UKH

Is there any evidence of this in the new strain?

I know the 70% value has been questioned,  and a trade off between the two parameters is still not fully understood or fully supported.

I'm clearly no expert, but I too question exactly how the same virus through mutation in less than a year, can become 70% more transmissible. I don't get it.

Is it somehow more likely to be breathed in, or has this new variant developed changes that increase its ability to infect cells better than the original virus? 

If its cell infection abilities have altered, would the vaccines still be effective? And if so, why would it still be effective - given that the variant's characteristics have changed significantly?

The latter - it's a change to the "spike" that lets it into the cell.

They may or may not.

Because it's still similar enough in terms of the structure of the spike.

It's only a small change so it's highly unlikely to affect the vaccine. But it's why we need as many people to take the vaccine as possible, the longer you give it the more chance it will eventually get away from the vaccine protection (not that it purposely does that).

To my knowledge there isn't any solid evidence of this, as of yet.

The report of the new strain, B1.1.7, suggests there is a possibility that the new strain is actually more virulent based on the N501Y mutation of the receptor binding domain on the spike protein. This amino acid residue has previously been characterised as being important in binding to ACE2 receptors. The suggestion that the mutation increases virulence is based on a mouse-adapted strain having this particular mutation and being able to produce human-like clinical symptoms, without resorting to a human-ACE2 mouse transgenic line.

So yeah, jury's still out I guess.

Looks like a similar variant exists in South Africa too..

https://www.bbc.co.uk/news/live/world-africa-47639452?ns_mchannel=social&am...

I suspect it's probably everywhere if it's been here since October.

"Transmission virulence trade-off"

Is there good evidence this trade-off exists at all? 

From what I've read, the South African one is thought to be a separate instance of a mutation with similar effects, rather than directly related.

I suppose if that mutation makes it more viable it's likely to evolve independently in several places, makes sense.

Yes, took two seconds on google scholar.

https://onlinelibrary.wiley.com/doi/10.1111/evo.13692#:~:text=In%20short%2C...).

Abstract

The virulence–transmission trade‐off hypothesis proposed more than 30 years ago is the cornerstone in the study of host–parasite co‐evolution. This hypothesis rests on the premise that virulence is an unavoidable and increasing cost because the parasite uses host resources to replicate. This cost associated with replication ultimately results in a deceleration in transmission rate because increasing within‐host replication increases host mortality. Empirical tests of predictions of the hypothesis have found mixed support, which cast doubt about its overall generalizability. To quantitatively address this issue, we conducted a meta‐analysis of 29 empirical studies, after reviewing over 6000 published papers, addressing the four core relationships between (1) virulence and recovery rate, (2) within‐host replication rate and virulence, (3) within‐host replication and transmission rate, and (4) virulence and transmission rate. We found strong support for an increasing relationship between replication and virulence, and replication and transmission. Yet, it is still uncertain if these relationships generally decelerate due to high within‐study variability. There was insufficient data to quantitatively test the other two core relationships predicted by the theory. Overall, the results suggest that the current empirical evidence provides partial support for the trade‐off hypothesis, but more work remains to be done.

How much does this trade-off apply in the emerging pandemic phase?  It seems to me that it's exerts a more gradual selective pressure in the endemic phase which may take many centuries to push the trade-off through.  Where's we're in the first half of the pandemic sigmoid so basically exponential, and the damned thing spreads well before it kills, so I don't think that selective pressure exists.

I don't know, but i'd be surprised at centuries. In virus terms that's a long time.

I was just wondering if there is any tracking of other rates associated with the virus in areas we know this strain is more prevalent. Hospitalization rates, Age-associated fatality rates etc (admittedly there's so many confounding factors on top (race, health, poverty etc).

I'm not saying a virulence trade off has to occur at all, that's pretty obvious from the literature, but it does seem to at least partially support the trade off.

Yes, and that basically says there's no strong evidence for the trade-off between transmission and virulence. 

"Is there good evidence this trade-off exists at all?"

I posted an article which finished with: "Overall, the results suggest that the current empirical evidence provides partial support for the trade‐off hypothesis, but more work remains to be done."

And without reading the paper you have decided that equates to no strong evidence.

I think it's exactly what I said in my OP which was "and a trade off between the two parameters is still not fully understood or fully supported." No where did I argue that this trade off definitely occurred, or was a strong relationship. I just asked was there any evidence of a change in its virulence, someone mentioned this yesterday on another thread.

In true UKC style you seem to be creating an argument because you are bored.

Hello. I have read the paper. If you are going to pull the "2 seconds on google" reposte you'd better come up with something that supports your argument. 

Edit: Sorry I don't mean to come across harshly, but it drives me (professionally) mad that assumptions about biology with very little evidence that they actually exist are perpetuated as fact. 

It's obvious and intuitive that a virus that kills people quickly would transmit more if they survived a bit longer to pass it on. But it's not obvious that a virus that becomes more infectious by other means due to a random mutation would necessarily become less dangerous. It doesn't work in reverse. We already know what the mutations in this variant are and the scientists were theorising that they would make this strain more infectious even before the empirical evidence was clear. It's not because the virus allows people to hang around and mix for longer, it's because the virus has specific changes that enable it to enter cells more easily (that's the theory at least.) 

What I've seen in the news would support this it seems. Vallance was happy to be quite explicit today that the disease is basically the same - he didn't feel the need to word his point on that anything like as carefully as he did what he said about vaccines. Hospitalisations are rising fast in the badly affected regions in the public data so presumably Vallance has enough confidence from what he has seen that this variant isn't reducing the hospitalisation rate significantly.

Having said all that I do agree it's critical to watch how the death rate develops through January and whether the CFR goes up or down at all.

Edit to say, there is a good discussion of this topic in the article posted by Eric9points on the other covid thread. My explanation above is a bit over simplistic.

September according to the Gov. web site.

Intuition is very often not a great guide for non-linear population-scale effects. Sorry to pick up on this, but the really perfect example of why this is not always true is if there was an infectious disease that transmitted from the infectious dead really well to living susceptible host: witness Ebola in West Africa 2014, due to cultural behaviours associated with funerals.

A second counter-argument to this is any infectious disease of density dependent population (e.g., much wildlife) where immunity is earned the hard way (maternal immunity doesn't last). Admittedly, this hopefully doesn't apply to any human population... 

I've not read in to the recent Ebola outbreaks, so what sprang to mind for me was Kuru.

Having a host with complex behaviours and social dynamics really changes things.

Fair point well made. I did realise afterwards I had been overly simplistic and probably should have stuck to the core message in my post.

Ignoramus here. Stating the obvious but from a different viewpoint surely the mutated virus is far more dangerous in that more people infected=more hospitalized=more deaths (especially if hospitals are overwhelmed). Also IF the mutated virus can enter cells easier (I think this has been suggested) then IF disease severity is sometimes related to number of virions initially infecting the host then for a given number of virions more will be  successful which MIGHT result in more cases of severe disease.