathogens/article?id=10.1371/j...

>> The 1918 pandemic strain A/Brevig Mission/18 was reconstructed with a pathogenicity-reducing mutation in PB1-F2 (S66N). The resultant 1918 S66N virus was attenuated in mice having a 3-log lower 50% lethal dose and caused less morbidity and mortality in mice than the wild-type virus. Viral lung titers were also decreased in 1918 S66N–infected mice compared with wild-type 1918 virus–infected mice. In addition, both viruses with an S at position 66 (WH N66S and wt 1918) induced elevated levels of cytokines in the lungs of infected mice. Together, these data show that a single amino acid substitution in PB1-F2 can result in increased viral pathogenicity and could be one of the factors contributing to the high lethality seen with the 1918 pandemic virus.<<

[madhadron]

This is a very poor way of looking at it. H1N1 is considered a subtype rather than a strain, and there are many H1N1 strains around. It makes more sense to think of the 1918 strain going extinct and some of quasispecies descendants of it persisting.

[rolph]

[1] is a repeated concern, that has roots in early virology e.g myxomatosis and rabbits overpopulating australia.

https://en.wikipedia.org/wiki/Myxomatosis

the coronavirus breaks past this dynamic as there is disjunction between transmission and onset of symptoms. thus morbidity is not a selective pressure upon transmisibility of the coronavirus.

[fallingfrog]

Do you know this for a fact or is that just a plausible idea you came up with? It sounds plausible enough but it also sounds plausible that if symptoms were delayed even more or failed to show up at all it might be transmissible for longer, meaning that that there would still be selective pressure towards less virulent strains.

[rolph]

this is fact, this is evolution. when reproduction occurs this is success, this is fitness to reproduce. if a host is killed, or inconveinienced enough to lay ill and not contact others, that is a selective factor that favours reduction of morbidity. in the case of coronavirus reproduction and transmission occurs before morbidity occurs in the index host. there is no selective pressure to become less virulent. there is selective pressure to change host, to evade recognition by the immune system.