CORONAVIRUS 2020: RHYTHM OF THE DEATH III

[Zetetic]

A defining feature is that it doesn't kill at speed - it already has a lengthy incubation period that's often symptomless but still supports transmission. (And even when does it kill, in the West at least, that's often at length in a way that supports transmission to carers.)

There needs to be an actual mechanism of selective pressure. At the moment I can't really see that other than the pressure wrought by humans actively hunting it.

[Zetetic]

it will soon run out of potential hosts.

COVID-19's fatality rate isn't really directly relevant to this though, compared with the effects of vaccination (which is I grant, indirectly related to its power to kill, because that's why we've developed and distributed vaccines) or even immunity from prior infection.

[BlodwynPig]

OPEN THE PUBS

[Chedney Honks]

I've pretty much lost interest in it now. Whatever we do from now on is like big fuck. We already totally fucked it. Should have done it properly thirteen months ago instead of bimbling along like cunts and I include everyone in that except the Happy Few who were on the right page from day one. Whatever happens now is down to the rest of the world and looks like they're pretty much as big cunts as even we are. Moving to Oz.

[Zetetic]

Nature published an article that the variants are showing signs of convergent evolution.

Can you link to this?

There's some pre-prints that make explicit reference, for example this, regarding "the rise of S:677 polymorphic variants". And E484K seemed to emerge and gain popularity independently in at least three different places.

Is there any evidence that any of these are linked to (pleasant) differences in disease progression and severity?

(Edit: I note that we worried B1.1.7 might be more severe as well as more transmissible and possibly more capable of reinfection - and the only reason that increased severity would have been a disadvantage is because it helped provoke a stronger response from government.)

[Zetetic]

Edit glitch.

[BlodwynPig]

Can you link to this?

There's some pre-prints that make explicit reference, for example this, regarding "the rise of S:677 polymorphic variants". And E484K seemed to emerge and gain popularity independently in at least three different places.

Is there any evidence that any of these are linked to (pleasant) differences in disease progression and severity?

(Edit: I note that we worried B1.1.7 might be more severe as well as more transmissible and possibly more capable of reinfection - and the only reason that increased severity would have been a disadvantage is because it helped provoke a stronger response from government.)

https://www.scientificamerican.com/article/the-coronavirus-variants-dont-seem-to-be-highly-variable-so-far/?utm_source=Nature+Briefing&utm_campaign=1bc0fb97f8-briefing-dy-20210326&utm_medium=email&utm_term=0_c9dfd39373-1bc0fb97f8-44212433

It's also critical that we make significant investments in building an early-warning system to detect new SARS-CoV-2 variants as well as many other emerging pathogens, both known and yet to be discovered. Viral genome surveillance and sequencing is the key. The reason why many variants have been detected in the U.K. is because of visionary investments by researchers and public health officials in these technologies.

Why thank you... it is actually our team doing this.

[Chedney Honks]

Thank you, my dude.

[Zetetic]

https://www.scientificamerican.com/article/the-coronavirus-variants-dont-seem-to-be-highly-variable-so-far

Which mentions the examples I did, and unfortunately supports the view that there's very little selective pressure towards lower disease severity (in contrast to transmissibility and immune evasion etc.).

Why thank you... it is actually our team doing this.

I think we're now actually sequencing every (viable) sample in our country. Or would be if Deloitte/DHSC didn't keep fucking up and sending them elsewhere...

(We're hoping this might help unpick what's actually going on in care home outbreaks. Unfortunately wastewater continues to be of no use in our bit of the world.)

[Zetetic]

Edit glitch!

[BlodwynPig]

.

[Zetetic]

Wastewater? The work is going but we still don't have anything that we can actually use [nb]like a standardised summary dataset that we can build products something that other people can understand, on top of, to help anyone make any decisions[/nb], unfortunately.

I know, because I'm going to weekly meetings on it now and sometimes trying not to scream.

[BlodwynPig]

Wastewater? The work is going but we still don't have anything that we can actually use [nb]like a standardised summary dataset that we can build products on top of, to help anyone make any decisions[/nb], unfortunately.

I know, because I'm going to weekly meetings on it now and sometimes trying not to scream.

Some ***** *** guys come to the meeting I chair every two weeks - be happy if they make some requests there.

[Zetetic]

I think what they might need is showing that someone else (i.e. you) is actually using the data to support decisions.

We seem to be stuck in a place about constant worrying about validation and interpretation - which I recognise I am perhaps insufficiently fussed about, but on the other hand it'd be good to have some sort out of output before the next pandemic.

I get the strong impression from some of these people that they've relatively little interest in helping tackle COVID-19, here-and-now, compared with proving the validity of the approach for the future - but I'm too easily frustrated.

[Shoulders?-Stomach!]

The UK has "gone from being cavalier to crippling caution" in its approach to Covid, a former head of drug maker GlaxoSmithKline has said.

Sir Richard Sykes, who is now chairman of the Royal Institution, said the possibility of a third wave of infections in the UK was concerning but "very, very unlikely".

"We have gone from being cavalier to crippling caution and I think that's dangerous," he told BBC Radio 4's Broadcasting House.

"There could be, but it's very, very unlikely that there will be a third wave."

In a wide-ranging interview, Sykes defended Oxford jab maker AstraZeneca's supply strategy - but he criticised the firm for its communciations amid a row over supplies with the EU.

And reflecting on the achievements of all the vaccine manufacturers, Sykes said: "What we've done in nine months is create a vaccine that is ninety-something percent effective, and absolutely safe, and got it into millions of people. I think has to stand as one of the great achievements of mankind."

This guy sounds like a total cunt

[MojoJojo]

Which mentions the examples I did, and unfortunately supports the view that there's very little selective pressure towards lower disease severity (in contrast to transmissibility and immune evasion etc.).

Wouldn't people with symptoms self-isolating provide a selective pressure towards less severe symptoms, which you'd expect to correlate with lower fatality?

Granted, that's probably small compared to transmissibility etc...

[BlodwynPig]

This guy sounds like a total cunt

Dangerous? for whom? typical capitalist dick fuck cunt shit arse wanker evil idiot goon jerk slop of a man

[BlodwynPig]

Wouldn't people with symptoms self-isolating provide a selective pressure towards less severe symptoms, which you'd expect to correlate with lower fatality?

Granted, that's probably small compared to transmissibility etc...

Unless they want the pangolins to be the next dominant species on the planet. The Rise of the Pangolins.

[bgmnts]

Dangerous? for whom? typical capitalist dick fuck cunt shit arse wanker evil idiot goon jerk slop of a man

Its easier just to say Tory.

[Zetetic]

Wouldn't people with symptoms self-isolating provide a selective pressure towards less severe symptoms, which you'd expect to correlate with lower fatality?

My guess is that it depends a lot on the actual details of the disease course.

If it maintains - in the vast majority of people - a pre-symptomatic period of transmission of a few days followed by a few days of at-worst mild-cold-like symptoms and transmissibility after that, then I can't see how the "ultimate" or whatever severity matters much to its fitness (until we're talking about civilisation-level responses).

[Zetetic]

More suggestion that B1.1.7 is more severe:
https://www.medrxiv.org/content/10.1101/2021.03.04.21252528v2

(Picked up by Nature's research updates.)

[Cuellar]

Hopefully this will push the lockdown easing back a bit. The amount of 'plans' I'm already getting roped into:

"What are your Easter plans?[???]"
"Oh let's have so and so round on Friday"
"Shall we go and see such and such?"

NO. It's got to stop.

[BlodwynPig]

Hopefully this will push the lockdown easing back a bit. The amount of 'plans' I'm already getting roped into:

"What are your Easter plans?[???]"
"Oh let's have so and so round on Friday"
"Shall we go and see such and such?"

NO. It's got to stop.

Dumb fucks. OPEN THE PUBS

[Mobius]

We've just had a 3 day lockdown in Brisbane and it sounds like it's going to be extended today, so Easter is cancelled GET IN

[BlodwynPig]

We've just had a 3 day lockdown in Brisbane and it sounds like it's going to be extended today, so Easter is cancelled GET IN

It's not cancelled though, is it. Are do Aussies have massive rave ups on the beach on Easter? Plus, Easter is an illusion anyway. Means nothing. Do some gardening, have a BBQ with your household.

[George Oscar Bluth II]

Which mentions the examples I did, and unfortunately supports the view that there's very little selective pressure towards lower disease severity (in contrast to transmissibility and immune evasion etc.).

Total amateur here but: isn't the problem with covid that it's novel, ie that none of us had seen it before so our immune systems are completely unprepared for it. The reason the other coronaviruses aren't as bad isn't because they're inherently "less deadly" but because we all get exposed to them early in life, get the antibodies and can fight them off in repeat visits. The low fatality rate from covid in children is surely part of this.

Plus the long incubation period anyway means the end result doesn't matter if even the worst affected can go round spreading it quite easily for a few days.

[Zetetic]

the reason the other coronaviruses aren't as bad isn't because they're inherently "less deadly"

My ignorance here is nearly complete, but my understanding is that it is believed is a difference in the severity of disease that's down to the particulars of the COVID-19 virus and not just a lack of pre-existing immunity. I note that it does seems to be essentially less fatal than SARS or MERS were, for example.

(All complicated further by the fact that death from all sorts of respiratory viruses often seems to involve cytokine storms, and not just immediate damage from viruses hijacking cells in the respiratory tract and - one way or another - the destruction of those cells?)

Plus the long incubation period anyway means the end result doesn't matter if even the worst affected can go round spreading it quite easily for a few days.

This is my, equally amateur, assumption: the disease course after the first week or so only matters for transmissibility insofar as the response it's provoking from our societies to distance and develop vaccines.

I can vaguely imagine a scenario where there's a surviving low-severity descendent of SARS-CoV-2 that 1) we don't notice emerging at scale and 2) collectively tolerate in a way that we're not tolerating COVID-19, because it tends to be even less severe. But this handwavy hypothetical doesn't really imply anything about the actual strains that we're seeing emerge at scale now and the pressures behind their selection.

[George Oscar Bluth II]

Yeah you're right that the lower fatality rate than SARS and MERS is important, seems to be the reason Covid took off and those both burned themselves out.

Quite interested in the idea that the other coronaviruses arrived with us like this. Some people think the "Russian flu" of the 1890s could have been one of the endemic coronaviruses, for instance.

[NoSleep]

The significant difference between Covid-19 and SARS or MERS is that, because the two latter severely affect all who contract them, it is easier to isolate them. Covid-19, conversely, can be transmitted by the many people who contract it but show no symptoms.

[Zetetic]

Perhaps most importantly, SARS and MERS didn't have a pre-symptomatic transmission period to speak of - identification and isolation worked, because pretty much only people actively displaying symptoms were transmitting it.

This is all related, I guess, insofar as there presumably isn't a "pre-symptomatic transmission? Y/N" gene and a "fatal in x% of cases? 7/17/70%" gene in coronaviruses, but rather the disease course and distribution of severity emerges from the overall behaviour of the virus and how people's immune systems respond to it.