I think it depends on the type of aircon - local or centralised, % recirculation.
At my work the test department for example cant really not use aircon, as the test procedure specifies a fairly narrow range of ambient temperature.
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I don’t know if you subscribe on-line but this article in the Telegraph explains some of the problems with the R number https://www.telegraph.co.uk/news/202...d-way-measure/
It can be both! R does not tell you how many have got it/have had it - it simply tells you how many are infected by the average person with infection.
Most have not had it because most have not yet been exposed to it; when exposed, most get it. Of those, all are asymptomatic to start with, yet can spread it; some never develop significant symptoms, a % never develop any symptoms. Of course some unlucky ones end up in hospital, some very unlucky ones die.
Trolling in my opinion is disagreeing without explaining why.
You have suggested I don't understand how R works, but you haven't advised why.
Posts #1225 and/or #1229 set it out.
As for the Telegraph article, I think we covered this before you joined the forum in your current guise but you may well have read and or commented on it in one of your other guises.
Simpson's Paradox shows how R can distort the reality, especially marked when the cases are low and small pockets of infection make the R number jump - as pointed out by Dr Jenny Harries in her appearance at the Downing St press conference on Monday when she advised that the R number can mislead at this stage of the pandemic.
https://unherd.com/2020/05/what-the-...dont-tell-you/
This might help you.
The last best guesstimate I saw of the overall U.K. infection rate was 5% of the population, with London and the south east viewed in isolation at around 20%. Herd immunity is effective at 82%
Interesting phone call this morning...
Firstly, furlough ending and back to office from next wednesday! Although potential to revert to part-time/part-furlough in the future if necessary.
Secondly, director was rushed into hospital a week ago with suspected heart-attack. After extensive testing he has a perfectly healthy heat/lungs for his age. However he did suffer quite badly with Corona a coupe of months back, and the pains are suspected as related to this. Apparently the hospitals are seeing a few similar occureneces of chest issues in people who have had corona...
This is what worries me most about catching the virus, I think I would be very unlucky to die from it (being quite fit and healthy for my age) but I do fear long term or irreparable damage to organs somehow. My twilight years would be little fun with a heart or lungs that only functioned 50% (for instance).
I do fear that the "death numbers" may only be the tip of the iceberg when it comes to damage done.
Some different estimates of R:
https://www.mrc-bsu.cam.ac.uk/now-casting/
What we are seeing is unexpected rates of poor resolution of lung changes on imaging. In diseases like influenza any chest x ray changes during the active phase generally resolve. But covid often seems to leave behind changes that are much slower to resolve. This raises the spectre of pulmonary fibrosis, a permanent of sometimes progressive deterioration in lung function...like miners or dust workers lung disease.
I'm sorry Mike, and I appreciate your background, but we have been presented with an assessment that R=4 up to lockdown.
If that R4 "tells you how many are infected by the average person with infection" then it tells you that we will have a huge and rapid rise in the infection - in fact it would be so huge that it would start hitting herd immunity before 10 weeks.
As to how many infections there are/will be in a population with an infection with an R of X depends on 1/ how many cases you start with 2/ the cycle time and 3/ how many cycles you have before taking measures to change R. There are formulas for this - epidemiologists will know this - are they wrong? I know some have come up with somewhat different results for R, but of course R is not fixed (unless you define it as such), and varies with both both time and place.
The biggest unknown - and an obvious influencer - is the cycle time - how long from being infected before someone then starts to infect others. If this is just a day, numbers will rise very quickly, if it is 2 weeks, it will clearly take much longer. Again, epidemiologists will know this, and have ways of estimating cycle time from the data available.
Do you feel R was a lot lower, and lockdown has had little influence, or that R was high, and far more have been infected than than the generally accepted 5% (10% in London)?
I feel the R of 4 might be about right.
I understand the cycle time is thought to be around 5 days - that seems the settled thought.
As I've set out previously an R of 4 (as set out in the piece I think you referred to earlier), a cycle time of 5 days, would mean from just 1 person, we would have had circa 1/3 of the population infected prior to lockdown.
I don't "know" as such. All I see is assertions that don't stack up.
An R of 4 (backed up by the speed and depth a processing plant can be gone through) just doesn't sit alongside a 5% level of infection in the population.
So something is wrong.
I know that some cases of Covid with no actual symptoms have had changes in their lungs on CT. Even with "ordinary" pneumonia it can take ages for even CXR appearances to return to normal, much less CT appearances.
I would be surprised if people end up with progressive fibrosis, but clearly some people's acute lung damage is fatal, and others, some quite young, have needed lung transplants.
There is clearly a lot we do not yet know about the longterm effects of Covid.
https://www.researchsquare.com/article/rs-35331/v1
Something for the forum experts to have a look at.
apparently up to 81% have a had some T cell response to COVID, which would mean lots of people have immunity.
Thank you for finding this WP.
Whilst I will defer to the better knowledge of experts, as this is a serious research article, for those who are interested in knowledge about the virus there is much to read. For those without the time to wade through it I have lifted two parts, below in bold, one of which mentions the 81% figure WP mentioned
Using predicted or randomSARS-CoV-2--derived peptide pools, two very recent studies reported preexisting SARS-CoV-2-directed T-cell responses in small groups of unexposed as well as SARS-CoV-2 seronegative individuals, thereby suggesting cross-reactivity between human common cold coronaviruses and SARS-CoV-210,11
Notably, we detected SARS-CoV-2 cross-reactive T cells in 81% of unexposed individuals. To determine if these T-cells indeed mediate heterologous immunity and whether this explains the relatively small proportion of severely ill or, even in general, infected patients during this pandemic32,33, a dedicated study using e.g. a matched case control, or retrospective cohort design applying our cross-reactive SARS-CoV-2 T-cell epitopes would be required.
Does this mean that the 81% who have a T cell response are completely asymptomatic or that some are while others will just have a mild illness?
MikeT provided this link last week.
https://thorax.bmj.com/content/early...nl-2020-215091
This study found that 59% of people on a cruise ship tested positive for Covid-19. However, interestingly it also revealed that 81% of those people were asymptomatic. Perhaps, these people had T cells that could fight it off as above and would probably not be revealed to have had the virus in an antibody test.
Much is being made about the apparent explosion of new cases in the USA at the moment. However, the states that are showing the large increases appear to be those that got off relatively lightly early on in the pandemic, such as Texas. There is no such spike in New York, which as we all know was previously very badly affected.
Another example to look at is South Africa. It had one of the most stringent lockdowns in the world and early on too. South Africans weren't even allowed to buy alcohol or cigarettes. They successfully suppressed the virus throughout March, April and much of May. But much good it has done them now. As the lockdown has eased, cases are now rapidly growing.
I guess the point I'm getting to is does in the end the virus have to get to around 20% of the population, who don't have some sort of immunity and then after that it will naturally tail off of it's own accord? In which case, unless a vaccine comes along before this level is reached, is lockdown a waste of time? I don't know, but it seems possible.
I don't think your conclusion from the article is correct or valid. I think you are over-interpreting what the article says. Note, however, that I am not claiming any expertise, or even any significant level of competency, in this or any associated field. (Neither am I claiming that I fully understand everything that is written in the article!)
My purpose in making this post is not to make any claims as to what the conclusions from the article should be, but rather simply to make the case that (based on my understanding) the conclusion that "up to 81% have a had some T cell response to COVID, which would mean lots of people have immunity" is not a correct nor valid conclusion to be made from the article. Certainly it is not, as far as I can see, a claim made anywhere in the article itself.
Here is a quotation from the second paragraph of the Discussion section:
"Notably, we detected SARS-CoV-2 cross-reactive T cells in 81% of unexposed individuals. To determine if these T-cells indeed mediate heterologous immunity and whether this explains the relatively small proportion of severely ill or, even in general, infected patients during this pandemic32,33, a dedicated study using e.g. a matched case control, or retrospective cohort design applying our cross-reactive SARS-CoV-2 T-cell epitopes would be required."
My understanding is that this does not mean that "81% have a had some T cell response to COVID". My understanding is that, on the contrary, these individuals have had NO exposure to SARS-CoV-2 / Covid-19. That's what the "cross-reactive" and "unexposed" parts of the quotation mean. My understanding is that "cross-reactive" means that these T cells have come about through exposure to something other other than SARS-Cov-2 (i.e., they are not SARS-CoV-2-specific T-cells). The 81% refers to the 185 individuals in the study who had NOT been exposed to SARS-CoV-2. Basically, my understanding is that what they are saying is that, of the 185 indiviiduals in the study who had not been exposed to SARS-Cov-2, 81% of them had been exposed at some time to something else which created T cells which are highly relevant and of interest in terms of the body's response to SARS-Cov-2 infection but which are not (obviously, because there has been no SARS-Cov-2 exposure) SARS-CoV-2-specific.
Neither does it mean that "lots of people have immunity" to SARS-CoV-2. It's possible that this is true, but the paper certainly does not say that this is the case. Rather, it specifically says that a dedicated study would be required to understand what the consequences of their findings are in relation to possible immunity from SARS-Cov-2 (see the quotation, above).
The study involved 180 individuals who had been exposed to SARS-Cov-2 and 185 who had not been so exposed. This seems a small sample to me if the objective of the study was to provide wide-ranging conclusions relevant to levels of infection and immunity. However, this was not the objective of the study. Rather, the objective was simply (!) to identify and characterise "SARS-CoV-2-specific and cross-reactive HLA class I and HLA-DR T-cell epitopes". (And, no, I don't claim to fully understand exactly what that means!)
Note, again, that all the above is based on my understanding. I would be happy to be corrected on any of my interpretations of what the article is saying (provided, of course, that sensible supporting evidence is provided).
I would suggest that it's also worth noting the comment at the top of the web page:
"This is a preprint. Preprints are preliminary reports that have not undergone peer review. They should not be considered conclusive, used to inform clinical practice, or referenced by the media as validated information."
It would be great if 81% of everybody had some resistance to covid-19 due to previous exposure to other corona virus’s and Prof Karol Sikora on Twitter was quite enthusiastic about this survey this morning too. I just think the high percentages infected in the two recent meat processing plant outbreaks (40% or so in Angelsea and 60% in Germany) tend to show that (even if some t-cell resistance is helping) there is still a high potential of catching and being able to spread the disease
I don't think the fact that so many caught the virus at these plants invalidates the idea that many people have some immunity to it. They will have tested everybody at these plants once it was established that there was an outbreak. But a large proportion will likely have had no symptoms. It would be very interesting to know quite how many.
Normally you would only go for a test if you were showing symptoms so we don't know how many people in the population have been exposed to Covid-19 and fought it off without realising it. They likely won't have produced any antibodies (because they didn't need to) so won't be picked up as being exposed to the virus by any antibody test.
The fact that so many people don't have symptoms is the main reason why it so infectious, many people won't realise they are passing it on.
It wasn't my conclusion. It was Prof Karol Sikora's. His conclusion as far as I am aware is not that 81% have immunity, but that many more than we are picking up from the anti-body tests.
40%? 50%? 70%...? who knows? But there's something in this.
It is early days absolutely, more work needs to be done. But it adds further information and it provides an explanation as to why a virus with a natural R assessed as over 3 and up to 5 that is rife in a population for 2 months at least before measures were put in place, only seems to have created 5-7% with anti-bodies.
Broadly speaking I think both you and WP are correct. Something is causing a lot of people who have been in contact with it to not produce anti-bodies, and the figures do not correspond with the accepted R(0) number. Until an expert comes up with a better theory to explain these irregularities, this makes a lot of sense.
I suspect that rural areas in Britain, that have had very few cases so far, will have sizeable outbreaks in the future, whilst areas like London, that have been badly hit, won't get it badly again (although there may be still be flare-ups).
In view of the all the demonstrations, raves, massing on South Coast beaches and football celebrations you would expect outbreaks breaking out around now in the areas where these people live. It will be interesting to see if this is the case, or whether the new outbreaks are confined to areas that have previously had very few cases. This will tell us if this is a valid theory, or just another blind alley.
Link to article from a couple of weeks ago that implies decline not due to immunity
https://www.imperial.ac.uk/news/1982...immunity-says/
Link to article from last week indicating herd immunity may come from a lower number of people infected than previously thought.
https://www.sciencedaily.com/release...0623111329.htm
I've also read articles that advise any immunity to this virus is short lived.
Guess we will just need to wait and see!
Imperial and oxford have made such wildly ridiculous and opposed predictions I am surprised anyone is still listening to any of them. Fantasy Ferguson resigned. He who said the swedes would have 50000 deaths if they pursued their policies. NOT.
Indeed WHO observations that some may get a second dose are far more likely to be a failure of tests.
A false positive, then later they get the disease. WHO were so invested in testing they have to say it was a double dose.
Having been vociferous in attacking government for lack of antibody tests, We now find BMJ saying that the tests are largely a waste of time. It says more about the medical professions penchant for self promotion and arguing regardless, than it does about COVID
One of the clear statements in wittons paper, is now generally accepted. That neither abbot nor Roche test are anything like as good as they claim. Even the test laboratory I used admitted it!
The first role of TCells is recognition of an invader ,so turning on immune response. Some are later involved in killing, helping etc, and later making antibodie.
The peptides in this study do indeed appear to trigger T cells in non covid patients. Far less than ex covid patients, but still significant.
Cross response is the norm we all rely on. It is why cowpox vaccine immunises against smallpox.
I think the future will show for example that South Korea succeeded despite their government action not because of it. After all - the Chinese hid it for weeks, and covid can progress assymptomatically. By the Time S korea acted they shut the stable door after the horse had come.
Could it be past exposure to other corona viruses tuning T cell response?
In science widely opposing views are the norm, I'll keep it simple for you....ask 50 scientists the same question and you get 50 different answers.
Re T cell response to Coronaviruses, it's been under review for many years, reports on immunity vary from 6 months up to 3 years, immunity to the the current Coronavirus is (obviously) under scrutiny but may be as little as a few weeks.
Until a proven/repeatable test method and outcome are available I will be keeping an open mind.
Hows the fight against the virus going in Portugal? We are hearing Brits have to quarantine when they return from holiday, maybe the relaxed lockdown we were told about wasn't such a good idea?
At least 52 answers amongst medics. Epidemiology modelling is appalling: also I have noticed before, medics don’t seem to “get” statistics or stochastic process. Even basic mistakes like assuming correlation implies cause.. They are worse than economists. The editor of lancet disagreed with himself. They write any misleading tosh to criticise the government.
The problem with some corona is mutations, which is the reason there is no lasting defence against common cold.
There is no evidence covid is mutating quickly so the jury is out but it could be many years.
Not being medically skilled on this topic, I have to use my maths/stats skills to weigh up the information we have and whilst having an open mind wouldn't you agree that the stats we have would suggest a much wider degree of infection in the public would seem likely than is indicated by the anti-body testing?
We can see how quickly it can spread in a range of situations, we can be pretty sure it was here in January and perhaps pre Xmas, and such a virulent virus, that is largely asymptomatic or mild cold like symptoms, could well have been knocking about for a month or two almost unnoticed.
I can get my head around that - there's a logic to it.
There doesn't seem to be a logic behind such a virulent virus only having got to 5-7% of the population. I can't look at the stats and work back to a way that this might have come about, because it would indicate that it wasn't so infectious if that was the case.
The anti body testing data is not robust enough at the moment to provide accurate numbers on those who have been infected or what immunity can be expected.
The statistical reports out there from the scientific community advise up to a 30% infection rate for England, others have suggested about half that, I think the govt put a figure of nearly 20% for London back in May with the rest of the country lower, but certainly more than 5%, all very interesting stuff but you know what they say about stats.
Well, no, it actually wasn't Sikora's conclusion. (And if you had referenced Sikora in your post people would have been able to check it for themselves.) It was similar in wording, but crucially different. I've now read Sikora's recent twitter posts (I hadn't seen them before I posted), and here's one (in full):
"I've said for some time that T cells were key to our immune response.
I've just read a preprint in which 81% of unexposed individuals had some T cell response.
This is significant, it could mean that lots of people have some immunity. More work to do, but v promising."
8:12 AM · Jun 29, 2020
You said "apparently up to 81% have a had some T cell response to COVID, which would mean lots of people have immunity." Your omission of the word "some" (as in 'some immunity'), and your replacement of the word "could" (as in 'could mean') with "would" (as in 'would mean'), are very important differences, as is your omission of the phrase "more work to do". (And your inclusion of the number 81% in the same sentence might have led some people to conclude that 'lots of people' meant '81% of people'.) That is, you took something which had uncertainty attached to it and removed that uncertainty completely. If you'd simply quoted Sikora in full, I'd have had no objection to your post. Clearly, there is a lot of uncertainty about what's going on with SARS-Cov-2 and it's important that we don't treat possibilities as though they were certainties. There is nothing wrong with recognising uncertainty.
Please note, I'm not trying to have a go at you. It's simply that, given how important this is, I think it's important that people don't embellish scientific findings. Some journalists do it quite regularly, of course but, surely, fell runners can maintain a higher level of integrity! (And I very much approve of your having included the link to the article. Providing references is good!)
Incidentally, I note that Sikora is keen to keep saying that people should keep following the rules - for example:
"As we ease out of lockdown, please keep following the rules. We need to keep forcing that number down."
2:54 PM · Jun 29, 2020·
"It's a stark reminder to all of us as the lockdown eases that we all have to take extra care. Wash hands, keep distance, avoid crowds."
7:56 AM · Jun 30, 2020
If you're referring to the 'lies, damned lies, and statistics' quotation, here's a good response to that, entitled "Truth, Damn Truth, and Statistics"
https://www.tandfonline.com/doi/full....2008.11889565
Here are a few extracts.
"It can be argued that in acknowledging our uncertainty and quantifying it, Statisticians are in some sense more honest in their statements about the world than others who make absolute claims. After all, we Statisticians don't claim to know things we can't know."
"What then is the source of the “damn lies” view? Statisticians are evidently taking great care to be honest, and readily admit their uncertainty. Liars usually assert their lies confidently in their striving to be believed. "
"Some people do use Statistics as part of a deliberate lie. They know they have elected a biased sample or cherry-picked results with low P-values. [...] Their use of Statistics is what Frankfurt has defined as bullshit."
There is another response to the "lies" quotation that's somewhere in the back of my mind but I can't bring it to the front. It might have been something Richard Feynman said. I might post it later if I can remember it!
More evidence seems to be emerging that a sizeable chunk of people have immunity from Covid-19, despite not having antibodies.
A Swedish study from blood donors in May, found that 30% of them had Covid-19 specific T cells. Many had no detectable antibodies - roughly twice as many as the number who did have antibodies.
Here is an article on it.
https://www.spectator.co.uk/article/...than-we-think-
Our friend Professor Sikora has also tweeted about it and linked to an article.
https://twitter.com/ProfKarolSikora/...74601108877312
This is only a small study of about 200 people so we obviously have to be careful about drawing too many conclusions. However if it was representative it would imply that certain places were getting close to herd immunity. In New York, it is estimated that 21% have produced Covid-19 antibodies so it might mean a further 40%+ have T-cell immunity. As I mentioned yesterday New York is not experiencing the large spike of infections that other states like Texas are.
Pedantic to a high level :D
Something for the forum experts to have a look at.
apparently up to 81% have a had some T cell response to COVID, which would mean lots of people have immunity.
I heard a discussion on the radio, I went to look at it, posted it here and invited more learned people than I to have a look. Not to pick over would or could :rolleyes:
My thoughts for what they are worth:
Covid 19 reacting T cells would be a more accurate description surely - and how do we know this is not cross reactivity with other Coronaviruses? And they have no antibodies, as that is an easier and more specific test - and they have not yet had Covid 19.
Most have not yet had it; whenever Covid 19 is given a chance - particularly inside with lots of vocal activity - it takes it. The idea that more must have had it is widespread, but I think its proponents under estimate the changes that most people have made to reduce their risk - partly voluntary, partly imposed.
I know the WHO have got a lot wrong, but I think their most recent report was about right.
Do remember - people without symptoms can and do spread it; 2 metres is better than 1 metre - 5 metres is better still; mixing with others inside is much riskier than doing so outside.