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Medicine Science

Coronavirus Emerged In Italy Earlier Than Thought, Study Shows (reuters.com) 185

An anonymous reader quotes a report from Reuters: The new coronavirus was circulating in Italy since September 2019, a study by the National Cancer Institute (INT) of the Italian city of Milan shows, signaling that COVID-19 might have spread beyond China earlier than previously thought. The Italian researchers' findings, published by the INT's scientific magazine Tumori Journal, show that 11.6% of 959 healthy volunteers enrolled in a lung cancer screening trial between September 2019 and March 2020, had developed coronavirus antibodies well before February.

A further specific SARS-CoV-2 antibodies test was carried out by the University of Siena for the same research titled "Unexpected detection of SARS-CoV-2 antibodies in the pre-pandemic period in Italy." It showed that four cases dated back to the first week of October were also positive for antibodies neutralizing the virus, meaning they had got infected in September, Giovanni Apolone, a co-author of the study, told Reuters.

"This is the main finding: people with no symptoms not only were positive after the serological tests but had also antibodies able to kill the virus," Apolone said. "It means that the new coronavirus can circulate among the population for long and with a low rate of lethality not because it is disappearing but only to surge again," he added. Italian researchers told Reuters in March that they reported a higher than usual number of cases of severe pneumonia and flu in Lombardy in the last quarter of 2019 in a sign that the new coronavirus might have circulated earlier than thought.

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Coronavirus Emerged In Italy Earlier Than Thought, Study Shows

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  • by Vihai ( 668734 ) on Tuesday November 17, 2020 @08:11AM (#60733908) Homepage

    It was published on a low-impact-factor journal from the same institution, the huge conflict of interest has not been disclosed, the peer review has been made in one day, there is no data on the methods and procedures, the conclusions extrapolate too much from the evidence.

    There are too many signs of pathological science...

    • by Anonymous Coward on Tuesday November 17, 2020 @08:35AM (#60733964)

      Italian here and following the news closely, I wanted to post the same. It is very early to say whether this is bogus or not. Most experts seem to agree that it is very, very unlikely that the virus was circulating so early, and in any case not with such numbers.

      However, consider the following: we know (by the satellite images of lines of ambulances in front of Wuhan hospitals) that the virus started spreading in China probably from end August. Northern Italy (in particular the Milan area) has very tight commercial connections with China, specifically in the textile industry. So it is not unthinkable that the virus jumped from China to Italy so early.

      • > we know (by the satellite images of lines of ambulances in front of Wuhan hospitals) that the virus started spreading in China probably from end August.

        No. No you don't. Suspect all you like, but you do not know.

        • by rainer_d ( 115765 ) on Tuesday November 17, 2020 @10:58AM (#60734428) Homepage

          > we know (by the satellite images of lines of ambulances in front of Wuhan hospitals) that the virus started spreading in China probably from end August.

          No. No you don't. Suspect all you like, but you do not know.

          Back in Early 2020, there were credible reports from exchange-students that Wuhan had seen an unusually large number of cases of pneumonia as far back as August and September.
          Given the large Chinese expat-community in Northern Italy and that Wuhan is a major transportation hub, it's not inconceivable that it was spread to Europe rather quickly.

          As we've seen, it takes a while to develop "critical mass" for the virus - and unless you are really testing a lot, a lot of mild cases just never register on the radar.

          • Back in Early 2020, there were credible reports from exchange-students that Wuhan had seen an unusually large number of cases of pneumonia as far back as August and September.

            No there weren't. Chinese hospitals didn't abnormally high cases of pneumonia until mid November. This is verifiable information, and not some crack report by some exchange students. It was the investigation of these elevated cases which identified the novel coronavirus as the cause.

            • If the reports were true, then China wouldn't have been able to contain it by shutting down Wuhan. It wouldn't have even made sense to try that strategy.

              The Chinese government wants to save face, but they aren't that nonsensical.
          • Back in Early 2020, there were credible reports from exchange-students that Wuhan had seen an unusually large number of cases of pneumonia as far back as August and September.

            There were also reports of large increase of flu cases in the US in late 2019 before 2020

            Given the large Chinese expat-community in Northern Italy and that Wuhan is a major transportation hub, it's not inconceivable that it was spread to Europe rather quickly.

            Oh, right, it's also not inconceivable that it was spread from Europe to China rather quickly.

      • However, consider the following: we know (by the satellite images of lines of ambulances in front of Wuhan hospitals) that the virus started spreading in China probably from end August.

        That research did not pass peer review [google.com] and has since been [bbc.com] rebut [archives-ouvertes.fr]:

        This claim received widespread media coverage despite the lack of validation from peers. This review serves as a pre-publication evaluation of the study. We identify several problems, even questionable research practices, including but not limited to: inappropriate and insufficient data,misuse and misinterpretation of statistical methods, and cherry-picking internet search terms. We also reflect on scientific publishing in a time of public emergency.

        Besides, how well did using satellite images as proof on politically charged issues work out prior to the Iraq War [nti.org]?

      • However, consider the following: we know (by the satellite images of lines of ambulances in front of Wuhan hospitals) that the virus started spreading in China probably from end August.

        No such thing happened in August. It wasn't until November that cases of pneumonia even started appearing questionably high.

        That's not to say that it's not unthinkable that there was a spread before this time, but the reality is the date of August is just being randomly pulled out of some places where the sun doesn't shine.

      • by mestar ( 121800 )

        Or from Italy to China, because, as you know, planes rarely fly somewhere and then don't come back.

        In other words, having lots of people traveling from China to Italy means that you also have many people traveling from Italy to China.

        So, the virus could have easily spread from Italy to China, because, as you said, Italy has very tight commercial connections with China.

    • by MrL0G1C ( 867445 )

      There are too many signs of pathological science...

      Pathological science is an area of research where "people are tricked into false results ... by subjective effects, wishful thinking or threshold interactions."

      So, the researchers found COVID-19 in samples from sewage from several cities in Italy, the earliest 2 sewage samples from 2 different cities are dated 19th December 2019. The virus was not found in sewage samples dated earlier than that 19Dec-19.

      I'm keen to hear how you think this is 'Pathological

    • I read something similar several months ago, I believe it was in Spain, they'd back-tested sewage for COVID and discovered it there before the outbreak started, perhaps in Dec (sorry, in a rush and don't have time to find the article again.) If keen on this do a search, there's already some precedent for detection of it before the main outbreak.

  • by Pollux ( 102520 ) <speter@[ ]ata.net.eg ['ted' in gap]> on Tuesday November 17, 2020 @08:16AM (#60733916) Journal

    It showed that four cases dated back to the first week of October were also positive for antibodies neutralizing the virus.

    So, we didn't find COVID-19. We found antibodies that match antibodies people are currently making against COVID-19.

    Which begs the question...are antibodies unique for each virus they fight? Or, is it possible that the antibodies found were antibodies that the body made previously fighting another coronavirus?

    Just trying to connect some dots here...Italy is a -huge- tourism nation. If there was COVID-19 in Italy back in September, we would have noticed something was wrong back in September. It would have spread everywhere, and whole nations would have seen by October or November tourists coming back from Italy bringing Coronavirus with them. But we didn't see that happen in October or November; we saw it happen in February and March. What if the human body makes the same antibodies (or ones similar enough to not be distinguishable in lab tests) to fight other coronavirii as it fights COVID-19? That would explain why a lot of people get COVID-19 but are asymptomatic, because they already have antibodies from other coronavirii that also stop COVID-19. That would fit the existing data we already know about COVID-19.

    Is there a doctor in the /. who can help answer these questions?

    • by DavenH ( 1065780 ) on Tuesday November 17, 2020 @08:31AM (#60733944)
      Not a doctor, this is just my speculation --

      My dad got very sick with pneumonia in late November 2019, a sickness that took 2 months to get over, a first of its kind case for him. Those around him experienced persistent (yet mild) flu-like symptoms on a ~12-day on/off cycle until summer, also a first. Perhaps this, and the Italian cases, were an ancestor coronavirus strain that predated SarsCov2 and hadn't yet the mutation that increased its virulence (R-factor)? This might explain some of the early antibodies, some odd sicknesses, and also why it wasn't a pandemic at the time.

      • by dryeo ( 100693 )

        OTOH, the wife got a bad cold that resulted in a very bad cough back in January (I had the same but mild and cough cleared up on its own). Within a couple of days of treatment with antibiotics, it cleared right up. This points to a bacterial infection causing the cough, likely triggered by a virus rather then Covid infecting her lungs.
        Most every autumn to winter, we get something similar, though without such an extreme cough.

    • by ganesaraja12 ( 963631 ) on Tuesday November 17, 2020 @08:34AM (#60733958)
      Crossreactivity of antibodies between different viral species of the same genus is a recognised phenomenon. Vaccinia infections (cowpox) to protect against variola (smallpox) is THE classic example - the same antibodies that killed cowpox also killed smallpox. We might be seeing a similar phenomenon here with a related non-SARS, non-COVID coronavirus. The thing about COVID-19 is so few actually develop functioning antibodies to the virus. The fact that it infects T-helper cells has something to do with this, I believe.
      • by dgatwood ( 11270 )

        The thing about COVID-19 is so few actually develop functioning antibodies to the virus. The fact that it infects T-helper cells has something to do with this, I believe.

        I see the paper you're talking about. Studies of HIV drugs show that lopinavir and similar showed no meaningful effect on the course of the disease despite preventing the infection of those cells, so I'm going to have to assume it isn't infecting them in the same sense that HIV does, and that the reasons for not getting neutralizing antibodies are something other than the depletion of those cells.

        But that's just a semi-educated guess. I could easily be wrong.

    • Re: (Score:2, Informative)

      > are antibodies unique for each virus they fight?

      No, they're specific to a protein expressed by a virus. Those may be unique but we get lucky when they're not.

      Much of the low-impact of nCoV-19 in more than a third of the population is due to people having existing antibodies to conserved-region proteins of common-cold beta-coronaviruses. That means structural proteins in the virus that existed in a direct or tree ancestor of nCoV-19.

      This is why households with kids have lower mortality - those buggers

      • Not so easy (Score:5, Informative)

        by DrYak ( 748999 ) on Tuesday November 17, 2020 @12:25PM (#60734790) Homepage

        No, they're specific to a protein expressed by a virus. Those may be unique but we get lucky when they're not.

        That's correct.

        Much of the low-impact of nCoV-19 in more than a third of the population is due to people having existing antibodies to conserved-region proteins of common-cold beta-coronaviruses. That means structural proteins in the virus that existed in a direct or tree ancestor of nCoV-19.

        It is entirely a valid hypothesis, I agree. But I haven't read substantial concrete research with results pointing in that direction. (Though it might be just because I definitely don't have the time to read everysingle last publication about SARS-CoV-2).
        At best there are several publications that point at cross-reactive T-cells (another target-specific component of the immune system, but how aren't *directly responsible with destroying* the virus itself), and the author hypothetising that the variability of outcomes might be partially caused by that.

        TL;DR: I don't say you're wrong, just that I haven't come accross much proof yet.

        This is why households with kids have lower mortality - those buggers brought home colds from school that caused an immune response to a protein that still exists in nCoV-19.

        Very unlikely. Most of the mortality in COVID-19 is imputable to the inflammatory response in the late stages of the disease, with the lungs self-destructing.
        That's why in late stage the corticoids provably help according to several large scale studies - by that time the inflamation is the main cause of bad outcomes and the corticoids help cut the inflammation.

        Younger kids have less mature immune systems which are less prone to such mass inflammation - thus younger kids have a lower chance (but not zero !) of self-destructing their lungs.
        (It's not the only disease. Smallpox is another disease which tend to be a lot less deadly in small children than, say, a big chunk of the entire adult american indian population).

        Full-disclosure: this linkage mechanism is a complete mystery to Orthodox Medical Science (e.g. Surgisphere reviewers).

        Parser failure error. Waht ?

        We could have just figured out which colds had the best targets and made a vaccine back in March for those cold viruses and gotten 85% effective vaccines by September, in preparation for the Northern Hemisphere winter. Instead we're spending trillions on mRNA vaccines from Big Pharma which are going to have the expected downstream consequences of new technology. The corruption is staggering.

        Okay, news flash: Except when you have a robust and well tested procedure in place to produce new vaccine sub-variant in a regular fashion, creating a vaccine takes *multiple years*, up to a decade maybe.

        (The only counter example being flu: the whole process is nowadays optimized to the point that from the moment the WHO emits a new list of potential strains to consider, we can have a vaccine ready in time for that winter's hemisphere. And even that perfectly organised pipeline can be disturbed by a sudden bump of demande - like the current recommendation to vaccine against flu, to have at least one less virus causing cold-like symptoms this winter.
        And that's after decades of development and fine tuning the current production flow.
        There is no other virus with such a quick reaction workflow. Yet. (Coronavirus is probably going to be the next to get one)
        Currently the influenza is the sole vaccine where you can reastically fine-tune something in a couple of months).

        Another news flash: there isn't currently any vaccine against common cold, including other members of the coronavirus family. So there's no other virus whose vaccine you could have fine tuned to "get effective vaccines by September, in preparation for the Northern Hemisphere winter".

        So building a new vaccine (roughly) from scratch is the only way to go.

        And now a

        • by Pollux ( 102520 )

          > Is there a doctor in the /. who can help answer these questions?

          There are some excellent physicians who keep up on the preprint server research but very, very few.

          Oh, hai. Though nowadays I work in research.

          And this is why I love Slashdot. There are -real- experts who give -real- answers to questions typically not found on the average internet forum.

          Thank you.

        • by kbahey ( 102895 )

          First, thank you for responding to the original poster. His comment was a combination of conspiracy theories, pseudoscience and speculation. Great job ...

          One comment though:

          Some vaccine type actually pretty close to your idea to modifying common cold vaccine: except that for practical reasons they are considering starting with rather different (but easier to handle) viruses - some vaccines (including the Russian sputnik project) are using Adenoviruses, which are more or less harmless to human but with SARS-

    • by Whateverthisis ( 7004192 ) on Tuesday November 17, 2020 @09:02AM (#60734054)
      Doctors don't know antibodies; that's a biotech question.

      Antibodies are a swiss army knife. They are shaped like a capital Y, with a stem and two arms that are modular and variable. What happens when your body is invaded for the first time by something the body considers foreign or a threat, it activates the immune system by launching a type of antibody called an IgM antibody. These are highly modular, and what happens is the body sends out massive amounts of these with lots of different types of the "arms". The arms bind to antigen, which are the proteins used by the invader that either surround the virus or bacteria, or are put off by the virus or bacteria to initiate some sort of function. Think of the IgM as a rapid prototype; it launches a thousand or even a million variations of the "arms" of the antibody to see which ones either tear teh virus apart or stop the antigen it uses to attack your body, starving the virus of it's target cell to replicate.

      Over time the body figures out which is most effective at neutralizing the invader, and it produces IgG antibodies. These are the most common antibodies, and basically it's "arms" now target which parts of the invader it found to be most effective. Maybe it's a surface protein that allows the antibody to tear the virus apart, maybe it's something that starves the virus of a critical life function and it dies off without replicating. The IgM antibody is often why being infected the first time you have a bad response, but the transition to IgG means the next time you have the disease your body is prepared to fight it. This is also by the way how vaccines work; they are attempting to trigger your body's ability to go through the IgM to IgG process, and if you have a lot of the IgG floating around in your body then when you get infected with a disease your body is armed to the teeth to fight it; the virus invades your body but you don't even notice because your immune system is ready.

      So to your question. Your antibodies are unique to you in the "stem" but are generally similar amongst species so all humans are pretty similar. However there is a weak point in each invader that due to the immune system's ability to rapidly prototype, it will eventually find that weakpoint. The weakpoint is specific to the invader, so the "arm" of the antibody ends up being specific to the virus regardless of whether you or I have different genetics. So that's a long winded answer, but the answer is YES, at this stage of detection they are finding IgG antibodies and they are virus specific, and different people will generally have over time the exact same "arm" of the antibody to a specific disease.

      Also, by the way, this is worth reading up on. The immune system and how it functions is utterly fascinating the more you dig into it.

    • by kbahey ( 102895 )

      Which begs the question...are antibodies unique for each virus they fight? Or, is it possible that the antibodies found were antibodies that the body made previously fighting another coronavirus?

      Ezayak ya ebn baladi ...
      I an not a doctor, but I was a pharmacist.

      Antibodies are formed as a response to proteins on the surface of pathogens (bacteria, fungi, viruses, ...). Proteins are just a sequence of amino acids that are folded into a particular 3D shape.

      It has been known even before the discovery of bacteria

  • So... (Score:2, Funny)

    by Ecuador ( 740021 )

    So, can we now call it the Italian flu? And make sure to pronounce it "aye-talian".

  • by HamidPayaamAbbasi ( 7143815 ) on Tuesday November 17, 2020 @08:31AM (#60733942)
    I actually work as a systems administrator for an apparels company that often travels to Italy and China and I got really really sick in December with all the now classic COVID symptoms. I don't usually bother talking about it because there is no 11 month in test for COVID but when the stirs of lockdowns started happening in February I knew it was that and stock piled my home before everyone cleared out the grocery stores in the first run. Besides this semi-anonymous post on this board I never saw the point of talking about it considering how idiotically politically charged this has all become and just stay home in a self imposed quarantine working remotely for he next year or three until this clears up. I do not want to feel like I can't breathe again.
    • by ISayWeOnlyToBePolite ( 721679 ) on Tuesday November 17, 2020 @09:18AM (#60734082)

      You could take an antibody test https://www1.nyc.gov/site/coro... [nyc.gov] it's free. Couldn't find T-cell immunity tests in the 15s i was willing to spend searching, you might have better luck.

    • It could have been some other flu as well. Almost a decade ago I had a particularly nasty case that knocked me on my ass for three days where I just stayed in bed outside of going to the bathroom or drinking water. There wasn't any kind of indication that it was worse than any other year, but it just caught me at the right time when it was able to run me over.

      Without any kind of diagnosis I would suggest that you avoid trying to read too much into what you had.
    • by Sloppy ( 14984 )

      with all the now classic COVID symptoms

      Did you have loss of taste or smell?

    • by kbahey ( 102895 )

      What you got may have been COVID or some other severe respiratory illness. The symptoms are shared with other pneumonia, ...etc.

      You can rule out if what you got was COVID or not by taking an antibody test. If you don't have the antibodies, then what you got was most likely not COVID. If you have the antibodies, it could have been from December 2019, April 2020, or September 2020. So no sure way to tell if you got it before 2020, or later.

    • by thegarbz ( 1787294 ) on Tuesday November 17, 2020 @01:28PM (#60735026)

      I actually work as a systems administrator for an apparels company that often travels to Italy and China and I got really really sick in December with all the now classic COVID symptoms.

      You think that's bad. I've had classic COVID symptoms nearly every year for most of my life. Hell in 2009 I ended up in hospital with a severe pneumonia infection as a result.

      It's amazing how many times I've had "COVID symptoms" during the standard flu/common cold season.

  • "It means that the new coronavirus can circulate among the population for long and with a low rate of lethality not because it is disappearing but only to surge again

    Like this is some surprise to us now?

    Anyone capable of putting the pieces together has realized this for at least 4 months now.

    And in particular, it means that this virus will not be under control until there is absolutely universal and ubiquitous testing. That means every single person, adult or child, who ever has any occasion whatsoev

  • by hey! ( 33014 ) on Tuesday November 17, 2020 @12:28PM (#60734798) Homepage Journal

    The serologic assay used in this study is an in-house designed RBD-based ELISA, namely, VM-IgG-RBD and VM-IgM-RBD, and is a proprietary assay developed by using spike glycoprotein ...

    (Emphasis mine)

    ELISA tests can cross react with similar antigens (e.g. proteins from other coronaviruses), which is why they're usually not considered a gold-standard test. They're good enough for screening and for diagnosing in a situation where you've got other supporting evidence, but maybe not to prove something with a low Bayesian prior probability. Also tests are only as good as the reagents you're using, and these reagents are proprietary. A test designer's assertion of his test's capabilities isn't something you can take uncritically; the test needs to be verified by other researchers before you rely on it.

    That doesn't mean the paper is wrong. It just means nobody should be drawing any conclusions from it yet.

A committee takes root and grows, it flowers, wilts and dies, scattering the seed from which other committees will bloom. -- Parkinson

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