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March 28, 2024, 09:16:56 PM

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Sourced Coronavirus Information & Links

Started by Sheffield Wednesday, March 14, 2020, 09:42:19 AM

Previous topic - Next topic

pancreas

Quote from: massive bereavement on March 25, 2020, 11:56:58 AM
If the tabloids/msm pick up on this article then its' only going to encourage people to ignore instructions to stay at home and shut businesses. She may turn out to be right, but there's the possibility that publishing that piece could literally be responsible for additional deaths and longer term breathing difficulties.

Partly agree. It isn't the responsibility of science to stifle its own internal debates because the media will pick up on something—it should be held account for responsible information. On the other hand, what she's suggesting is so way out there that I think there is a case of putting a cork in it.

The only thing she's advocating is serum testing, which I guess would be a good idea in any case.

Zetetic

And indeed everyone is aiming at it anyway.

QuoteIt isn't the responsibility of [academics] to stifle [their] own internal debates
This isn't internal, of course.

Zetetic

Quote from: pancreas on March 25, 2020, 11:43:09 AM
My main concern with it is that it can't be extremely infectious at the same time that you believe loads (but not all) people have had it.
They fiddle about with the time of introduction, not the rate of transmission (which they keep as between 2.25-2.75).

I'm not sure really what the point of this is other than "look, I can do some modelling". I work with children who I'm fairly sure could have knocked this out in a hour or two (and they wouldn't have made Figure 2 unfriendly to the red-green colourblind).

massive bereavement

Seeing increasing references to two different strains, the S strain and the L strain, seems to be a big debate as to whether or not there is a significant enough difference to justify labelling them as separate strains or if one is more deadly than the other.

Meanwhile, "The Icelandic genetics company DeCode Genetics has tracked 40 mutations of coronavirus in Iceland. A probable scenario is that the virus develops to become more contagious, but less dangerous for those affected, says Danish virologist..... We have the genes from more than 400 infections. The interesting thing about that sequencing is that we can track where the virus came from. Some came from Austria. There is another type from people who were infected in Italy. And there is a third type of virus found in people infected in England. Seven people had attended a football match in England. '"

https://www.information.dk/indland/2020/03/forskere-sporet-40-mutationer-coronavirus-alene-paa-island

Quote from: Zetetic on March 25, 2020, 08:23:27 AM
What an astonishingly pointless piece of work, given that mass serological testing is what everyone's aiming at whenever they can already.

tldr - If you decide that the proportion of people getting severely ill is very, very low then lots of people have probably already had it.

https://www.dropbox.com/s/oxmu2rwsnhi9j9c/Draft-COVID-19-Model%20%2813%29.pdf?dl=0

I think what they are saying is that if the death rate from the disease is lower, then we must have had more infection in order to get the number of deaths we have seen. Is that right?

Zetetic

And it was would have needed to be introduced a bit earlier to enable that level of infection.

pancreas

Yes, but it doesn't explain why the number of deaths is growing at an exponential rate from a fairly clear first death of just a few weeks ago. Even if 50 deaths were misattributed to normal flu or something else, I don't see how we would be on the current trajectory we are on in terms of the number of deaths. Do you see my point?

Zetetic

Not really - the model suggests that if for some reason you decide it has a really low fatality rate you would probably have expected to see a few deaths a few days sooner (which we could have missed, or just got lucky), but you'd still expect to see an exponential rise of deaths (following the exponential rise in infections, but a much smaller proportion).

I'm not sure why you think it would make the trajectory look radically different after the first few deaths. (And it looking different for those first few deaths is matter of extremely good case finding, I guess.)

But we've no good reason to believe the assumption of an extremely low IFR, do we?

Nice if it turns out to be true, but nothing to affect decision making now.

Think it'd look similar if you had 1M infected and 1% chance of death, or 10M and 0.1%. At least you'd need a better model to distinguish the difference, and more detailed statistics.

On the other hand, a load of tests have been performed and I'm pretty sure we'd have noticed the tons and tons of very sick but not dead people, so I'm skeptical.

Zetetic

And you'd be getting far more positives from the symptomatic healthcare worker testing that's going on this week and last week, if only by chance, I reckon.

(Noting that this testing won't tell if you've had it only if you've got it.)

buzby

#220
Quote from: Zetetic on March 25, 2020, 01:06:58 PM
I'm not sure really what the point of this is other than "look, I can do some modelling". I work with children who I'm fairly sure could have knocked this out in a hour or two (and they wouldn't have made Figure 2 unfriendly to the red-green colourblind).
Speaking as someone who is, it's bloody awful!

The Iceland figures are interesting, especially the people infected after attending a football game in the UK. I wouldn't mind betting it was the Liverpool-Atletico Madrid game, where 3000 Madrid fan were allowed to travel to attend even though Spain's league games were being played behind closed doors at the time.

pancreas

My point is that you can take the #deaths from the FT data and draw a line back to roughly where t=0 ought to be. Sunetra thinks we were all getting it as early as Oct last year. That doesn't mesh.

Zetetic

The paper's suggestion is late January in the most extreme (lowest fatality rate) case, if I'm reading it correctly.


Wouldn't it be fairly easy to test that theory? Just test 1,000 or so people who have not displayed symptoms to see if they have or have had it. (I mean fairly easy for a competent government, obviously 1,000 extra tests are not easy to come by it seems)

Zetetic

It should be easy within a few weeks, I believe.

pancreas

I did read recently that they've done testing in New York and found 28% infection.

kalowski


Dewt

Do you have to stick the cotton bud in your brain?


oy vey

It acts by giving you the virus and confirming successful injection. Results have been very positive so far.




Head Gardener



steveh

Few bits from Nature:

- Seems to cause T-cell death so your immune system is compromised making it more likely you will get other infections: https://www.nature.com/articles/s41423-020-0424-9

- Things that are now known about immunity: https://www.nature.com/articles/d41586-020-00798-8

- Vaccine progress: https://www.nature.com/articles/d41573-020-00073-5

steveh

This is a good summary of what's currently known about longer-term effects: https://www.latimes.com/science/story/2020-04-10/coronavirus-infection-can-do-lasting-damage-to-the-heart-liver

- Could be some years for normal lung function to return.
- Can weaken the heart, even if no respiratory problems.
- Impaired liver function can persist past the infection.
- Severe cases causing blood clots.
- As-yet unknown effects on other organs with ACE2 receptors, including the kidneys and brain.

Dewt

I am very interested in not getting this virus and I will live like a hermit until there's a vaccine.