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Coronavirus.

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edwin_m

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I did see something about this posted last night but it was then removed, I believe the link went to a dead end. Originally in the Financial Times but now finding it's way to many outlets, it's about a study from the University of Oxford where they believe Coronavirus was here much earlier than originally thought. It actually makes quite a lot of sense, to me anyway.

https://www.standard.co.uk/news/hea...n-oxford-university-study-finds-a4396721.html
Good if true, but I think we have to err on the side of caution unless and until this is independently verified - there's too much hanging on it to do otherwise.

If it has been around for some time then it's surprising it wasn't noticed earlier, especially when people started dying in China and the authorities here would have been specifically looking for deaths with similar symptoms. Is it possible that a less deadly strain was going round and then mutated? If so then we'd have to be confident that the one confers immunity to the other.
 
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Mogster

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I know that the plural of anecdote isn't data, but over the New Year holiday I was ill with the full house of coronavirus symptoms - fever, myalgia, uncontrollable coughing and breathing difficulties. When the coughing fits came I couldn't breath in, had a "stridor" (a noise like a wheeze but on trying to inhale, caused by the airways closing up), turned blue in the face and nearly passed out a couple of times. The dry cough persisted for weeks and I'm only just over it. I don't know what bug I had but I've never experienced anything like it. It does make you wonder if coronavirus has been in the U.K. longer than we think.

Last December an elderly relative of a co-worker was hospitalised with a viral lower respiratory infection that started as a dry cough. The lab were unable to identify the virus and eventually the relative died due to an extended immune response that proved resistant to all treatment.

As you say it’s anecdotal and not data, but yes, it does make you wonder...
 

Mogster

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Prof Ferguson shredded that paper in at the Health Select Committee hearing this morning. Having said that there needs to be a lot of testing to establish the number who have had to feed into the modelling as it has huge impact overall (a big weakness of the current IC work). The Oxford work was based on data up to last Thursday morning so some underlying assumptions are different now.

Other Prof F. snippets:
R0 looks like it is nearer 3 than 2.5 based on latest work. Distancing therefore has much bigger impact.
R0 only expected to drop by 10-15% in warmer dry weather based on previous Corona Virus experience e.g. to 2.55 - 2.7 if R0 is 3.0.

Well he would wouldn’t he, his team wrote the other paper... His reputation is on the line.

Anyway it seems major serological studies are starting to wind up to answer these questions.

https://www.reuters.com/article/us-...s-for-unseen-coronavirus-spread-idUSKBN2161S4

AMSTERDAM (Reuters) - Dutch health authorities have begun a major project testing blood donation samples to see how many people in the Netherlands may have already had the new coronavirus, often with symptoms so mild they hardly noticed.
 

Bletchleyite

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If it has been around for some time then it's surprising it wasn't noticed earlier, especially when people started dying in China and the authorities here would have been specifically looking for deaths with similar symptoms. Is it possible that a less deadly strain was going round and then mutated? If so then we'd have to be confident that the one confers immunity to the other.

There are believed to be two known strains around, one more serious than the other. It is quite possible that the less serious one got out first. There are a few articles knocking around on this but I can't find a conclusive enough article to be worth quoting.
 

Djgr

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hwl

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Mogster

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There are believed to be two known strains around, one more serious than the other. It is quite possible that the less serious one got out first. There are a few articles knocking around on this but I can't find a conclusive enough article to be worth quoting.

There have been rumours in the media but I don’t think the existence of the “more virulent form of CoV2” has been confirmed.

Different individual CoV2 virus’s will have genetic differences the same way that you and I are genetically different. The genetic differences mostly don’t affect how the virus makes proteins and so the way it functions, the same way people’s genetic differences don’t affect the way they function mostly. The differences do allow scientists to identify when people have contracted similar “strains” and so where and when they may have contracted the virus though which always amazes me.
 

Mogster

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So it could be that half of the population already have immunity and are sitting on their backsides at home for no purpose?

Yep. The economy of the entire world depends on this information... No pressure... :lol:
 

hwl

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Yep. The economy of the entire world depends on this information... No pressure... :lol:
The both papers somewhat have been some what demolished in the guardian this evening, (conclusion we need antibody testing data):

https://www.theguardian.com/science...xposes-the-problems-and-pitfalls-of-modelling

Coronavirus exposes the problems and pitfalls of modelling

Models based on assumptions in the absence of data can be over-speculative and ‘open to gross over-interpretation’
The lessons to be learned from the coronavirus pandemic will keep scholars and university lecturers busy for decades to come. Chief among them is the value of modelling, and the fact that an uncritical reliance on their findings can lead you badly astray.

Take a recent model from Oxford University. It assessed how well different outbreak scenarios fitted the rise in coronavirus deaths in the UK and Italy. The most extreme UK scenario assumed that only a tiny fraction of people were at risk of serious illness. It also estimated that, as of last week, 68% of the population had been exposed to the virus. The study, which has not been published or peer-reviewed, unleashed a flurry of headlines declaring that coronavirus may have infected half of the people in Britain. That is 34 million people.

But as infectious disease modellers and public health experts, including the Oxford team themselves, have pointed out, the model used assumptions because there was no hard data.

No one knows what fraction of the public is at risk of serious illness. The study merely demonstrates how wildly different scenarios can produce the same tragic pattern of deaths, and emphasises that we urgently need serological testing for antibodies against the virus, to discover which world we are in.

Paul Klenerman, one of the Oxford researchers, called the 68% figure the most extreme result and explained that “there is another extreme which is that only a tiny proportion have been exposed”. The true figure, which is unknown, was likely somewhere in between, he said.

In other words, the number of people infected in Britain is either very large, very small, or middling. This may sound unhelpful, but that is precisely the point. “We need much more data about who has been exposed to inform policy,” Klenerman said.


The Oxford model was useful in emphasising the need for serological testing, but not for grasping the scale of the pandemic in the UK. As Prof James Wood, a researcher in infection dynamics at Cambridge University, put it: “The paper does substantially over-speculate and is open to gross over-interpretation by others.”

Devi Sridhar, a professor of global public health at Edinburgh University, said the Oxford study set out a hypothesis and nothing more. “It’s like me sitting here and putting into very fancy equations what would change if we had a vaccine tomorrow. I could model how a vaccine would save lives and you would see headlines reading ‘New vaccine is going to save lives.’ But we don’t have a vaccine.”

The modelling from Imperial College that underpinned the government’s belief that the nation could ride out the epidemic by letting the infection sweep through, creating “herd immunity” on the way, was more troubling.

The model, based on 13-year-old code for a long-feared influenza pandemic, assumed that the demand for intensive care units would be the same for both infections. Data from China soon showed this to be dangerously wrong, but the model was only updated when more data poured out of Italy, where intensive care was swiftly overwhelmed and deaths shot up.

Nor was that the only shortcoming of the Imperial model. It did not consider the impact of widespread rapid testing, contact tracing and isolation, which can be used in the early stages of an epidemic or in lockdown conditions to keep infections down to such an extent that when restrictions are lifted the virus should not rebound.

It is not a question of whether models are flawed but in which ways are they flawed, and models can still be enormously valuable if their shortcomings are appreciated. As with other sources of information, however, they should never be used alone.

“Models are a useful input among many when you are doing public policy, but you have to use triangulation. You have to look across different sources of information and not just rely on one. It’s more messy and complex than just saying ‘OK here’s a number’, but you get to a more accurate answer for our world,” Sridhar said.

Never have the words of the British statistician George Box rung truer than in this pandemic: “All models are wrong, but some are useful.”
 

Mogster

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The BBC is reporting Ferguson told the select committee this morning

...that the latest research suggested as many as half to two-thirds of deaths from coronavirus might have happened this year anyway, because most fatalities were among people at the end of their lives or with other health conditions.

Hmmm
 

Djgr

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Yep. The economy of the entire world depends on this information... No pressure... :lol:

But if it turned out to be true and you were one of the 50% would you be mainly relieved or mainly annoyed?
 

Meole

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Looks like he's gone to his holiday home in Scotland to self isolate. Not sure how symptom-free Camilla managed to blag herself a test. There is a long line of succession to the throne, so if we do loose a few royals there is a queue of people ready to step up to the job.



What advice do they give in your local area to people with mild coronavirus symptoms?
Thought advice is that second homes are out of bounds ?
 

JamesT

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Unnecessary travel is. I'd suggest that if you were already in a second home at the point of the lockdown starting, staying there would be valid - it's being suggested he was already there, isn't it?

Apparently he traveled up on Sunday and was tested on Monday. But it’s also reported that he was displaying mild symptoms over the weekend, in which case surely it would have been better to have stayed where he was and self-isolated rather than waiting for a test?
 

Peter Kelford

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There is a awful lot happening behind the scenes to keep the show on the road.
Builders are being allowed to build so I'd assume so.

Looks like he's gone to his holiday home in Scotland to self isolate. Not sure how symptom-free Camilla managed to blag herself a test. There is a long line of succession to the throne, so if we do loose a few royals there is a queue of people ready to step up to the job.
Private hospitals?

I saw something that suggested Raab was the "designated survivor"!
Theoretically, they should get the youngest member of the cabinet, with the least family obligations and least medical complications into this role.

Probably Châlons sur Marne (now called Châlons en Champagne) which is the junction on the main line from Paris Est with the line for Verdun. Verdun was the location of the longest WW1 battle involving the French.
I thought that at first. Thanks.
 

Mogster

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But if it turned out to be true and you were one of the 50% would you be mainly relieved or mainly annoyed?

I’d be very relieved if it meant things could return to normal and there was a rapid way out of this crisis. The global economic fallout of the current situation scares me more than the healthcare aspects.
 

Meerkat

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The BBC is reporting Ferguson told the select committee this morning
Hmmm

So two thirds of them would have died this year......but not in the next few weeks, and it's the peak that is the scary bit.

How does that explain the death of 21 year old Chloe Middleton who had "no underlying health conditions"?

Hmmm

Aside from no one saying it is ONLY a danger for old people are they sure she had no underlying issues, or just no underlying issues that they knew about?
 

Bletchleyite

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Aside from no one saying it is ONLY a danger for old people are they sure she had no underlying issues, or just no underlying issues that they knew about?

That's I guess a possibility, unless an autopsy has already been completed (assuming it even will be). It is not at all unusual for people to literally drop dead at running races (particularly very accessible ones like Parkrun) from serious heart conditions that they never knew they had. And I suspect I wouldn't even know I had asthma if I wasn't a runner, it's the only thing that's high-intensity enough to cause an issue, even cycling doesn't.
 

Bayum

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That approach does make a lot of sense as people with the worst symptoms apparently have autoimmune lung damage.
Yeah, the infection itself doesn’t cause the problems, more how the body reacts to it. My understanding is that ARDS is the immune system going haywire. Body recognises the infection and seeks to get rid - raises temperature, invokes other symptoms - muscle aches etc. In the lungs themselves, the alveoli are filling with fluid causing the ground glass opacities on the CT scans, but this isn’t enough. The body goes on another onslaught causing a cytokine storm, where the immune system just goes crazy. Tocilizumab is an anti-IL6 molecule and so reduces a significant portion of the immune process happening.
 

Bayum

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How does that explain the death of 21 year old Chloe Middleton who had "no underlying health conditions"?

Hmmm
We don’t know she had ‘no underlying health conditions’ unless further work is done. The 21 year old football coach who died last week was in the same category, until analysis showed he actually had leukaemia. Besides that, there’s always been a warning that deaths have occurred in all age groups, but people have become fixated on this idea that ‘most’ means ‘me’ and ‘those with underlying health conditions’ means I’m absolutely fine because I have none of the risk factors. We know from China that a good number of deaths were amongst people NOT aged 60+, no underlying health conditions or whatever. Indeed, the first whistleblower doctor, man in his prime, died from the virus.
 

Mogster

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Yeah, the infection itself doesn’t cause the problems, more how the body reacts to it. My understanding is that ARDS is the immune system going haywire. Body recognises the infection and seeks to get rid - raises temperature, invokes other symptoms - muscle aches etc. In the lungs themselves, the alveoli are filling with fluid causing the ground glass opacities on the CT scans, but this isn’t enough. The body goes on another onslaught causing a cytokine storm, where the immune system just goes crazy. Tocilizumab is an anti-IL6 molecule and so reduces a significant portion of the immune process happening.

Yes the IL6 inhibitor does make sense.

The NHS will be offering hospitals convalescent plasma collected from recovered patients very soon.
 
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