No salvation in the denominator

As I mentioned before, doofi at Oxford have suggested  that vast number of people have already contracted coronavirus, and that the fraction of those infected that become ill is thus much smaller than it looks.  There was never any chance of this. PCR positivity rates were not high, and in a fast-growing epidemic, most cases would be new enough to be PCR-positive.

Now, a new study shows that this notion is not correct. ” 164 close contacts tested by PCR and serology. 16/164 of contacts PCR+ & all PCR+ also serology+. Additional 7/164 were serology+ but PCR-.”

There are some people that have contracted disease and don’t show up on PCR – but not many.

 

 

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58 Responses to No salvation in the denominator

  1. Maciano says:

    Greg,

    Is there something about this virus what makes it so contagious? There are a lot of lockdown-ish measures in Europe and you still see quite a lot of new daily cases.

    Also, I don’t get why certain places seem to become so problematic so fast; South Tirol, Bergamo, Madrid, Brabant, NR Westphalen, New Rochelle, Wuhan. It’s like the virus can survive in certain places for some time, outside the human body, without getting damaged.

    From the get-go I’ve been quite surprised how fast this thing spread around. Much faster than ebola or zika AFAICT.

    • Lee-Hsung Wang says:

      the explosion in specific places might not have much to do with specific places [except that many of these places have a lot of international travel and high population] but simply the logic of earlier infection + exponential growth.
      Even for those with experiences with exponential curves it is often hard to understand what this intuitively means; exponential growth plus random time lagged seeding will give you these sudden hotspots.

      • Reader506 says:

        My thoughts exactly. The “random time lagged seeding” is potentially more variable than one might think since the virus doesn’t have to spread at a constant rate, and the early stages can be more variable over time. The first infection might only infect one other person, who in turn might only infect one as well, until finally after 10-15 days the virus makes it to a gathering where it can get 5 people in one shot and spreading really begins In contrast a sick person might arrive in NY City and and infect 20 people in 2 days riding the subway.

      • Maciano says:

        Thnx, yes. It must be.

        Even more reason to start mass and fast testing everyone constantly

  2. dearieme says:

    I’m not surprised by how easily it spreads. I’m more surprised that in many places it seems to be somewhat less deadly than I’d have guessed from the actions of the Chinese government. Perhaps LHW’s explanation holds there too.

    I assume the German figures to be an artefact: I hope I’m wrong because if they aren’t then we should all learn from Germany. Although, I caution myself, it’s early days yet.

    P.S. I’ve received my first e-mail from a business urging me to pay my account swiftly because they’ve had to close down (except the accounts office, apparently). I will: I have every sympathy with their plight.

    • Anonymous says:

      The main route of transmission into Germany were young ski vacationers, probably with younger-than-average social circles. So, it’s very likely an artefact of disproportional infection of younger people in the beginning.

    • reiner Tor says:

      What makes you think it was not deadly? Actually it seems deadlier now than two months ago. Back then I thought mortality would be around 1% – with an intact and efficient healthcare system. (It was already clear back then that once hospitals get overwhelmed, it would be a different story.)

      Now it seems to be closer to 2% rather than 1%, in Korea there are still unresolved cases and their mortality rate of all cases so far has slowly inched up to above 1.5%, and will probably reach 2% over time. Which is pretty bad, even if most of those killed are in less than stellar health.

      • dearieme says:

        I’m mildly surprised that 1%-2% was enough to terrify the sort of regime that earlier murdered people by the tens of millions. Maybe that’s because it’s a somewhat different regime nowadays.

        • reiner Tor says:

          I would guess the regime would prioritize the survival of 66-year-old males randomly killed by disease to a much higher extent than distant peasants. So that might have been one factor.

          Another factor is that, of course, 1-2% is only true as long as the healthcare system is still intact and efficient. Which is not going to be a case once the epidemic reaches a significant part of the population – it seems that a breaking point has already been reached in Lombardy or at least locally in and around Bergamo, and probably Wuhan or some parts of the city were there for a week or two in late January and early February as well.

          So probably mortality would’ve been around 5%, and would’ve endangered the life of a certain 66 year old guy, who just happened to call the shots. Even if he were Mao Zedong, that latter part might’ve been enough, but he’s probably no Mao Zedong.

          By the way, is there any evidence that an epidemic with a 5% mortality rate (after the breakdown of the healthcare system) is less ruinous economically than a total lockdown? I have yet to see evidence of this. I would guess that the economy would go down the toilet anyway. For example other countries might close your borders for you, even if you don’t. This would cripple your tourism and airlines. Internal tourism and air travel (as well as railways) would suffer because panic would set in, and people would avoid travel. Other countries will also go into lockdown even if you don’t, so your economy would be pulled down by them anyway. Even internally, restaurants would close for lack of patrons, but perhaps not before some of the best star chefs would die of Covid-19. People would avoid going to work (they could report sick – there’d be no-one to check if it’s true or not; also, being sick often takes several weeks with this disease, even for those who would eventually recover), or they would just simply fall sick or even drop dead on the job, preventing them from doing work, so even crucial industries like nuclear plants might stop working (with potentially catastrophic consequences, at least in the case of nuclear plants), or be at risk of breaking down. Since some of the most experienced and highly trained professionals and managers in lots of industries would die, this would wreak longer term economic havoc. Healthcare itself is providing some 5-10% of GDP in most countries (in the US it’s 17%), its breakdown might affect its long-term performance, especially after lots of doctors drop dead from the disease (due to high viral load).

          Apropos, high viral load. Probably ordinary people would get higher viral loads in the absence of some kind of lockdown measures. Grocery store clerks, for example, but lots of others, too, since there’d be more chances of picking it up from any surface, and SARS-CoV-2 would be ubiquitous, there’d probably be lots of infections where people would pick it up from more than a single source. So mortality could get higher still. Also, without a lockdown (which, to be sure, each country has imposed or will soon impose – no politician is going to be so stupid to just watch several percentage points of the population drop dead in chaotic conditions), the virus is going to evolve into a more virulent version. (It’s purely hypothetical, to repeat, because even Iran closed the shrines and stopped Friday prayers, just like Saudi Arabia canceled the Hajj.)

          So it’s not 1-2% mortality (of mostly economically unproductive people) which is the most frightening (though it’s frightening in itself, and could cause lots of damage, not least of all to a certain 66-year-old), but the secondary effects etc., which might result in something way worse.

          To repeat the most important point, what I outlined above is purely hypothetical. I cannot imagine a government which doesn’t introduce at least some kind of moderate lockdown in the face of this. There’s been a lot of noise from Trump about reopening the economy by Easter etc., but I don’t think it will happen. Trump will stare into the abyss, the chaos and the dead, and the abyss will stare back at him. There’s no way he’ll reopen the economy until the epidemic is under control.

  3. Just saying says:

    There are cases where people infected with coronavirus repeatedly test negative on PCR, with the occasional intermittent positive result.

    https://www.researchsquare.com/article/rs-17319/v1

    They say this may be related to the stage of the disease and/or the viral load. It was noted that in early stages, when viral load is low, the test may give a false negative. Might this also apply to late, post recovery stages?

    Is it possible that people are stuck in a no mans land where symptoms have receded, virus is still present at a low level (missed by PCR), but antibody test still shows negative?

    It has been speculated that the disease severity may depend on infectious dose.

    If so, might there be essentially two versions of the disease?

    A high infectious dose version found in medical facilities, care homes, etc. This is the one that is having a deadly effect on young and healthy medical workers.

    And a infectious dose version, spreading in parallel, through more casual contact?

    With SARS 1, there was a correlation between initial viral load and disease severity.

    https://www.cmaj.ca/content/171/11/1349

    Same mechanism is suspected with SARS 2

    What happens to healthy people who get infected with the lowest possible initial infectious dose? Can PCR and serology tests detect a person like this? Is he immune after recovery?

    • Ben says:

      PCR has a poor sensitivity to begin with so yes, its usefulness is limited in mildly symptomatic individuals.

      Seroconversion seems to take 7-11 days after infection in the case of COVID-19, i.e. it’s mostly useless for acute illness, but it should be useful for detecting immunity (assuming there’s protective immunity after recovery).

      People who actually develop pneumonia are also investigated via CT imaging which seems to have much better sensitivity than PCR (but is less specific). PCR followed by CT should be able to distinguish COVID-19 related pneumonia in most.

      • Serology Lag says:

        Current evidence provides a longer lag

        https://www.medrxiv.org/content/10.1101/2020.03.23.20041707v1.full.pdf“Results The seroconversion rate for Ab, IgM and IgG in COVID-19 patients was 98.8%
        (79/80), 93.8% (75/80) and 93.8% (75/80), respectively. The first detectible serology
        marker is total antibody and followed by IgM and IgG, with a median seroconversion
        time of 15, 18 and 20 day post exposure (d.p.e) or 9, 10 and 12 days post onset,
        separately. The antibody levels increased rapidly since 6 d.p.o and accompanied with
        the decline of viral load. For patients in the early stage of illness (0-7d.p.o),Ab showed
        the highest sensitivity (64.1%) compared to the IgM and IgG (33.3% for both,
        p<0.001). The sensitivities of Ab, IgM and IgG detection increased to 100%, 96.7%
        and 93.3% two weeks later, respectively. “

        Rather than about 8 days post infection (which is about the lag time to symptoms, if there are any?), about 2-3 weeks.

        Deaths and serologically estimated total prevalence are thus somewhat comparable (about same time lag to initial infections, barring perhaps a 2-3 days in the balance).

        (Death – https://wwwnc.cdc.gov/eid/article/26/6/20-0320_article“However, given the critical need to consider time lags to death when calculating case-fatality risk (3), we used time lags from a recent study from China (4). Yang et al. (4) reported that the median time from symptom onset to radiological confirmation of pneumonia was 5 days (interquartile range [IQR] 3–7 days); from symptom onset to intensive care unit (ICU) admission was 11 days (IQR 7–14 days); and from ICU admission to death was 7 days (IQR 3–11 days). Therefore, a median of 13 days passed from pneumonia confirmation to death ([11–5] + 7 = 13).”)

        That’s neat it means you can just go:

        (Known Deaths in Area)/((Serological prevalence in area)*(Total Pop of Area)),

        to generate an estimate of true IFR for that region (then once you have a bunch of regions you can regress on median age to get a rough age adjusted true IFR at true national median age). Without having to worry about estimating back serological prevalence another 7 days.

        Notwithstanding low bound false positives.

    • reiner Tor says:

      If symptoms depend that much on viral load, then herd immunity might just be the worst idea ever. Because the more freely the virus roams the land, the more frequent high viral load infections (or infections from multiple sources) will be.

    • Just saying says:

      New article from science-y people arguing that the volume of exposure is likely to be linked to symptom severity.

      “Small initial exposures tend to lead to mild or asymptomatic infections, while larger doses can be lethal.

      From a policy perspective, we need to consider that not all exposures to the coronavirus may be the same. Stepping into an office building that once had someone with the coronavirus in it is not as dangerous as sitting next to that infected person for an hourlong train commute.

      This may seem obvious, but many people are not making this distinction. We need to focus more on preventing high-dose infection.”


      “Low-dose infections can even engender immunity, protecting against high-dose exposures in the future.”

      People should take particular care against high-dose exposures, which are most likely to occur in close in-person interactions — such as coffee meetings, crowded bars and quiet time in a room with Grandma — and from touching our faces after getting substantial amounts of virus on our hands. In-person interactions are more dangerous in enclosed spaces and at short distances, with dose escalating with exposure time. For transient interactions that violate the rule of maintaining six feet between you and others, such as paying a cashier at the grocery store, keep them brief — aim for “within six feet, only six seconds.”

      This may represent a hidden benefit of living in the suburbs with only a few people in your home and practicing social distancing. You might get it through brief casual contacts, but unless you are particularly vulnerable, you’re liable to get a small dose and only spread a small dose to others.

      It may also help explain lower death rates in German speaking areas of Switzerland, compared to French and Italian speaking areas.

      Would be an interesting and positive coincidence if true, since social distancing is a good fit for a disease with this characteristic. On the other hand, it means we really shoulda had masks, even if they weren’t perfect ones.

  4. AJD says:

    Greg,

    I’ve been following your analysis (and that of others), and I’m fully in agreement that this one is a serious risk, and worth the extreme measures to try to stomp the effective R0 down below 1. Once we’ve done that, and the spread drops off, is it practical to reduce said distancing measures (before a vaccine), or would COVID-19 just return full-force? With a natural R0 > 2 and close to 1m confirmed infections worldwide already, it seems unbelievable that we’d be able to kill it off completely (a la SARS and MERS). Am I wrong there? Is it practical to kill it pre-vaccine?

    If not, Is there some system of testing, tracing, monitoring, etc. that could believably keep effective R0 <= 1 for many months?

    • gkai says:

      Obviously it’s not 50% in the UK. Not even in Italy.
      But as obviously, the detected cases are not the whole story. It can not, else given that many countries are still in the exponential growth phase, and that there is multiple doubling time between contamination and death, you don’t get death rate by diving total reported dead by total detected cases.
      This death(t)/contamination(t) ratio is skewed, the death rate is something like death(t)/contamination(t-T_sick).

      So what is the actual contamination at this time, in the UK for example. It is between detected cases (22000) and crazy model assumption (33000000), but where?

  5. gothamette says:

    I thought that the “half the population is already infected” folks were basing it on infection earlier than December 2019 (in the West). This is a lie.

    There’s a lot of crap on the ‘webs about much earlier infection, with ppl testifying about dry coughs in October. These are made-up symptoms.

    • swampr says:

      I thought it was interesting that Italian doctors said they’d seen unexplained pneumonia as early as October. The nextstrain.org link you posted convinced me otherwise. Wuhan was clearly the spreading center, even if Italy was very early. Supposedly most Italian cases trace back to the Webasto outbreak in Germany.

      It’s possible that there were weakly infectious strains already around in China for some time that suddenly mutated in the fall somewhere and exploded in Wuhan. Some villagers living near the Yunnan bat caves they studied intensively showed CoV antibodies in 2012. Likely it is this way in many parts of China. Of course the people doing that research were based in … Wuhan.

    • gcochran9 says:

      It is easy to retcon this sort of thing. There really are mildly similar common illnesses, especially for mild cases.

      • gothamette says:

        Yes, this. And there are still ppl saying “just flu.” Still, right now, as we speak. I mean, type.

  6. Anonymous says:

    How specific is the serology test?

  7. swampr says:

    What do you all think of the Kinsa fever data? Convincing? A simple drop of fevers wouldn’t mean much since most fevers aren’t Covid. In Guangdong province only .15% of 320,000 people tested in fever clinics were positive even though it had one of the bigger outbreaks there. But Kinsa is saying they detected an anomalous spike in fevers they believe was Covid starting in March that subsequently declined.

  8. Rob says:

    I don’t get why anyone thought earlier widespread infection seemed reasonable. If a few percent infected now causes a run on ventilators, wouldn’t a 50% infection rate have filled up the ventilators and been noticed months ago? Was it just the hope desperate people have when reasonable hopes are exhausted? Don’t the limeys know god smiles on drunks, fools, and Americans?

    Cochran, what do you think of Robin Hanson’s idea of bringing back variolation for the coronavirus? Hanson focuses on infecting with a very low number of visions, but wasn’t the other half of variolation introducing the pathogen through a route it hadn’t evolved to exploit, like orally or nasally with smallpox. Would subcutaneous SARS-CoV-2 establish a self-limiting infection that spared the lungs? Capillary walls do express ACE2, so does some skin. If we can’t get a vaccine up and running before next winter, would variolation be an option? Even if it worked, would the FDA ever approve it?

    http://www.overcomingbias.com/2020/03/variolation-may-cut-covid19-deaths-3-30x.html

    I still think someone should see if it infects horses. Though there aren’t as many horses around as their used to be. How different can their Ace2 proteins be?

    • gcochran9 says:

      It’s worth investigating. Not many people remember variolation. You mention two potential mechanisms in variolation: I doubt if much is known about either, since it was abandoned a long time ago. There’s another possible mechanism, which might well be the main one: people used inoculum from mild cases of smallpox. There are/were two strains of smallpox, variola major and variola minor: the cfr for ordinary smallpox is 30%, the CFR for variola minor is 1%..
      It is said they used smallpox scabs that had been dried for some time – fresh scabs were more likely to cause a full-blown, dangerous case. That sounds like low viral count, maybe.
      Another problem with smallpox variolation: it was contagious, and thus you were a risk to others.

      Now, with coronavirus, we don’t have a mild strain to use, but low virion count and unorthodox entry are possible. Worth investigating, I’d say. But so are many other approaches.

      • 415 reasons says:

        If you use an old scab presumably it’s got a lot of DEAD virions in addition to a tiny number of live ones. At that point you’re talking about a vaccine. To me a big question is why can’t we figure out a vaccine much faster. It’s not like something bad will happen if we say it can’t happen quicker than 18 months, right?

    • John Massey says:

      Researchers in Hong Kong are doing it with golden Syrian guinea pigs, which have very similar ACE2 to humans.

    • John Massey says:

      Infecting them, I mean. The disease progression in the guinea pigs is remarkably similar to that in humans, and after recovery they have antibodies. The researchers have applied for approval from the Medical Council to do trials on infected humans, injecting them with antibodies from guinea pigs, if I understood the story correctly.

      We’ll see.

  9. David Chamberlin says:

    If there is no salvation in the denominator, and no salvation in drug therapies in the near future and it’s doubling every three to five days then there are just a few more factors to add. What percentage of the public has it now, what is the mortality rate when the hospitals are over run, and what percentage of the public will get it before it peaks and dies down. This projection https://covid19.healthdata.org/projections is flat wrong yet is being cited by people who should know better and maybe they do.

    Most folks want to be optimistic so I keep this to myself. We are a math nerdy bunch who don’t like liars no matter how well intentioned they are.

  10. John Massey says:

    Some people seem remarkably dumb. There is no ‘lock-downish’.

    Story from Reuters: https://www.scmp.com/news/world/united-states-canada/article/3077880/coronavirus-why-prato-home-italys-biggest-single

    • gothamette says:

      On 2nd read, I have a different response.

      One: lock downs really do work, yeah.

      Two: The Chinese-Italians of Prato knew what the deal was, the Italians didn’t. A few people warning friends is nice, but it’s not enough. I don’t blame the Italians. They didn’t know what hit them. It would have been nice if China had issued a blunt warning to the rest of the world. But they didn’t.

      • John Massey says:

        On January 11, Chinese scientists published the complete genome sequence of the virus on open platforms. On January 24, Chinese doctors and scientists reported the first description of the new disease in The Lancet. They urged world governments to carefully monitor this new threat because of its pandemic potential. They strongly recommended the provision of personal protective gear for health workers and testing for the virus to be done immediately on suspected cases. They warned that the mortality rate would be high. On January 23 when Wuhan was completely locked down, many people in the west screamed about infringement of human rights.

        What do you need, someone to hit you over the head with a baseball bat? Pin you against a wall and scream into your face? How blunt does a warning need to be?

        • gothamette says:

          I have the highest respect for Chinese doctors and scientists, especially that young man who died. I’m not criticizing them.

          I’m talking about the damned CCP. While using a bulldozer (rightly, correctly) on themselves, they were spreading propaganda about us. A highly placed official tweeted that the US created the virus and spread it in Wuhan.

          https://fortune.com/2020/03/30/china-coronavirus-propaganda-has-shifted-dramatically/

          They lied about numbers:

          https://q13fox.com/2020/04/01/china-lied-about-coronavirus-putting-world-in-jeopardy-us-intelligence-agents-say/

          This slimebag is a highly placed official in the Foreign Ministry:

          You yourself cited one of their pathetic attempts to pin the virus on the West, without doing due diligence and then slimed out of it by saying you were pulling my leg.

          Go fuck yourself, Massey.

          • John Massey says:

            What I said was not to allow yourself to be provoked by someone who was obviously trying to provoke.

            What I cited was what an Italian professor was saying. I would be lying if I said it is not fun to poke you with a pointy stick now and then, but you need to be a bit more perceptive – I’m not Chinese, I’m not a shill for the CCP and I’m not an apologist for China. I’m also not a sucker for the American right wing media. I am not remotely interested in politics and ideology; I couldn’t care less.

            What I want to know is the source of the coronavirus, which has still not been determined, and not for want of trying. I think on the weight of the evidence that it is very highly likely that it is within China, but I would be a lot more comfortable with certainty about how and where it happened.

            • gothamette says:

              There is a document that gets put up and taken down from the net that claims the virus came from a lab in Wuhan. A mistake, not a bioweapon. Bats were not being sold at that market. It’s a badly translated document and may be crap, but who knows.

              Click to access 114720192-5eb8307f-017c-4075-a697-348628da0204.pdf

              • John Massey says:

                There is a paper by American and Australian scientists, to which I no longer have the link (but you could find it), that concluded it was neither a deliberate nor accidental lab release. The Chinese paper, that keeps getting retracted by the authors but being put up again by who knows who, suggesting it was an accidental lab release, was spurious. Cotton was pushing this theory in the USA, but he was wrong, like he is about everything.

                Conclusion: It was not a lab release, accidental or otherwise. It was not some planted bioweapon. It is almost certainly a disease which has somehow jumped from some species of bat into humans, almost certainly somewhere in China. The Huanan seafood market in Wuhan certainly became an epicentre for the disease to spread in the initial outbreak of cases that got noticed by late December as anomalous, but it appears not to have originated there.

              • gothamette says:

                ” somehow jumped from some species of bat into humans, almost certainly somewhere in China. ”

                So, not necessarily Wuhan?

              • John Massey says:

                Not necessarily.

                Wuhan is pretty unremarkable as Chinese cities go, but what distinguishes it is that it is a central transport hub: an interchange for the world’s largest high speed rail network, and also a domestic air travel interchange.

                Just about anyone going from anywhere in China to anywhere else in China passes through Wuhan. It is also only 4.5 hours by high speed rail from Hong Kong, so HK people going to various parts of the Mainland all pass through Wuhan, and anyone entering China using HK as an entry point all pass through Wuhan, unless they are only going to Guangdong Province.

                Wuhan became the epicentre because Wuhan is at the centre of everything.

              • gothamette says:

                It either jumped from bats to humans somewhere, or into an intermediary species.

                If from bats, it wasn’t the Wuhan market.

                If some intermediary species, then maybe Wuhan market.

                Is that it?

              • John Massey says:

                No. The first five documented cases in China had no possible contact with the Huanan market in Wuhan. So however it got into humans, either directly from some species of bat or via some intermediate animal, it looks unlikely that occurred in that market.

                Further, the closest genetic match of the coronavirus so far found in bats is only 96%, which is not close enough – it needs to be 99%. The same with any recombinant coronavirus found in pangolins – the closest is only 91-92%. Not close enough.

                Chinese scientists have exhaustively tested all of the animals being sold in the Huanan market, and haven’t found it.

                There is the theory that humans could have contracted a coronavirus from bats, and that it has been circulating at low level in humans in China, maybe for years, before mutating into something highly contagious enough to become epidemic, but that is still just a theory.

                No, cats were not on the menu in the Huanan market. Neither were dogs. The animals were wild animals, or farm bred wild animals (but those farms in China, which have now all been shut down, hopefully, were often just a front for marketing wild animals that had been poached).

                Repeat – Chinese scientists have not found a close enough match for the coronavirus even in bats, and they have documented some 400 different coronaviruses in bats. So when you say it came from bats, that is a very highly likely bet, but it has yet to be conclusively determined.

              • gothamette says:

                “mutating into something highly contagious enough to become epidemic, but that is still just a theory.”

                Or mutating in some intermediary species before becoming contagious enough.

                Going back to the idea that the virus circulated in people at a low level before mutating into something more lethal – would this show up in a test?

                Has this ever happened in the history of virology?

              • John Massey says:

                You’re asking me? I’m a civil engineer.

                All I know is that some people who know stuff considered this a likely enough possibility to propose it as a possible explanation.

              • gothamette says:

                I read stuff like this a lot, and also in the respected medical press, so please, where did you read that the first five cases were NOT associated w/the wet market????

                https://www.businessinsider.com/coronavirus-pandemic-timeline-history-major-events-2020-3

              • gothamette says:

                “The first five cases”

                OK, after asking you where you got that 42 times and receiving no answer, I did my own research and found:

                https://www.nejm.org/doi/full/10.1056/NEJMoa2001316  

                *On December 29, 2019, the first 4 cases reported, all linked to the Huanan (Southern China) Seafood Wholesale Market, were identified by local hospitals using a surveillance mechanism *

              • gothamette says:

                “No. The first five documented cases in China had no possible contact with the Huanan market in Wuhan.”

                Link? I’ve looked & cdn’t find source.

            • John Massey says:

              That paper was published two weeks ago in Nature Medicine by an international team drawn from the Scripps Research Institute in California, the University of Edinburgh, Columbia University in New York, the University of Sydney and Tulane University in New Orleans.

              Go to it. I’m busy.

            • gothamette says:

              “What I want to know is the source of the coronavirus, which has still not been determined, and not for want of trying. I think on the weight of the evidence that it is very highly likely that it is within China, but I would be a lot more comfortable with certainty about how and where it happened.”

              The source was bats. What you mean is the intermediary.

              Now, this might sound crazy but why not. Could it have been cats? Do they sell and eat cats at the market?

              https://www.biorxiv.org/content/10.1101/2020.04.01.021196v1

              • John Massey says:

                Pet cats and dogs have both been infected by their owners in Hong Kong, but they did not become sick from the disease, and there is no evidence that cats or dogs can infect humans, although it is evident from that paper that cats can infect each other.

                Neither were on the menu at Huanan market, as far as I have been able to determine. That is not to say that someone somewhere in China might have been eating infected cats or dogs.

                Guangdong Province has seen fit to go beyond the new national legislation banning the marketing and eating of wild animals, and has also strictly prohibited the consumption of cats and dogs, which suggests they had a reason for doing that. I have never personally witnessed cats or dogs being sold for human consumption anywhere in Guangdong Province or heard of people doing it, but there was nothing stopping people from opportunistically killing and eating stray cats or dogs, even if it was not a widespread practice. It is now illegal.

    • gothamette says:

      A remarkable story.

      Why do you think that the Israeli CFR is only 0.4%?

      24/5500, approx.

      (They’ve got 100 on life support so this will surely go up)

  11. dearieme says:

    Angus Dalgleish, a cancer immunologist, had a piece in the Telegraph yesterday. Because of its paywall I’ll just copy and paste a bit.

    “I have been involved with a number of clinical trials involving vaccines and other immune therapies. One of these is a mycobacterial product known as IMM-101, which has proved an effective treatment in both melanoma and pancreatic cancer studies. Intriguingly, a number of participants in trials I have worked on have remarked that, since taking this “vaccine”, they have not suffered any flu or cold symptoms, often having succumbed every winter previously. Many were elderly, with more than one serious illness.”

    He goes on to say that he’s persuaded colleagues in Norway to incorporate this stuff into an experimental vaccine. Then:

    “I would like to propose that, as a short-term immunity boost, NHS workers should be provided with IMM-101 shots. IMM-101 is available immediately, and is safe, having been approved for cancer trials.

    There is no proof that this will work on Covid-19, I am told repeatedly when I have proposed this. Statisticians tell me that anecdotes are meaningless. But IMM-101 shares properties with the BCG vaccine, which protects against tuberculosis, and may help us fill in the gaps.

    My colleagues and I have dissected the mechanism of action of IMM-101 and have shown that it stimulates the innate immune system that protects us from attack by viruses. The cells stimulated by IMM-101 include natural killers (NKs) and secrete cytokines which are known to kill viruses.

    Many of these properties are shared with the BCG vaccine. BCG is not as effective, nor as safe, as IMM-101 in the context of immune-boosting clinical trials (unlike the BCG, an IMM-101 shot can be given again if the reaction fades; the BCG can also cause ulcers and infections at the injection site). Nonetheless, given its common basic properties with IMM-101, BCG does provide some fantastic statistical support for our proposal.”

    Keep on trying, chaps.

  12. gothamette says:

    Why are more men dying of C19 than women?

    • Jacob says:

      My hot take on this is that hyperglycemia (also heart disease, blood pressure, obesity to varying degrees) is an independent predictor of death for COVID-19 patients. Not only would it explain relative death rates for diabetics, men, and to a lesser degree the elderly, but it has been proven in the previous SARS-CoV. The latter virus, which we could think of as an older cousin to SARS-CoV-2, coincided with acute hyperglycemia in about half of patients in a sample selected from SARS patients with no history of diabetes.

      https://link.springer.com/article/10.1007/s00592-009-0109-4

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