Very funny

No, really, just great:

I’ve been chuckling about this all day so I had to share it with you.

Fergus Walsh, the BBC’s medical correspondent, has written about how he was ‘gobsmacked’ to repeatedly test positive for the coronavirus antibody (meaning, obviously, that he has had the virus).

53 thoughts on “Very funny”

  1. Not terribly surprising. The average BBC journalist see their job as propagandists for the approved opinions, not fearless seekers of truth. A thousand flowers blooming worries them just as much as it did Mao 🙂

  2. Repeatedly?

    In the context of the article it makes sense actually – he was trying out a range of those quick-result test-yourself consumer kits that everyone initially thought were going to be gamechangers until more careful testing showed they were too inaccurate to be medically useful. On the basis of how much they had been dissed, it perhaps wasn’t unreasonable to think he might get different results from the different brands of tests (and he almost did, with one of them only barely showing the second line that indicates a positive result). His surprise wasn’t so much that the tests agreed with other per se but that they agreed he was positive, when he had never had, during the operative period, even the slightest hint of any symptoms, and he would have been looking out carefully for them. He had thought that although many infections were known to be minor, you’d probably get a smidgeon of a hint, feel an off-day perhaps. But nada.

  3. How far back do those antibody tests work, will you still show up positive if you had the Kung Flu in January?

  4. Degree in English Literature, and a post-grad Diploma in Journalism. His job is to entertain by writing entertainingly about the manifold play of human emotion and meaning.

    Bonus due.

  5. OT, but today is what used to be known as Empire Day.

    How very strange that a people who – by their confidence and good sense – once governed much of the world are now often too frightened to emerge from their front doors.

    But then, in the days of the Empire, we were not feminised into risk-aversion and into believing that feeling is a form of cognition, and the leftist termites had not weakened our social foundations.

    Still, I recommend irritating leftists by wishing them Happy Empire Day.

  6. Degree in English Literature, and a post-grad Diploma in Journalism

    Is that him? Makes complete sense. The “Health Correspondent” for the BBC was always going to be an Arts graduate with no medical training or experience.

    The flat out weirdest part of the article is that he describes having the main symptoms (for two weeks or so),has tested positive (with no chance of a false positive), yet (a) he insists he didn’t have the virus and then (b) says he was an asymptomatic carrier.

    I can only assume from this that he has no understanding of what the word ‘asymptomatic’ means, which is a bit of a problem for a Health correspondent on a national broadcaster.

  7. Theo: Well thank you sir, seeing as it’s my birthday today. Sadly Empire Day is no more, and it’s PC replacement was moved to March by fiat. They didn’t even ask me, the buggers!

  8. @Rob

    At the time he had the symptoms, there wasn’t evidence of COVID transmission in the UK. He’s probably correct to think it was another bug. Even if it does turn out there were some cases in the UK in December / January, there can’t have been many of them (or we would have seen it in short order in terms of hospital critical care/deaths). There are lots of people who think because they had the lurgies in Dec/Jan they must have been in the first wave of COVID and the vast majority of them must be wrong.

    The thing he was expressing surprise about was that if he had COVID later without realising it, then it really must have been totally asymptomatic. Didn’t feel a thing. Not even “I don’t feel 100%, my throat tickles, I feel a bit hot, but not quite bad enough to say I have a raised temperature or cough” but nothing at all. I didn’t think the surprise was unreasonable – being told something and actually experiencing it are different things.

  9. Degree in English Literature, and a post-grad Diploma in Journalism

    I mean WTF? Is he qualified as a super fan of Holby City perhaps?

    Latest in a long line of BBC “specialists” totally unqualified in their specialism. See also music graduate Paul Mason as one-time economics editor for Newsnight and Channel 4. It’s our licence money these pricks are hoovering up FFS

  10. MBE – Even if it does turn out there were some cases in the UK in December / January, there can’t have been many of them (or we would have seen it in short order in terms of hospital critical care/deaths).

    Seems reasonable, but based on what we now know about the low hospitalisation rate and death rate of the Chinese Cough, would we have noticed it? The Nightingales are all empty.

  11. Thanks for reading it, MBE. I didn’t want a connection to velvetgloveironfist on my permanent record.

  12. ” There are lots of people who think because they had the lurgies in Dec/Jan they must have been in the first wave of COVID and the vast majority of them must be wrong.”

    Why ‘must’ they be wrong? They may be wrong, might be wrong, on balance of probability be wrong, but ‘must’?

    What if the current wave of CV is the second one, a more virulent strain than the first which was largely indistinguishable from ordinary flu, either in symptom or death rate? The first maybe came through the UK in Dec/Jan, second one (the current one)a month or two later. Given its increasingly likely that the virus escaped from the lab in October 2019, and was obviously widespread in Wuhan by December, and international travel means if its in place A it’ll be in place B 5000 miles away within days if not weeks, I can see no reason why it couldn’t have been quite widespread within the UK over Christmas and the New Year.

  13. @Steve/@Jim

    Across Europe, including the UK, there’s an extensive “sentinel system” for tracking respiratory diseases, including doing genetic analysis on the next batch of nasties. By December they would all have been on the lookout for COVID.

    https://www.ecdc.europa.eu/en/seasonal-influenza/surveillance-and-disease-data/facts-sentinel-surveillance

    However, I’ve clearly breached Cromwell’s rule:

    https://en.m.wikipedia.org/wiki/Cromwell%27s_rule

    So I’ll recast the “must” as “overwhelmingly likely”. My understanding is that enough serious cases of COVID have some otherwise unusual features that a largeish outbreak (one that produced a number of serious cases) would have been pretty noticeable. If in December a few China returnees had minor or no symptoms, passed it on to zero/one/two others with no superspreading and by chance it all died out, that’s not so implausible. A lot of the research seems to be pointing to superspreaders as the source of a large proportion of transmissions so chains of transmission that don’t include such an event are quite likely to just peter out. But the idea of many thousands of people having had COVID early, and there are loads of people who think they did, seems harder to reconcile with what’s known. Also, if there was a very widespread “ultra-mild strain” that did the rounds in Dec/Jan, it’s done very well to dodge showing up in genetic analysis.

  14. Folks are good at putting two and two together and making numbers greater than four. Despite statistical improbability, very few people who have had coughs, colds, temperatures, loss of sense of smell, even discoloured toes, since December, put them down to anything other than coronavirus.

  15. I think MBE has a point about superspreaders, even superspreading events.
    You can make a simple model with 80% of the spreading being done by 20% of the population.
    If overall R=3, this could comprise 5 people of whom A infects 12, and the other four infect 3. If the incoming infection avoids type A people or events, then it peters out quickly.
    Someone found in Wuhan that 11% of the people accounted for 80% of the infecting.

  16. “What if the current wave of CV is the second one”

    Possible.

    A couple of months ago, Gamecock had a day or two of loss of smell. A WEEK later, he heard loss of smell was a symptom of Covid. Well damn! He self evaluated, and had no syptoms whatsover. Was it Covid? Don’t know.

    If it were determined that he has antibodies for it, he wouldn’t be surprised.

    Here’s the thing to me: the U.S. has 1,600,000 confirmed cases. This stuff spread very easily, at least for a while. So I expect there to be ten million Americans exposed, if not tens of millions.

    The mystery now is why is it receding. Spring in the Northern Hemisphere, autumn is the Southern? Ramping up down there? Was summertime what protected Africa for months?

  17. MBR: “Also, if there was a very widespread “ultra-mild strain” that did the rounds in Dec/Jan, it’s done very well to dodge showing up in genetic analysis.”

    But there are… HCoV-NL63 and HCoV-HKU1 are both endemic here. NL probably since “forever”, HK since 2005/6-ish. Both can cause that lovely “lingering cold/cough” we had running around from November to early Januari, and both do give a positive result when you test for “CoVid antibodies” with the cheap tests.
    And both are not exactly “mild” … It’s more that the specific set of complications that make SARS2 so nasty is much, much rarer with those two…

    Which also means having run into one of those two does give you (partial) immunity to HCoV-SARS2. At reasonable virus titers.. Daring the bull to a chicken run is still a bad idea…

    The mild strains haven’t dodged genotyping.. They’re simply part of the usual Winter Crud and as such do not rate above “minor annoyance” .

  18. They promised millions of deaths which haven’t arrived. Many of the 1000s that supposedly have arrived are listed because of crook reporting not the “deadly pandemic”.

    Fuck “waves”–just end the LD while something of the economy is left to save.

  19. The Meissen Bison

    Fergus Walsh:

    I’m rarely ill, but I did have a bout of pneumonia in early January.

    Does pneumonia come in “bouts”?¹ This is the language of the hypochondriac with a chest infection.
    _______
    1) Obvs the pneumonia who haunts these threads with his stinking teeth and festering armpits comes in prolonged bouts. I mean the other kind.

  20. By December they would all have been on the lookout for COVID.

    Eh? I don’t think so. Even the Asian nations specifically geared up for SARS 2 weren’t looking then and China was suppressing any hint that it might exist.

  21. How very strange that a people who – by their confidence and good sense – once governed much of the world are now often too frightened to emerge from their front doors.

    The people who carved out the British Empire were very different from those who inhabit Britain today. The genes may be much the same, but the culture ain’t.

  22. There was a report a while back that the main strain in China was the B Strain, which had mutated from the A strain found mainly in Australia and the US. It then went to Europe where it mutated into the C strain in Italy. The European B strain then went to New York.This was why the Japanese and Taiwanese – hardly the biggest fans of the CCP – suggested it may have come from Oz and or US in the first -lace back in October But obviously that can’t be true cos China Man bad.

  23. Steve
    May 24, 2020 at 10:31 am

    How far back do those antibody tests work, will you still show up positive if you had the Kung Flu in January?

    One you start making anti-bodies you will always make those anti-bodies – to the end of your life. So, if your test only tests for anti-bodies that are connected to a specific disease, once you get a positive test (which, at a minimum, indicates a strong exposure even if you never came close to being symptomatic) you will always get a positive test.

    There’s a set of completely different things needed to check for the actual disease and anti-body tests are a quick and cheap way of showing you who doesn’t need those more expensive tests.

  24. @ Mark T
    Yes, I read that claim elsewhere – pity that it involved time travel to make the chain of events possible.
    There are two more plausible options: the first being that the A strain is a mutation of the B strain. The second is a bit complicated but still more plausible than time travel: the cases in Washington State are alleged to have arisen from an American services sports team returning from a match in China prior to the Chinese government admitting there was an epidemic, so that implies that some of the Chinese army were infected but the government hushed it up until after a mutated virus caused a lethal outbreak in Wuhan and the whistleblower doctor died.

  25. @Grikath

    Do the cheap’n’nasty tests antibody show positive results if you’ve had those other coronaviruses (which aren’t strains of SARS-CoV-2) too? I hadn’t realised that. Presumably makes them even dodgier unless that really does provide immunity against COVID-19 and I don’t think the jury’s in on that one – for what little it’s worth this New Scientist article is a few days old and reckons the current verdict is pointing more towards “doesn’t help” than “protective”: https://www.newscientist.com/article/2244096-coronavirus-and-covid-19-your-questions-answered/

    @Aggers/Steve

    Memory doesn’t last forever. This is for SARS (“Duration of Antibody Responses after Severe Acute Respiratory Syndrome”):

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851497/

    Among the cohort of patients with known transmission histories, we were able to obtain a complete collection of serum samples from 18 patients at 6 months, 1, 2, and 3 years. The IgG levels of these 18 patients were analyzed separately to obtain an IgG trend that more accurately represented convalescent SARS patients (Figure 2). All 18 patients had positive IgG at 6 months and at 1 year (i.e., 100% positive); only 1 patient became IgG negative at 2 years. However, at 3 years, the positive percentage dropped to 55.56%.

  26. Bloke in North Dorset

    MBE,

    You make some fair points but you also need to address the likelihood of some having pneumonia and then within 3 months (allowing for 1 month antibodies to form) later being infected by the novel coronavirus and being asymptomatic?

  27. @MBE May 24, 2020 at 10:24 am

    I assume you didn’t read the linked article where Fergus, on 23 May 2020, writes:

    “I’ve not had any symptoms in recent months. I’m rarely ill, in early January. I was off sick for about 10 days and had a cough and a high temperature. I couldn’t shake it off
    …how many people have had coronavirus without knowing it, so-called asymptomatic cases – people, it seems, like me..

    Asymptomatic???

    Given we now know Wuhan Virus started in mid October 2019, Fegus must be exceptionally dumb to still believe his January SARS infection was certainly not CV-19

    “…the vast majority of them must be wrong” – Must? really? Must?

    “…a largeish outbreak would have been pretty noticeable” – because outbreak followed normal bell curve you dismiss early cases as fake? :facepalm

    “…By December they would all have been on the lookout for COVID” – Whut? When China was still denying it spread human to human in late January (to allow China New year parties?)

    “…dodge showing up in genetic analysis” – nope, it has; least serious strain is 250 times less serious than most

    Above has been posted here before – read more

    I must say, you’ve excelled today as a Newmoania clone

  28. @Jim
    +1 The European CV-19 virus is a mutation of the original China/Far East virus

    @Mr Ecks
    +1 “Promised millions of deaths”

    Wuhan Virus: Global Epidemic, Pandemic? No
    Started mid Oct 2019, now in Month Seven and
    Global Population ~7.8 Billion – 7,800,000,000
    – May 05, 2020, 17:48 GMT – Wuhan Virus Global Deaths 255,595 (~0.003%)
    – May 10, 2020, 17:37 GMT – Wuhan Virus Global Deaths 282,516 (~0.003%)
    – May 24, 2020, 18:25 GMT – Wuhan Virus Global Deaths 345,536 (~0.003%)

    Annual Flu Deaths in UK is ~20,000-35,000 and all cause annual deaths in UK ~680,000

  29. @TMB

    You mean :

    Often, if your immune system makes antibodies against one microbe, it gets a head start for fighting a related one later on. But this doesn’t always apply. There is evidence that encountering a virus can sometimes lead to worse symptoms in subsequent infections involving the same virus or a similar one.

    from that article?
    That’s prime Guardianista level crud. As is most of the rest of the article. Then again.. it’s Newscientist..

    Umm no… And an edited-in [TLDR] warning… and a [Simplified!] warning to boot.

    The immune system detects glycoproteïns. Specifically ones that do not contain a code that spells “this is Us.”
    If a glycoproteïn is detected that’s not part of the expected set, the alarm is raised, and a cascade is triggered. This amplifies the original alarm so that it propagates. The total level of “alert signal” then determines the actual response, with different systems reacting to different types and levels of alarms.

    As part of the immune reaction you produce more of the detector proteïns to find those specific glycoproteïns. While long-lived for proteïns, these have a shelf life and will degrade over time and get recycled. This depends on a number of factors, including Quantum, so there’s no hard rule stating how long you’ll have these detectors scouting for you. Some last mere weeks, others years.
    So you will lose your immunity against [X] eventually if you don’t encounter [X] anymore for a long time. So if a pathogen is so common you run into it regularly, your immunity stays up.
    Of course, pathogens have the unfriendly habit of tinkering with their glycoproteïn profiles, so the system isn’t watertight. But in biology nothing is..

    One feature of the detection system is that it is precise, but not exact. This means the detection system can and will detect “code families” instead of one specific code when it comes to clycoproteïns, based on “if it fits, it sits.”
    The good thing about that is that related pathogens tend to have related glycoproteïn codes, so a specific detector can detect multiple pathogens if they share the same code family.
    This is where the article starts going South already, because they mix microbes and viruses.
    Microbes are complete living cells, like bacteria. They are HUGE, especially compared to most of our cells, and have a veritable rainforest worth of glycoproteïns on their surface. Within species/families they are also quite consistent, so there’s good odds that if you encountered [X] and built up the detection for it, it’ll also catch cousin [Y] and possibly uncle [Z].
    Viruses are much, much smaller and are built up with only a couple of glycoproteïns, one of which is the main detector for their host cell. This means the detection surface is a lot smaller and much more specific, so the chance of the antigen for [X] also detecting cousin [Y] is generally a lot smaller. Especially since viruses do play the glyco-shuffle quite readily.
    However… The glyco-proteïns needed to find their host cells and attach to them are very specific and can’t be changed too much though. So as long as a virus strain keeps the same detector(s) or other parts of its body there’s a good chance your body will recognise cousin [Y], at least partially. This is why the Flu Shot generally works, sort of, for most people.

    Same mechanism, same relative chances of “family” detection, completely different underlying principles as to “why”.

    As for the “Worse Symptoms”… This is an allergic reaction, which does not originate in the detection system, but in the cascade used to propagate the detection signal. Which for some people has a disproportionate reaction to certain antigens causing reactions far more excessive than the original detection signal warrants. Sometimes so excessive it actually kills them if there’s no intervention.
    People usually associate allergies with pollen, bees, peanuts, shellfish.. Celery is on the table, as is, for some unholy reason, garlic. And some people are so unlucky they are allergic to parts of their own body.
    The same principle, however, works as well with actual pathogens: people can have severe reactions to a bacterium or virus… The mechanism is exactly the same..

    And note the some people.. Not everyone drops dead after sniffing a single peanut, or getting stung by a bee, or….
    In fact, that level of allergy is quite rare. And none of it is the peanut’s or the bee’s fault. The problem is with the people being unlucky enough to have an immune system that’s not “up to spec”.
    And the article lumps those exceptions with the rest, calls it “possible” , and proceeds adressing it as “probable”.
    This “journalistic” trick may be …acceptable… in a gossip rag, or the Guardian ( or any other brit newspaper.. it’s just the flavour that differs..) . It’s completely unacceptible when you claim “Science”. ™Lions!!.

    And no, the cheap tests aren’t shoddy.. They’re chemistry. Chemistry works.
    But like a proper bit of computer code, you do need to include the right logic ( in this case, set of anti-antigens) to get a specific result.
    The cheap ones do [X] OR [Y], the really reliable ( and expensive) ones do [X(n)], [Y(n)],[Z(n)] in a matrix. Makes a difference.

  30. The Meissen Bison

    @Grikath
    You had me worried for a moment that I was cleverer than nature had intended.

  31. Grikath

    You seem like a random person on the Internet who sounds current on tech biology …

    Care to venture an opinion? – specifically on the possibility of in vitro testing for “bad” cascade reaction to particular trigger proteins?

    Testing for catastrophic immune reaction seems to have direct utility and lasting value. Is it a stupid idea ?

  32. @BIND

    “You make some fair points but you also need to address the likelihood of some having pneumonia and then within 3 months (allowing for 1 month antibodies to form) later being infected by the novel coronavirus and being asymptomatic?”

    Having a nasty case of pneumonia during the cold’n’flu season is, unfortunately, neither pleasant nor particularly rare.

    As for COVID-19: for someone in London having caught it isn’t all that unlikely, seroprevalence studies suggested about 17% of London adults have caught it at some point (see https://www.bbc.co.uk/news/live/world-52749186 but NB there were some wide confidence intervals on that!) and that’s broadly in line with the fact that reported cases have been higher in London, though obviously actual cases are going to be a multiple of reported cases. Since the reporter had been working during the epidemic rather than staying at home, that chance must be higher even before we consider the specific risks attached to being a health journalist, which might well be greater than for many other jobs bearing in mind the situations you’re likely to be exposed to. So it could easily be a 25% chance of catching COVID-19 in these three months, and I’d be surprised if it were lower than 10% even allowing for uncertainty in the seroprevalence sampling.

    And the proportion asymptomatic is a matter of dispute. Oxford Uni’s Centre for Evidence-Based Medicine had a look at this: https://www.cebm.net/covid-19/covid-19-what-proportion-are-asymptomatic/

    Unfortunately their general conclusion was “the data are poor” and while no study suggested asymptomatic infections were a trivially small proportion, it could be anything from 5% to 80%.

    A more recent study but with a small sample size reckoned it could be closer to 75%: https://www.lshtm.ac.uk/newsevents/news/2020/almost-75-people-board-diamond-princess-covid-19-may-have-been-asymptomatic

    If we went with 25% chance of a working London journalist being infected in the last three months and 40% chance of infections being asymptomatic, that’s a 10% chance overall, which isn’t all that small. Multiply that by the chances of getting pneumonia earlier in the year for the standard, non-COVID reason and there’s the likelihood you want.

    In contrast, what are the chances of being one of the first cases of COVID-19 in the UK and going down with pneumonia? Just the chances of contracting COVID that early must be extraordinarily long odds indeed. Even if COVID cases had been at a constant rate since January, your chances of being right at the start of it would be tens of times smaller than your chance of catching it in the middle or later. But combine that with the initially exponential-ish rate of growth and the proportion of early cases becomes a tiny part of the whole. Combine that with the arguments against large-scale transmission that early in the year without it being noticed, and the odds only get longer. Finally an additional reduction in probability must be applied – he needed a case severe enough to have pneumonia (which we know for middle-aged men would only occur in the minority of cases) but not bad enough that the medics would notice it didn’t resemble a typical influenza-like illness.

    To reiterate: it wouldn’t surprise me at all – I rate it as far more likely than not – that the first recorded UK case and the first recorded UK transmission were not the first case or transmission, just the first to come to medical attention. But there were thousands of people with pneumonia in early 2020 for all the normal boring reasons, and if even a slim-but-nontrivial proportion of those had COVID-19 then – since the majority of COVID infections don’t lead to such bad symptoms – there would have had to be a lot of minor and asymptomatic infections too, so that would have required a substantial outbreak. Yet somehow this outbreak needs to have evaded the sentinel system across Europe, not caused those weird cases with distinctive COVID symptoms that would have alarmed respiratory specialists, not noticeably kicked up the death rate, and despite the complete lack of social distancing – Joe Public weren’t paying much attention to the threat at the time, at least behaviourally – not kicked off into a massive and unmistakable exponential growth for a couple more months. Yet we know that of those Londoners with the boring run-of-the-mill pneumonia in January, something like 5-10% could easily have gone on to have an asymptomatic COVID-19 infection in the last 3 months. So a positive antibody test is not a particularly convincing smoking gun.

    Early isolated cases that produce short or no chains of transmission so just fizzled out without anyone noticing, that I can buy. But you’d have to be extremely unlucky to get caught up in one and it’s unlikely unless you or a close contact – or a close contact of a close contact, perhaps – had recently returned from the epicentre in China. (I can see a case that the job of health correspondent does make you more likely to be exposed to this than the average person!)

    There are lots of people who claim that their January illness was “almost certainly” very early COVID. I think a lot of them will get a surprise if they take an antibody test, and even those who claim vindication from a positive result should be extremely cautious in that interpretation.

  33. @Grikath

    Apologies, I should have quoted the bit I meant. I know it’s the NS and the “pop” in “pop science” is sadly very operative. I was looking for something very specific, which is what the state of play was in terms of crossimmunity from other coronoaviruses already in circulation – I know it’s something that’s been under investigation and if there was anything really definitive that had come out without me noticing then I was hoping it would have passed to the NS’s attention. Certainly earlier this year a lot of scientists were being quoted sceptically about whether “common cold” coronaviruses would give useful protection against COVID-19. There was a more optimistic paper I vaguely remembered seeing a week or so ago but I can recall it now – https://www.cell.com/cell/fulltext/S0092-8674(20)30610-3 “Targets of T cell responses to SARS-CoV-2 coronavirus in humans with COVID-19 disease and unexposed individuals”:

    Importantly, we detected SARS-CoV-2−reactive CD4+ T cells in ∼40-60% of unexposed individuals, suggesting cross-reactive T cell recognition between circulating ‘common cold’ coronaviruses and SARS-CoV-2.

    But I don’t know if there are any studies showing how beneficial this has proven in practice?

    Perhaps “shoddy” is a bad word-choice for the cheap tests, but the British government bought millions of the things, evaluated them (at Porton Down I think) and recognised they were neither sensitive nor specific enough to actually use: https://www.theguardian.com/world/2020/apr/09/uk-government-urged-to-abandon-poor-finger-prick-antibody-tests-coronavirus

  34. @Pcar

    You’re right re the chronology thanks. Public health authorities in the UK were looking for the virus in January, quite early on, but not December.

    “…dodge showing up in genetic analysis” – nope, it has; least serious strain is 250 times less serious than most

    You got a link for that? Seems at odds from what I’m hearing from virologists when they communicate with the press/public e.g.

    https://nextstrain.org/help/coronavirus/FAQ#is-one-strain-of-the-covid-19-virus-more-severe

    https://www.medicalnewstoday.com/articles/is-there-more-than-one-strain-of-the-new-coronavirus

    https://www.theatlantic.com/health/archive/2020/05/coronavirus-strains-transmissible/611239/

    “…a largeish outbreak would have been pretty noticeable” – because outbreak followed normal bell curve you dismiss early cases as fake? :facepalm

    Epi curves aren’t really bell curves, they’re not symmetrical for starters. And at the starts and ends it really matters that they’re discrete rather than continuous, because the stochasticity dominates there rather than a smooth trend. Obviously somebody’s got to be the early cases. But the chances of it being any particular person are very low and I can’t see any especially convincing reason to think Walsh is one of them. There’ll be loads of people who caught pneumonia for other reasons, then contracted COVID-19 later. Given the timings, this seems far more likely than the alternative. (For it to be an evens chance would need there to have been loads of COVID-19 pneumonia cases at that time too, somehow without being noticed – and that would imply the epi curve was pulled left of where we think it was, yet with exponential growth it surely wouldn’t have stayed unnoticed for long.)

  35. @MBE
    That Cell article is the Real Deal. A quick scan of it, and keeping the same caveat the authors did…
    Yes, seems that there’s a significant amount of cross reaction derived from “common cold” CoVid infections. So the endemic viruses do give a measure of immunity.

    My personal caveat is that it does not seem to prevent actual infection.. The proteïns caught in the “generic CoVid trap” that give the strongest reactions are mostly helper proteïns which get released after the propagation cycle is completed. So there’s a …delay there, with the immune system actually reacting to the debris as well as the viral bodies.

    Bookmarked it for giving it a serious read.

    @Tomo
    If I could figure out a way to duplicate our immune system to that level in vitro I’d be picking up a Nobel, probably several, next year…. ( and a, in my eyes more prestigious, igNobel if I slant one of the necessary publications as Silly Enough..)

    It’s like trying to copy a cloud-based multi-vendor distributed-computing solution ( to spam some IT jargon) onto a single laptop. When all you have is a Commodore64 to work with…
    Our immune system is a single “organ” that’s distributed all over our body instead of a single spot you can point to. Even getting one bit to work in vitro would land you serious accolades, let alone the whole bunch.
    Can’t be done with current tech/knowledge.

  36. @Grikath May 24, 2020 at 9:36

    Agree. MBE’s Ref usual left negative and erroneous speil

    Pre-Med course at school in 80s taught immune system learns and remembers, then applies and adapts to future infections

    This CV-19 hysteria seems to be based on ignorant assumption immune system never encountered a SARS/CoronaV before

    Gov’t and MSM calling it “novel, never before… virus” feeds the hysteria

    @MBE
    Refs in posts days/weeks ago. Mostly Docs/Profs, some on Specie UK/US

  37. @MBE May 24, 2020 at 11:41 pm

    Across Europe and USA samples from SARS patients Nov/Dec/Jan have been (re)tested and CV-19 revealed as cause

  38. @PCar
    “This CV-19 hysteria seems to be based on ignorant assumption immune system never encountered a SARS/CoronaV before”

    Hmmyeaahh.. But don’t discount the fact that at any given time generic CoVid infection/immunisation is estimated at about 4-5% of the population. Definitely not enough to create a “herd immunity” barrier..
    So for all practical purposes the CoVid/SARS virus is novel and unknown to a large portion of the population..

    If the results from the Cell article are corroborated, it does offer a quick-and-dirty solution solution though…

    Not unlike the original smallpox immunisations with cowpox, ensure that most of the population get a bout of the endemic and less dangerous Coronavirus variants…
    I can see the screaming headlines already.. “Govt Mandates Illness As Cure!!!” 😉

  39. Bloke in North Dorset

    @MBE,

    I accept that the probability of him getting pneumonia and then becoming an asymptomatic C19 victim is greater than him becoming one of the first C19 victims, but the probability of the latter isn’t zero, and its the way he dismisses it that makes Chris’s post amusing.

    The NHS website on pneumonia reckons there’s a 0.5% to 1% chance of catching pneumonia, although a little higher in winter. I also see that he is in his late 50s and everyone I’ve met who’s had it was knocked sideways by it, so I would expect him to have inadvertently self-isolated, which could be the reason for him not becoming a spreader. Without knowing his lifestyle its hard to know whether he would have been infecting other people whilst infectious before the symptoms showed had it been C19.

    Out of interest I went back and saw that the first confirmed UK cases were on 31 Jan and the first London case on 12 Feb in someone who had recently arrived from China. Whist that points to him not having C19 in January it doesn’t dismiss it either. Those first cases were the ones who were severe enough to present at hospital. and we don’t know how many people had it beforehand and had just got on with their life thinking they had a bad cold, flu, or even pneumonia :).

    Anyway, some good links in there from you and the others, so its been a worthwhile discussion.

  40. PF (still gremlins)

    WRT timing, there were people coming back from Ischgl specifically in mid January (Sussex) with a whole load of symptoms that were straight off the Covid check list, and that had been in that particular apres ski bar etc. They were never tested. And then quite a lot of obvious follow on cases (same symptoms) locally after that. Reported in the DT a month or two back.

  41. @Pcar

    Re “…dodge showing up in genetic analysis” – nope, it has; least serious strain is 250 times less serious than most

    Having looked for it, I think the thing the Speccie was referencing was the one reported here: https://www.scmp.com/news/china/science/article/3080771/coronavirus-mutations-affect-deadliness-strains-chinese-study

    By “250 times less serious”, I think that isn’t a reference to mortality but comes from a Chinese study in which: To verify the theory, Li and colleagues infected cells with strains carrying different mutations. The most aggressive strains could generate 270 times as much viral load as the weakest type. These strains also killed the cells the fastest.

    On the other hand there were a lot of virologists quoted in
    https://www.medicalnewstoday.com/articles/is-there-more-than-one-strain-of-the-new-coronavirus and in https://www.theatlantic.com/health/archive/2020/05/coronavirus-strains-transmissible/611239/ who were very sceptical about the “different strains” idea, and a later study by the University of Glasgow reckoned the observed mutations didn’t have functional significance so there was really only one “type” of the virus in circulation: https://www.sciencefocus.com/news/no-evidence-of-coronavirus-mutating-into-more-dangerous-strains/ and paper published at https://academic.oup.com/ve/article/6/1/veaa034/5827470

    Re “Pre-Med course at school in 80s taught immune system learns and remembers, then applies and adapts to future infections” – well yes, that’s the biology 101 stuff, but crossimmunity from one virus to another isn’t perfect. For example, catching one strain of flu doesn’t necessarily give you protection against the next … and SARS-CoV-2 is different enough from the “common cold” coronaviruses for the experts to be sceptical that most of the population would have any substantial protection. And the immune response wanes over time, which was the point of Steve’s question – the link in my answer showed that for the original SARS, people could test positive on an antibody test a year after infection, but not three years later.

    Across Europe and USA samples from SARS patients Nov/Dec/Jan have been (re)tested and CV-19 revealed as cause

    Don’t think that’s quite right, there haven’t been any cases of SARS since 2004 I believe? But replace “SARS” with “pneumonia”, and yes, a handful of cases were identified eg https://www.bbc.co.uk/news/world-europe-52526554 … Like I said there must have been some early cases, particularly imported ones and some of their close contacts (or contacts of contacts: the famous example of the French fishmonger who was retrospectively diagnosed as having had it at the end of December, for example, had a wife who worked at an airport) . But it is extremely unlikely any individual pneumonia case back then would have been due to COVID-19 as there can only have been a handful of cases, or else we would have seen that exponential growth in cases much earlier. There’s also the phylogenetic evidence – that seems to suggest the virus can’t have emerged in humans in China much earlier than November (which underlines how early Nov/Dec and even Jan cases in Europe must have been), nor can there have been substantial transmission in the UK before it was first documented in late February. If there’d been a large outbreak in January that was undetected at the time, it would show up in phylogenetic analysis due to early UK-specific mutations; my imperfect understanding is that as late as March, UK phylogenetic evidence was pointing to cases being driven by recent imports, see https://www.cogconsortium.uk/news/analysis-of-covid-19-genomes-reveals-large-numbers-of-introductions-to-the-uk-in-march/ and the technical reports https://www.cogconsortium.uk/news/

  42. @BIND

    Cheers. Perhaps Walsh should have been more open-minded. On the other hand, my issue with “we don’t know how many people had it beforehand and had just got on with their life thinking they had a bad cold, flu, or even pneumonia” is that while that number remains unknown, it must be very tightly bounded above, by (a) the requirement that all these cases, and anybody else they infected, to remain undetected at the time, (b) the requirement not to have exploded into exponential growth – a single big superspreading event or a couple of smaller ones, and we’d have known about it very quickly, (c) the requirement that UK transmission in Jan or earlier left no obvious trace in the phylogenetics. It’s for that reason I think the probabilities must be several orders of magnitude apart, and the UK members of the “January Covid Survivors Club” must be overwhelmingly mistaken. I could be wrong, and perhaps retrospective analysis of December/January samples and more detailed phylogenetic analysis will reveal that, but I don’t think there’ll turn out to have been more than a handful of relatively isolated cases, mostly imported, in January.

  43. Oops, spam trap.

    @Pcar

    Re “…dodge showing up in genetic analysis” – nope, it has; least serious strain is 250 times less serious than most

    Having looked for it, seems the study the Speccie was referencing was the one reported here: https://www.scmp.com/news/china/science/article/3080771/coronavirus-mutations-affect-deadliness-strains-chinese-study

    By “250 times less serious”, I think that isn’t a reference to mortality but comes from a Chinese study in which: To verify the theory, Li and colleagues infected cells with strains carrying different mutations. The most aggressive strains could generate 270 times as much viral load as the weakest type. These strains also killed the cells the fastest.

    On the other hand there were a lot of virologists quoted in the articles I posted above who were very sceptical about the “different strains” idea, and a study (later than that Chinese one) by the University of Glasgow reckoned the observed mutations didn’t have functional significance so there was really only one “type” of the virus in circulation: https://www.sciencefocus.com/news/no-evidence-of-coronavirus-mutating-into-more-dangerous-strains/ and paper published at https://academic.oup.com/ve/article/6/1/veaa034/5827470

  44. @Pcar

    Re “Pre-Med course at school in 80s taught immune system learns and remembers, then applies and adapts to future infections” – well yes, that’s the biology 101 stuff, but crossimmunity from one virus to another isn’t perfect. For example, catching one strain of flu doesn’t necessarily give you protection against the next … and SARS-CoV-2 is different enough from the “common cold” coronaviruses for the experts to be sceptical that most of the population would have any substantial protection (though I’d be interested to see some actual figures for health outcomes). And the immune response wanes over time, which was the point of Steve’s question – the link in my answer showed that for the original SARS, people could test positive on an antibody test a year after infection, but not three years later.

    Across Europe and USA samples from SARS patients Nov/Dec/Jan have been (re)tested and CV-19 revealed as cause

    Don’t think that’s quite right, there haven’t been any reported cases of SARS since 2004 I believe? But replace “SARS” with “pneumonia”, and yes, a handful of cases were identified eg https://www.bbc.co.uk/news/world-europe-52526554 … Like I said there must have been some early cases, particularly imported ones and some of their close contacts (or contacts of contacts: the famous example of the French fishmonger who was retrospectively diagnosed as having had it at the end of December, for example, had a wife who worked at an airport) . But it is extremely unlikely any individual pneumonia case back then would have been due to COVID-19 as there can only have been a handful of cases, or else we would have seen that exponential growth in cases much earlier. There’s also the phylogenetic evidence – that seems to suggest the virus can’t have emerged in humans in China much earlier than November (which underlines how early Nov/Dec and even Jan cases in Europe must have been), nor can there have been substantial transmission in the UK before it was first documented in late February. If there’d been a large outbreak in January that was undetected at the time, it would show up in phylogenetic analysis due to early UK-specific mutations; my imperfect understanding is that as late as March, UK phylogenetic evidence was pointing to cases being driven by recent imports, see https://www.cogconsortium.uk/news/analysis-of-covid-19-genomes-reveals-large-numbers-of-introductions-to-the-uk-in-march/ and the technical reports https://www.cogconsortium.uk/news/

  45. @Pcar

    For what it’s worth, I think TMay would describe it as “SARS means SARS” – rather than there being a generic condition called “SARS” which has, as one of its possible causes, the more specific SARS coronavirus.

    Wiki says: “Severe acute respiratory syndrome (SARS) is a viral respiratory disease of zoonotic origin that surfaced in the early 2000s caused by severe acute respiratory syndrome coronavirus (SARS-CoV or SARS-CoV-1)” https://en.wikipedia.org/wiki/Severe_acute_respiratory_syndrome

    NHS says: “SARS (severe acute respiratory syndrome) is caused by the SARS coronavirus, known as SARS CoV. Coronaviruses commonly cause infections in both humans and animals. There have been 2 self-limiting SARS outbreaks, which resulted in a highly contagious and potentially life-threatening form of pneumonia. Both happened between 2002 and 2004. Since 2004, there have not been any known cases of SARS reported anywhere in the world.” https://www.nhs.uk/conditions/sars/

    The WHO says: “SARS (Severe Acute Respiratory Syndrome). Cause: SARS coronavirus (SARS-CoV) – virus identified in 2003. SARS-CoV is thought to be an animal virus from an as-yet-uncertain animal reservoir, perhaps bats, that spread to other animals (civet cats) and first infected humans in the Guangdong province of southern China in 2002.” https://www.who.int/ith/diseases/sars/en/

  46. @MBE

    How wiki defines Severe acute respiratory syndrome (SARS) is irrelevant. Gov’t and Media say Covid-19 is a Severe acute respiratory syndrome (SARS), which it is. Usage precedes dictionary defn.

  47. @Pcar

    I believe the correct generic term is “SARI”, short for “severe acute respiratory infection”, so that also covers serious cases of MERS and COVID-19. Analogous to “ILI” as a catch-all for “influenza-like illness”. Hence we see sentences like “Recent travellers returning from the Middle East who develop SARI should be tested for MERS-CoV” rather than “who develop SARS”, which is a separate (and hopefully vanquished) disease.

    That’s the WHO surveillance case definition anyway:

    SARI case definition
    An acute respiratory infection with:

    * history of fever or measured fever of ≥ 38 C°;
    * and cough;
    * with onset within the last 10 days;
    * and requires hospitalization.

    https://www.who.int/influenza/surveillance_monitoring/ili_sari_surveillance_case_definition/en/

  48. I started feeling a bit grotty on Sunday. (Spoiler alert, I’m feeling much better today.) I rarely seem to get these bugs, the last time I can remember having to take to my bed for a few days was several years ago. I didn’t have many of the ‘symptoms’ of Covid – temperature, persistent cough, anosmia etc.

    I was noticeably worse on Monday, so at 1pm I logged on the .gov web site and booked a test, got an appointment for 30 minutes later (8 miles away) and we were all done and on our way back home by 2:15pm. We’ve just got our test results, which were negative (as I expected). The procedure was easy, and because the testing was being done by the army, very efficient.

    I was a bit surprised to have picked up a different bug (presumably, but the test is only ~70% reliable) despite observing lockdown pretty closely. I’m lucky that my sister is a GP and she provided me with helpful guidance throughout.

  49. “Gov’t and Media say Covid-19 is a Severe acute respiratory syndrome (SARS), which it is.”

    The classical definition of “syndrome” includes unknown cause*. The cause of CV-19 is known. It is not a syndrome.

    *AIDS became HIV, once the cause was learned.

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