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Thread: Disease and pandemics thread (because it's science)

  1. #2071
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    Quote Originally Posted by Jens View Post
    And another week or so of figures (increase in deaths during the last day):

    92 3.2%
    93 3.7%
    94 3.8%
    95 3.6%
    96 3.2%
    97 3.2%
    98 2.6%

    The 2.6% is the lowest since it was on day 45, which was when it was leveling off in South Korea and starting to take off in Italy. It's still almost 5,000 people dying per day, but it's off from the peak of almost 8,500 registered ten days ago. I suppose it's a sign that the social distancing is having some effect.
    Here is the latest batch:

    99 2.0%
    100 2.7%
    101 4.7%
    102 2.9%
    103 2.6%
    104 3.8%
    105 0.4%
    106 1.6%
    107 1.7%

    Again, it has gone down in general. There is a glitch, where there was a large jump on day 104, followed by a really small increase on day 105, but apparently that was because the US misreported and then fixed it the next day, so that the US ended up with a negative death count on that day.
    As above, so below

  2. #2072
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    Quote Originally Posted by Jens View Post
    Yes, I didn't write that directly because I was trying to be polite. I sort of meant that, in the sense: if I am on a train and there is somebody who smells like cigarettes, I will tend to avoid sitting next to them. So it is possible that they maintain more distance, perhaps passively rather than actively. And hence are less prone to being infected. But is just one confounding factor to the idea that smoking may protect you from COVID.
    As a recent sinner, I didn't see the need to be polite. It's a journey of self discovery and home truths. The unfortunate part is, as a smoker you really can't smell it. Other smells are fine, but until you stop for a few days, the smell of stale smoke and ash trays is nonexistent. It's very strange and shocking when you realise.(at least for me it was).

  3. #2073
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    According to Worldometer, only 750 Covid deaths in the USA yesterday. That's the lowest since March 29.

    They use a day based on GMT and it's always lower on Sundays because of reporting, but still kind of good news. Now we just need to hope that the reopenings don't create a second wave. My small county had it's first new case in several weeks a couple of days ago; a 90-year-old person.
    Cum catapultae proscriptae erunt tum soli proscript catapultas habebunt.

  4. #2074
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    Not sure about that figure, 750, is it right?
    sicut vis videre esto
    When we realize that patterns don't exist in the universe, they are a template that we hold to the universe to make sense of it, it all makes a lot more sense.
    Originally Posted by Ken G

  5. #2075
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    There is one, and only one strain of SARS-CoV-2:
    There is only one strain of SARS-CoV-2. The first virus isolate, taken from a Wuhan patient in December 2019, is the same strain as the most recent isolate taken anywhere else in the world in May 2020. So far no one has shown that any of these virus isolates differ in any fundamental property. I can hear some of you shouting, but isn’t a nucleotide change enough to make a strain? The answer is a resounding NO. Every virus expelled by an infected individual differs from the next by many base changes. It would be foolish and of little utility to call each patient isolate a strain. That term is reserved only for special changes that confer a new property to the virus.
    Explainable via the founder effect:
    There is no doubt that viruses with the D614G change are emerging in different geographical regions of the world. Until proven otherwise, their emergence is likely due to the founder effect. Let’s say a virus with D614G emerges during replication in a person’s respiratory tract. If viruses with that change infect the next person, and the next, and so on, then the D614G change will predominate. The change is simply a single nucleotide polymorphism of little consequence. It is the noise produced by error-prone RNA synthesis by the virus. Viruses with D614S are simply virus isolates. They are not strains of SARS-CoV-2.
    Absence of a selective pressure:
    For an amino acid change such as D614S to be positively selected, as opposed to being maintained as a consequence of the founder effect, requires selective pressure. For such an already highly transmissible virus, the nature of such selection pressure is difficult to discern.

  6. #2076
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    Interesting news report from Australia on yet another batch of unusable serotology (antibody) tests here.

    The more technical comments about antibody tests in general are quite a surprise however (see emboldened quotes below):

    "The reality is, at the moment, they are not useful," said Professor Carola Vinuesa, one of the authors of the government report and co-director of the NHMRC Centre for Personalised Immunology at the Australian National University.

    "At the moment, the quality does not seem to be good enough for these tests to be deployed in large scale."

    "The sensitivity is not very good. They are not useful in being able to say 'you were infected'."

    Professor Vinuesa said no test currently developed was accurate enough to reliably detect antibodies.

    "Most individual results will be false positives," she said. "You cannot have most positive results being false."

    A spokesman later said the government ended up buying only 1 million tests, after a third supply contract was cancelled.

    "These tests have been purchased as they may have a role to play in population level serosurveillance," the spokesman said.

    The current COVID-19 test, known as PCR, can only tell if a person is currently infected. Antibody tests are considered crucial by epidemiologists because they will give, for the first time, a true estimate of the number of people who have caught COVID.

    But they are extremely difficult to make 100 per cent accurate.

    Antibody levels can vary significantly between people, with some having very low levels. In addition, the tests may also pick up antibodies to other viruses that are similar to COVID-19.

    "That gives the potential we are identifying people who have just been exposed to the common cold," said Professor Ivo Mueller, head of immunity at the Walter and Eliza Hall Institute.

    Professor Mueller's team is currently trying to make their own accurate antibody test - a process that is proving difficult.
    So, from this, one is left with the impression that both the the specivity and sensivity of Covid-19 serotology tests seem to not satisfy their intended purpose (which is unsettling .. in the least)?

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    Quote Originally Posted by Selfsim View Post
    Interesting news report from Australia on yet another batch of unusable serotology (antibody) tests here.

    The more technical comments about antibody tests in general are quite a surprise however (see emboldened quotes below):

    So, from this, one is left with the impression that both the the specivity and sensivity of Covid-19 serotology tests seem to not satisfy their intended purpose (which is unsettling .. in the least)?
    I've been thinking this for some time. All these countries that are so confident about identifying, tracking and tracing are on thin ice. Their figures could be completely off. What good is a million tests a day if the results are worthless?

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    Quote Originally Posted by headrush View Post
    I've been thinking this for some time. All these countries that are so confident about identifying, tracking and tracing are on thin ice. Their figures could be completely off. What good is a million tests a day if the results are worthless?
    Need to be a bit careful here. The article I posted was about antibody testing, which is conducted out of an attempt to get a rough approximation/sampling of the likelihood of past infections across a given population. It may well be that Australia doesn't have enough of sufficient population densities to achieve statistically meaningful epidemiological results specifically for SARS-Cov-2 past infections via currently available serolotology (antibody) tests. (I'm guessing here). The tests they rejected in Australia may achieve more meaningful results if used across more numerous, more geographically confined (and thus higher population densities) in other countries like the US, China, UK, etc (I don't know though).

    The PCR-RT swab tests however, which are used to identify the presence/absence of active SARS-Cov-2 virus infections are way more precise and when administered correctly, should produce way more accurate results in any given population. If these tests were administered to the level of 'a million tests a day', then I would pay very close attention to those results!

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    Quote Originally Posted by headrush View Post
    I've been thinking this for some time. All these countries that are so confident about identifying, tracking and tracing are on thin ice. Their figures could be completely off. What good is a million tests a day if the results are worthless?
    As Selfsim wrote, testing is mostly done with PCR rather than antibody testing. Antibody testing seems (from what I've seen) to be mostly used to randomly test people to see how many have been exposed (because you don't have to know you were sick to have antibodies). And tracking has another dimension, which is to trace possible contacts of a person who is known to have the disease and isolate them to prevent others from being infected.
    As above, so below

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    Just for the record, (and not that anyone should care), but I've now slightly changed my views about the potential infectiousness of patients testing positive (PCR test) during their recovery phase.

    The impacts, from an infection viewpoint, of what is being 'shed' during the final phases of a viral infection can in fact, vary widely in its effects, from enhancing or inhibiting, (speeding up or slowing down) the rate of subsequent host infection. This then legitimises scientific speculation about the possibility of naked virus particles surviving and propagating subsequent infection, without a membrane. This may or may not apply in the case of the SARS-CoV-2 virus infection (Covid-19).

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    Well, I'm getting confused here. I thought the pcr tests were ineffective because they gave false positives and could not distinguish between infected and contagious or used to be infected but no longer contagious.
    The cultured tests were, I thought, the only way to determine who was actually contagious. I think I confused the tests for antibodies with the cultured test.

  12. #2082
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    Quote Originally Posted by headrush View Post
    Well, I'm getting confused here. I thought the pcr tests were ineffective because they gave false positives and could not distinguish between infected and contagious or used to be infected but no longer contagious.
    The cultured tests were, I thought, the only way to determine who was actually contagious. I think I confused the tests for antibodies with the cultured test.
    PCR--tests for presence of SARS-CoV-2 RNA. In patients with symptoms, a good indication that they have the disease. In patients who have recovered from the disease, now demonstrated to be misleading as to their infectiousness, because a fragment of viral RNA that will trigger a positive PCR is not the same thing as an infective virion.

    Viral culture
    --demonstrates presence of infective virions. (Journalists have confused the picture by calling a postive PCR test combined with no growth on culture as a "false positive". In fact, it's very likely to be a true positive for the thing it's designed to detect. It just doesn't detect the most important thing about infectivity.) Viral culture is tricky and time consuming, and therefore not suitable for quick diagnostic testing of symptomatic individuals. Hence our reliance on PCR, which (in symptomatic individuals from a population in which the disease is reasonably prevalent) has low false positive and false negative rates.

    Antibody tests
    (= "serology")--many different tests, looking for antibodies to various SARS-CoV-2 binding sites, have been developed. Their sensitivity and specificity (ability to reject false negatives, ability to reject false positives) are still being tested. Many perform poorly. They can be used for two different purposes:
    1) Serosurveillance--monitoring the extent of previous infection in a large population. This doesn't require an extremely precise test, so long as the sensitivity and specificity are well understood--one can adjust for false positives and false negatives and come up with an order of magnitude estimate for the prevalence of antibody in the population, sufficient to help understand disease transmission and guide the release of lockdown. It's important that you make no judgements about an individual's health status on the basis of this sort of surveillance testing, however, because they could easily fall into a false negative or positive category.
    2) "Immunity Passport"--testing the immune status of a single individual. In this setting, the test needs to be extremely specific, particularly if the prevalence is low. Otherwise any positive test is more likely to be a false positive than a true positive. No tests currently being produced provide the necessary level of precision, and the WHO and numerous national health authorities have cautioned politicians repeatedly against "immunity passport" testing.

    Grant Hutchison

  13. #2083
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    Grant- That was a nice summary, thanks.
    The media has recently been talking about antigen testing. Is that something different?


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    Quote Originally Posted by Selfsim View Post
    Just for the record, (and not that anyone should care), but I've now slightly changed my views about the potential infectiousness of patients testing positive (PCR test) during their recovery phase.

    The impacts, from an infection viewpoint, of what is being 'shed' during the final phases of a viral infection can in fact, vary widely in its effects, from enhancing or inhibiting, (speeding up or slowing down) the rate of subsequent host infection. This then legitimises scientific speculation about the possibility of naked virus particles surviving and propagating subsequent infection, without a membrane. This may or may not apply in the case of the SARS-CoV-2 virus infection (Covid-19).
    Most viruses need the transcription enzymes they carry within their capsid to enter the cell along with them, so their isolated genetic material is not infective even if it is placed inside a cell.
    Postive-sense RNA viruses don't require transcription, because their RNA looks like cellular mRNA, so they don't need to carry their own enzymes. If their intact genome is purified and artificially injected into a cell in the laboratory, it can latch on to ribosomes and start churning out virions, rendering the cell infective. But I've seen no evidence that intact viral genomes are shed by convalescent individuals, and no evidence that viral RNA alone (in the absence of a virion to inject it into a cell) has caused infections "in the wild". Do you have any references demonstrating this?

    If such a thing did occur, we'd pick it up by viral culture, and correctly classify the affected individuals as being infective.

    Grant Hutchison

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    Quote Originally Posted by Extravoice View Post
    Grant- That was a nice summary, thanks.
    The media has recently been talking about antigen testing. Is that something different?
    An antigen is the thing to which an antibody binds. People have been loosely distinguishing between "antibody tests" (tests to see if you have been exposed to viral antigens and developed immunity) and "antigen tests" (tests for the presence of parts of the virus, particularly the PCR test for viral RNA).
    Antigen test--Have I got the disease?
    Antibody test--Have I had the disease?

    Grant Hutchison

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    Quote Originally Posted by grant hutchison View Post
    An antigen is the thing to which an antibody binds. People have been loosely distinguishing between "antibody tests" (tests to see if you have been exposed to viral antigens and developed immunity) and "antigen tests" (tests for the presence of parts of the virus, particularly the PCR test for viral RNA).
    Antigen test--Have I got the disease?
    Antibody test--Have I had the disease?

    Grant Hutchison
    Thanks Grant, very helpful information.

    Is there much difference in the way the sample is collected for each of your examples?
    Is a swab test more likely to be PCR or can viral culture be done that way too?
    I'm guessing serology requires blood.

    Thanks

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    Quote Originally Posted by headrush View Post
    Thanks Grant, very helpful information.

    Is there much difference in the way the sample is collected for each of your examples?
    Is a swab test more likely to be PCR or can viral culture be done that way too?
    I'm guessing serology requires blood.

    Thanks
    Yes, blood for serology, secretion swabs for PCR in COVID-19. Blood is where the immunity is, airway secretions are where the prime infective risk is. And there's early evidence that most people with secretions swabs that test positive for SARS-CoV-2 RNA don't show a positive PCR test on their blood. That's an interesting result, since some of the other coronaviruses do commonly cause viraemia (virus in the blood) during infection. But I know labs in the UK are still treating blood samples from COVID-19 patients as "high risk"--that is, as a source of potential infection.
    Notice (from my link) that some patients are excreting viral RNA in their faeces. Last time I looked, there was no convincing evidence that this was a significant route of infectious transmission, but it does hold out the possibility of an effective population surveillance method. PCR is extremely sensitive at detecting minute quantities of RNA, so checking sewer swabs regularly has the potential to flag up parts of a town in which someone has the infection, after which the sewer tree can be traced back upstream. There's work being done on developing that approach now. (The UK Prime Minister managed to cock this up and cause a mild panic recently, by getting confused about the difference between the sewage drainage system and the water supply. Mistakenly suggesting that the water supply might be contaminated with SARS-CoV-2 wasn't a great reassurance to anyone.)

    Grant Hutchison

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    Thanks again Grant. It's interesting that the authors of the report you linked suggest that samples taken from multiple sites might reduce the false negatives and improve the sensitivity.

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    It's certainly important to be able to know the fraction of people from any population you can randomly select from (it doesn't have to be the entire population, subpopulations work too) that have been infected, since then all you have to do is divide that fraction from the fraction of people in that same subpopulation that have died of COVID-19, and poof, you have the death probability from infection within that subpopulation. It would seem the easiest thing in the world to do, and of huge importance. So has anyone seen this done, and if not, why not?

    I've seen exactly two examples-- the claim by the Governor of New York that about 20% of people in New York City had been infected, and a study in Santa Clara county that said about 5% there had been infected. I also saw a claim by Swedish epidemiologists that 20% of Stockholm had been infected, but they did not say how they knew that or what subpopulation was sampled, so I won't count it. The subpopulations that we do have some information about were, for NYC, people in supermarkets, and in Santa Clara, people who answered a request (framed as a way to tell if they had been exposed, which clearly skews the respondents toward people with concern that they had indeed been exposed). The problem is, it is hard to know what fraction of those subpopulations died, because you can't ask someone if they died or not. The best you can do is assume the subpopulation is randomly sampled from those same places, NYC and Santa Clara county, and then look up the deaths there. I mentioned the outcome of that exercise above, but I'm not clear on what is regarded as forbidden speech on this forum, so I won't repeat the results. Suffice it to say that the fraction who get infected that die is obviously the single most important number you can know, because it informs the drawbacks of herd immunity strategies. That's why I find it so odd that, by now, that probability, for various subpopulations, does not feature prominently in all discussions about this disease. I don't think we can inform any policies until we have a handle on that simple number.
    Last edited by Ken G; 2020-May-13 at 04:02 PM.

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    Quote Originally Posted by headrush View Post
    Thanks again Grant. It's interesting that the authors of the report you linked suggest that samples taken from multiple sites might reduce the false negatives and improve the sensitivity.
    Stacking multiple tests is a general way of improving reliability. Hence the commonly used discharge criterion of "two negative PCR tests in succession" for hospitalized COVID-19 patients. Two false negatives in succession is less likely than a single false negative.

    Grant Hutchison

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    Quote Originally Posted by grant hutchison View Post
    ... In patients who have recovered from the disease, now demonstrated to be misleading as to their infectiousness, because a fragment of viral RNA that will trigger a positive PCR is not the same thing as an infective virion.
    My point all along has been that viral RNA contains all the information needed for it to become infectious. I have seen nothing which detracts from the implications of that.

    In fact, there are processes already known which enable it to go forward propagating as an active, infectious virion.
    The notion that viral RNA 'is not the same thing as an infective virion', when taken in isolation might be so .. merely by virtue of the respective definitions of 'virion' and 'RNA', but that is a trivial point in comparison with the potential for regenerating infection via these already known processes.

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    Quote Originally Posted by Ken G View Post
    It's certainly important to be able to know ..
    Its always good to see the scientific approach returning to a science thread in a science forum.

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    Quote Originally Posted by Selfsim View Post
    My point all along has been that viral RNA contains all the information needed for it to become infectious.
    And I've understood your point all along. I just remain unconvinced that your definition of "infectious" has any relevance to the real world of infectious diseases transmitting in nature, since it seems also to require that a printout of a viral genome should be viewed as something that can "become infectious".
    I'm always willing to examine evidence, though. Until that's offered, I'm not going to go around this house again.

    Grant Hutchison
    Last edited by grant hutchison; 2020-May-14 at 01:16 AM.

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    Quote Originally Posted by Selfsim View Post
    My point all along has been that viral RNA contains all the information needed for it to become infectious. I have seen nothing which detracts from the implications of that.

    In fact, there are processes already known which enable it to go forward propagating as an active, infectious virion.
    The notion that viral RNA 'is not the same thing as an infective virion', when taken in isolation might be so .. merely by virtue of the respective definitions of 'virion' and 'RNA', but that is a trivial point in comparison with the potential for regenerating infection via these already known processes.
    What already known processes are you talking about? Normally the viral RNA cannot enter the cell without the virion proteins to latch to a receptor and allow the RNA to be inserted. Do you mean that the RNA can enter a cell by itself?
    As above, so below

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    Quote Originally Posted by Jens
    What already known processes are you talking about? Normally the viral RNA cannot enter the cell without the virion proteins to latch to a receptor and allow the RNA to be inserted. Do you mean that the RNA can enter a cell by itself?
    Look, I find there are misleading, yet seemingly authoritative statements being made in this thread, which I care to challenge for the sake of clarity and further learning.


    Some examples are:

    i) ’In patients who have recovered from the disease, now demonstrated to be misleading as to their infectiousness, because a fragment of viral RNA that will trigger a positive PCR is not the same thing as an infective virion’.

    No process explanation has been given as to just how a positive PCR-RT result is triggered by ‘a fragment of viral RNA’.
    The PCR-RT test process specifically contains a step which aims at disposing of potential contaminants in an isolate .. so some explanation is called for here.

    ii) ’But I've seen no evidence that intact viral genomes are shed by convalescent individuals,

    Immune mediated cell killing involves apoptosis, an ordered shutdown that does not involve uncontrolled release of Damage-associated molecular patterns (DAMPs) and Pathogen-associated molecular patterns (PAMPs), amongst other things.

    If tests detect viral RNA, then it is coming from an active infection - either virions or infected cells. In the context of virology, ‘shedding’ does not refer to ‘fragments’ of viral RNA.

    iii) ’Most viruses need the transcription enzymes they carry within their capsid to enter the cell along with them, so their isolated genetic material is not infective even if it is placed inside a cell.’

    This is the first time the term ‘capsid’ has been used and yet, it is key to discussions on the process of infection.

    iv) ’and no evidence that viral RNA alone (in the absence of a virion to inject it into a cell) has caused infections "in the wild" ‘

    Some naked viruses, (non-enveloped, capsid enclosed RNA .. and I’m not referring to coronaviruses here), can leave cells via an alternative route involving enclosure in fully host-derived lipid bilayers containing both proteins and RNA.

    The exact combination of virions and host-derived molecules, in these cases, determines how these virus-containing particles spread infection and/or trigger antiviral immune responses.

    There is also some evidence that viruses evolved on multiple, independent occasions throughout the course of evolution by the recruitment of diverse host proteins that became major virion components. That being said, it is generally accepted that the origin of the first true viruses is still inseparable from the emergence of viral capsids.

    The above statements come from numerous reputable sources. Some, or none, may be relevant to how Covid-19 progresses and there are aspects not yet known about how this infection proceeds (and under what specific circumstances). I choose to read from reputable source materials rather than singular forum voices, (not wanting to take anything away from those voices). Sometimes the two sources do not connect .. and that forms the basis of valuable learning ground.

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    Quote Originally Posted by Selfsim View Post
    Look, I find there are misleading, yet seemingly authoritative statements being made in this thread, which I care to challenge for the sake of clarity and further learning.
    i) The PCR tests detect specific conserved sequences of viral genome, not the entire genome (which of course we know is subject to a degree of variability). PCR can't tell an intact genome from a fragment containing a conserved sequence.
    ii) No evidence to rebut my point, plus an unsupported claim. Free RNA is fragile, and degrades steadily over a period of days until it is undetectible by PCR because even the short conserved segments have all been broken. But the very first break in the genome strand stops it being a genome.
    iii) I believe it was not the first time I used the word "capsid". If it was, a request for clarification would have produced an explanation.
    iv) No evidence to rebut my point. It doesn't even seem relevant.

    Frankly, your objections are half-baked at best. If you care to post actual research in future, I'm willing to discuss it. I'll also respond to clear requests for clarification, and will acknowledge any errors brought convincingly to my attention. But I've no intention of responding to any more unfocussed sniping from the sidelines, or any of these belated, tangential and vague post hoc objections.

    Grant Hutchison

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    Disease and pandemics thread (because it's science)

    Thread closed pending moderator discussion.

    Thread reopened...but please read this before posting.

    This thread has been of concern to the moderation team for some time. We want discussion of mainstream science. We do. However, considering the sensitive nature of the current situation and with so much uncertainty about the science of COVID-19 at this point, we feel it must be as mainstream as it can be, with as little misinformation as can be achieved. The mainstream is squarely in CQ's remit, after all.

    To that end, we can't have endless arguments against what appears to be mainstream medical information just because they think they know better than a professional. They aren't helpful. We have a member we can view as an ‘expert witness’, if you will. That is, it isn't a fallacious appeal to authority if the authority has relevant expertise in the field and their statements comport with other expert sources. That doesn't mean that all experts have to agree nor does it mean the 'testimony' is unassailable. But let's be clear: ask questions if you need to but endlessly arguing against such information based on one’s lay interpretation of medical information (from sources named or unnamed, reputable or not) is tantamount to—if not actual—ATM advocacy.

    We know that some/many/most who favor unrestrained discussion of matters scientific will disagree with this stance. We understand. You're not wrong, in the general. It's just not right for this venue.
    Last edited by PetersCreek; 2020-May-21 at 02:57 PM.
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    Some good news: It looks like recovered patients are no longer infectious.


    https://www.google.com/amp/s/www.for...nfectious/amp/


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    Quote Originally Posted by Extravoice View Post
    Some good news: It looks like recovered patients are no longer infectious.


    https://www.google.com/amp/s/www.for...nfectious/amp/
    Looks like a nice epidemiological follow-up to South Korea's original work, taking viral cultures from those with persisent PCR positive tests, which they reported about three weeks ago.

    Grant Hutchison

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    Quote Originally Posted by Jens View Post
    Here is the latest batch:

    99 2.0%
    100 2.7%
    101 4.7%
    102 2.9%
    103 2.6%
    104 3.8%
    105 0.4%
    106 1.6%
    107 1.7%

    Again, it has gone down in general. There is a glitch, where there was a large jump on day 104, followed by a really small increase on day 105, but apparently that was because the US misreported and then fixed it the next day, so that the US ended up with a negative death count on that day.
    Here are the latest figures. It rose to over 3%, but then has gone back down to under 2% per day. The last figure is dodgy, because there are no cases or deaths reported from the US (presumably some reporting glitch), and France recorded a minus death count, so it must have been a recalculation of some type.

    108 2.6%
    109 2.1%
    110 2.5%
    111 3.2%
    112 1.7%
    113 1.5%
    114 1.5%
    115 1.6%
    116 1.7%
    117 1.8%
    118 1.8%
    119 1.4%
    120 1.4%
    121 0.8%
    As above, so below

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