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

  1. #1531
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    This qualifies as different from BNO News:


    BREAKING: Bronx Zoo says one of its tigers has tested positive for coronavirus
    This thing is really contagious right off the gate.

    ETA:
    The tiger which tested positive for coronavirus is 4-year-old Nadia, a Malaysian tiger. Her sister, 2 Amur tigers, and 3 African lions have developed a dry cough as well. All are expected to recover

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    Quote Originally Posted by Roger E. Moore View Post
    I'm going to hate it when COVID-19 shows up again this fall, alongside the flu, and we go through this all over again.

    What are the chances of comorbidity, I wonder.
    Where damage to the lung lining has been caused by an over-reactive immune system response to the virus, the outlook for withstanding subsequent pathogens/viruses, is not a pretty one.

    One has to wonder how long it takes for the lungs to rebuild a normal, healthy lining? (Smoking whilst that process is underway, would be sheer madness I'm afraid).

    I can see why infected (and subsequently recovered) front-line health workers would be reluctant to return to the battlefield.

  3. #1533
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    Quote Originally Posted by Roger E. Moore View Post
    What are the chances of comorbidity, I wonder.
    Coinfection? With flu and COVID-19? It happens. (The five patients in the report survived without needing Intensive Care.)
    Coinfection with SARS-CoV-2 and other respiratory viruses appears to be relatively common.

    Grant Hutchison

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    Quote Originally Posted by grant hutchison View Post
    Coinfection? With flu and COVID-19? It happens. (The five patients in the report survived without needing Intensive Care.)
    Coinfection with SARS-CoV-2 and other respiratory viruses appears to be relatively common.

    Grant Hutchison
    How is 'nasal tampon' a symptom? (I can understand the need for using such a device .. but a symptom???)

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    Quote Originally Posted by Selfsim View Post
    How is 'nasal tampon' a symptom? (I can understand the need for using such a device .. but a symptom???)
    I'm guessing it means "plugged nose".
    Cum catapultae proscriptae erunt tum soli proscript catapultas habebunt.

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    Quote Originally Posted by grant hutchison View Post
    The trouble with liquid ventilation is that it doesn't actually improve outcome in patients with Adult Respiratory Distress Syndrome (which seems to be what causes the severe lung problems of COVID-19).
    Grant Hutchison
    Drat!

    Here I was thinking that it could force out lighter fluids being denser than any edema—maybe as a lavage until the infection passed.Perhaps with oxygenation of the blood by other means.
    The reason I suggested medical personnel is that they would not panic as much at the thought of such treatment.

    In the future—instead of rolling Ventilators, perhaps hoses to a central—no, that might be a vector. Air ventilation seems hard on the lungs.

    One other thing:

    A man from Pinson by the name of Adam York had ECMO, after suffering something very like COVID in January 2018, according to The Trussville Tribune.

    I wonder if something in his body chemistry or genes might point a way out.
    Last edited by publiusr; 2020-Apr-06 at 08:20 AM.

  7. #1537
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    Quote Originally Posted by Selfsim View Post
    How is 'nasal tampon' a symptom? (I can understand the need for using such a device .. but a symptom???)
    Semantic nit pick: have we given up on the distinction between signs and symptoms? Symptoms are feelings. Signs are measurable and observable. The “flu” feeling is what it feels like when our immune system goes to work. It’s a symptom. The fever registers on a thermometer, it’s a sign. But the reference to signs has disappeared. Seems to be a loss of an important distinction to me.
    sicut vis videre esto
    When we realize that patterns don't exist in the universe, they are a template that we hold to the universe to make sense of it, it all makes a lot more sense.
    Originally Posted by Ken G

  8. #1538
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    Quote Originally Posted by Selfsim View Post
    How is 'nasal tampon' a symptom? (I can understand the need for using such a device .. but a symptom???)
    Trebuchet is correct: the sensation of having a blocked nose. A tampon is a blockage. Tamponade is the state of being blocked. I've never seen the expression used for anything other than an object you stick up someone's nose to stop bleeding, but sometimes these odd phrases appear when authors are writing English as a second language.

    Grant Hutchison
    Last edited by grant hutchison; 2020-Apr-06 at 11:59 AM.

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    Quote Originally Posted by profloater View Post
    Semantic nit pick: have we given up on the distinction between signs and symptoms? Symptoms are feelings. Signs are measurable and observable. The “flu” feeling is what it feels like when our immune system goes to work. It’s a symptom. The fever registers on a thermometer, it’s a sign. But the reference to signs has disappeared. Seems to be a loss of an important distinction to me.
    It certainly hasn't disappeared in medicine. Did it ever exist in common parlance?

    Grant Hutchison

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    A quick question, possibly for Grant.

    If smoking tends to cause more ACE-2 receptors in the lungs, how long would one have to refrain from smoking before the receptors return to a more normal level?

    Also, I'm assuming it's a function of the smoke rather than of the nicotine. Is that correct?

  11. #1541
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    Quote Originally Posted by grant hutchison View Post
    It certainly hasn't disappeared in medicine. Did it ever exist in common parlance?

    Grant Hutchison
    I thought it used to be common, but maybe I did not notice before this dominant news, with all these epicentres.
    sicut vis videre esto
    When we realize that patterns don't exist in the universe, they are a template that we hold to the universe to make sense of it, it all makes a lot more sense.
    Originally Posted by Ken G

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    Quote Originally Posted by headrush View Post
    If smoking tends to cause more ACE-2 receptors in the lungs, how long would one have to refrain from smoking before the receptors return to a more normal level?

    Also, I'm assuming it's a function of the smoke rather than of the nicotine. Is that correct?
    I looked around for this information recently, and couldn't find anything specific. People started to investigate in the aftermath of SARS, but I suspect research funding dried up when SARS came quickly under control. Also, sampling cells from deep in the lungs is quite invasive--it's not something you'd want to subject a person to repeatedly while they were giving up smoking.
    The minimum timescale would have to be the turnover time of surface receptors (days) or of the pneumocyte cells (a week).

    But ACE-2 is perhaps not actually the issue here. People who smoke are more susceptible to respiratory viruses generally, including those like flu with no ACE-2 affinity. And the general protective mechanism in the lung take months to recover when a person gives up smoking. Also, the biology and epidemiology remain unclear:
    SARS-CoV-2 is known to use the angiotensin converting enzyme 2 (ACE2) as a receptor for cell entry. There is a complex and unclear interplay between COVID-19 and the renin-angiotensin-aldosterone system.1 Until recently, smoking and nicotine were found to down-regulate ACE2 expression in the lung and other tissues.2,3 More recent analyses suggest that up-regulation of ACE-2 caused by smoking could be detrimental for COVID-19.4,5 However experimental data suggest that infection with SARS-CoV and SARS-CoV-2 leads to down-regulation of ACE2, and this downregulation is detrimental due to uncontrolled ACE and angiotensin II activity.6,7 It has been observed that decreased ACE2 availability contributes to lung injury and ARDS development.8,9 Therefore, higher ACE2 expression, while seemingly paradoxical, may protect against acute lung injury caused by COVID-19.
    This preliminary analysis does not support the argument that current smoking is a risk factor for hospitalization for COVID-19. Instead, these consistent observations, which are further emphasized by the low prevalence of current smoking among COVID-19 patients in the US (1.3%), raises the hypothesis that nicotine may have beneficial effects on COVID-19. This could be attributed to its immunomodulatory effects and its interaction with the renin-angiotensin system. However, other confounding factors need to be considered and the accuracy of the recorded smoking status needs to be determined. However, the results were remarkably consistent across all studies and were recently verified in the first case series of COVID-19 cases in the US.
    Grant Hutchison

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    Quote Originally Posted by profloater View Post
    Statistics: looking at deaths in the USA, upper respiratory tract is given as 41 per 100,000 slightly higher than strokes. Then influenza with pneumonia adds 14 per 100,000. Adding those for the population gives about 180,000 per year, USA, and these are the deaths which will accelerated by this virus. Plus some of course.

    Will this year’s figures attribute a high proportion to this pandemic?
    The thing to recognize about the COVID-19 pandemic is that this disease is both more contagious, and more deadly, than any of the other prevalent flus,and unlike other flus, has no vaccine. This means that pretty much no matter what we do, the deaths from COVID-19 will be significantly higher than all other flu deaths combined-- maybe by 1-2 orders of magnitude. The death rate from complications from smoking and pollution will stay more or less constant, and whether or not those deaths are tolerable is a question for elsewhere. But the key difference between them and COVID-19 is that the deaths from COVID-19 are very much under our own control. When people look at the current death rates and compare them with various other things, they are making an implicit assumption that the COVID-19 death rate is characterized by what we are seeing now, but we must recognize it would already be much higher if draconian measures were not widely in place throughout the world. This is the key difference between a pandemic with exponential growth capability, and all those other medical concerns you are contrasting it with. So your "just statistics" are apples and oranges.

    It should be noted that the global death rate from the flu epidemic of 1918 was up to 100 times the death rate from common flus. It certainly seems like COVID-19 has a similar potential, so that's another statistic to bear in mind.

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    Quote Originally Posted by schlaugh View Post
    So I'm in the grocery store, dutifully wearing my 3-layer cloth mask, and I have a violent sneeze. And I'm one of those people who may sneeze a few times in a row.

    Now what?
    Treat your mask as infected. Why is this any different from what you do if you sneeze into your elbow? I don't understand why everyone is just fine with "cover your cough" but make a big issue out of wearing a cloth mask, that contrast makes no sense. If I'm in a store and someone sneezes three times, and several of them get out before the elbow gets up there, I'm out of that store immediately and wishing that person had a mask on. (I'm probably out of the store even if they have a mask, but I'm still glad they did.) I realize the sneeze is not itself a symptom of COVID-19, my concern is they might also have COVID-19.

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    Quote Originally Posted by Roger E. Moore View Post
    What are the chances of comorbidity, I wonder.
    I would guess pretty low, because a lot fewer people will get the other deadly flus given all the safeguards that will be in place against COVID-19. Even so, COVID-19 should dominate all flu deaths, and won't need, or get, much help from other flus. That's a side benefit of the measures against COVID-19, it saves you both the millions that would die from COVID-19, but also hundreds of thousands that would have died from other flus.

  16. #1546
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    Quote Originally Posted by Ken G View Post
    The thing to recognize about the COVID-19 pandemic is that this disease is both more contagious, and more deadly, than any of the other prevalent flus,and unlike other flus, has no vaccine. This means that pretty much no matter what we do, the deaths from COVID-19 will be significantly higher than all other flu deaths combined-- maybe by 1-2 orders of magnitude. The death rate from complications from smoking and pollution will stay more or less constant, and whether or not those deaths are tolerable is a question for elsewhere. But the key difference between them and COVID-19 is that the deaths from COVID-19 are very much under our own control. When people look at the current death rates and compare them with various other things, they are making an implicit assumption that the COVID-19 death rate is characterized by what we are seeing now, but we must recognize it would already be much higher if draconian measures were not widely in place throughout the world. This is the key difference between a pandemic with exponential growth capability, and all those other medical concerns you are contrasting it with. So your "just statistics" are apples and oranges.

    It should be noted that the global death rate from the flu epidemic of 1918 was up to 100 times the death rate from common flus. It certainly seems like COVID-19 has a similar potential, so that's another statistic to bear in mind.
    Well the USA death figures are rising with cases with about 1% at 8 days delay. On quite big numbers now. It’s too soon to say but the Oxford model has a rapid growth of immunity with little or no signs, not like 1918. That model includes the city living factor. City folk mix a lot more than country folk and closer together. So the dots all over USA might not go the way of NYC. Of course I am biased by my situation. I really hope the Oxford Model is right, and not the Imperial one, but both are being reworked from the evidence.

    Living isolated, I doubt if I have any immunity, so what to do when restrictions lifted? We really need antibody tests, then those wrist bands, I think that will happen but probably not till June.
    Last edited by profloater; 2020-Apr-06 at 05:25 PM. Reason: Important typo
    sicut vis videre esto
    When we realize that patterns don't exist in the universe, they are a template that we hold to the universe to make sense of it, it all makes a lot more sense.
    Originally Posted by Ken G

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    Here's an unrelated question. From the start of the pandemic, the common information in the US was that you can't get COVID-19 from eating infected food, ostensibly because stomach acid destroys the virus, notwithstanding the obvious fact that the throat comes before the stomach. What's more, the common mode of getting infected was invariably described as touching an infected surface, and then touching the eyes or nose. Over and over we heard eyes and nose, and even if someone coughed, it was about the droplets lying in wait on a surface, which we would pass to our eyes or nose. Two dozen times I must have heard that mantra.

    That always surprised me, because with common viruses we are always told not to share food with an infected person. So what is the current opinion, is the mouth not a place to worry about infection? If an infected person prepares our food, will eating it not subject us to contagion? Not once have I even heard that mode of infection mentioned, and I don't know if there is science behind it or if people are just afraid of hurting the restaurant industry.

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    Quote Originally Posted by profloater View Post
    I really hope the Oxford Model is right, and not the Imperial one, but both are being reworked from the evidence.
    And until there is actual evidence,one must ask, does one prepare for the model they like, or the one they don't?
    Living isolated, I doubt if I have any immunity, so what to do when restrictions lifted? We really need antibody tests, then those wrist bands, I think that will happen but probably not till June.
    I agree, it would sure be nice to see if there is immunity. I can't think what the Oxford model is based on, I don't see much evidence that people are getting immune in broad numbers. Most people regard the China numbers as bogus, and South Korea avoided widespread infection from the start. So has Germany, but maybe these are weather-related, there appear to be local explosions for reasons that I don't think are known. But I have yet to see credible evidence that anywhere that had an explosion has seen a mysterious reduction in cases that must be attributed to herd immunity and not to lockdown measures. Perhaps we just need a little more time in Italy and we will know, but I'm not holding out the hope that this will just go away by some magical immunity mechanism not present for the 1918 flu. It would sure be nice though! (And yes, only nice for those in dense areas, for the rest we must hold out for the vaccine.)

  19. #1549
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    Quote Originally Posted by Ken G View Post
    Here's an unrelated question. From the start of the pandemic, the common information in the US was that you can't get COVID-19 from eating infected food, ostensibly because stomach acid destroys the virus, notwithstanding the obvious fact that the throat comes before the stomach. What's more, the common mode of getting infected was invariably described as touching an infected surface, and then touching the eyes or nose. Over and over we heard eyes and nose, and even if someone coughed, it was about the droplets lying in wait on a surface, which we would pass to our eyes or nose. Two dozen times I must have heard that mantra.

    That always surprised me, because with common viruses we are always told not to share food with an infected person. So what is the current opinion, is the mouth not a place to worry about infection? If an infected person prepares our food, will eating it not subject us to contagion? Not once have I even heard that mode of infection mentioned, and I don't know if there is science behind it or if people are just afraid of hurting the restaurant industry.
    Well viral sore throat is very common, including now for our PM, is it food or breathing? Viral gastro trouble is , presumably , eating although Related vomit is highly infectious by breathing , so my guess is food prepared by a carrier is infectious or contagious in that case.
    sicut vis videre esto
    When we realize that patterns don't exist in the universe, they are a template that we hold to the universe to make sense of it, it all makes a lot more sense.
    Originally Posted by Ken G

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    Disease and pandemics thread (because it's science)

    Slightly off topic, can anyone give an executive summary of what the ACE2’s normal function is?
    My attempts at Googling either return articles above how it lets viruses into cells, or are so technical that I get lost halfway through the first sentence.


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    Quote Originally Posted by Extravoice View Post
    Slightly off topic, can anyone give an executive summary of what the ACE2’s normal function is?
    My attempts at Googling either return articles above how it lets viruses into cells, or are so technical that I get lost halfway through the first sentence.
    https://en.wikipedia.org/wiki/Angiot...rting_enzyme_2

    ACE2 lowers blood pressure by catalysing the cleavage of angiotensin II (a vasoconstrictor peptide) into angiotensin 1–7 (a vasodilator)
    So, it alters an enzyme to control the dilation of blood vessels.
    "I'm planning to live forever. So far, that's working perfectly." Steven Wright

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    Quote Originally Posted by Noclevername View Post
    https://en.wikipedia.org/wiki/Angiot...rting_enzyme_2



    So, it alters an enzyme to control the dilation of blood vessels.
    Thanks.


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    Quote Originally Posted by grant hutchison View Post
    I looked around for this information recently, and couldn't find anything specific. People started to investigate in the aftermath of SARS, but I suspect research funding dried up when SARS came quickly under control. Also, sampling cells from deep in the lungs is quite invasive--it's not something you'd want to subject a person to repeatedly while they were giving up smoking.
    The minimum timescale would have to be the turnover time of surface receptors (days) or of the pneumocyte cells (a week).

    But ACE-2 is perhaps not actually the issue here. People who smoke are more susceptible to respiratory viruses generally, including those like flu with no ACE-2 affinity. And the general protective mechanism in the lung take months to recover when a person gives up smoking. Also, the biology and epidemiology remain unclear:

    Grant Hutchison
    Thanks Grant, that's helpful even if the results are unclear.

  24. #1554
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    Quote Originally Posted by Ken G View Post
    Here's an unrelated question. From the start of the pandemic, the common information in the US was that you can't get COVID-19 from eating infected food, ostensibly because stomach acid destroys the virus, notwithstanding the obvious fact that the throat comes before the stomach. What's more, the common mode of getting infected was invariably described as touching an infected surface, and then touching the eyes or nose. Over and over we heard eyes and nose, and even if someone coughed, it was about the droplets lying in wait on a surface, which we would pass to our eyes or nose. Two dozen times I must have heard that mantra.

    That always surprised me, because with common viruses we are always told not to share food with an infected person. So what is the current opinion, is the mouth not a place to worry about infection? If an infected person prepares our food, will eating it not subject us to contagion? Not once have I even heard that mode of infection mentioned, and I don't know if there is science behind it or if people are just afraid of hurting the restaurant industry.
    What you don't want is a blob of virus-loaded secretion sitting in contact with a mucous membrane--any mucous membrane, but eyes, nostrils and lips are the most commonly contaminated by virus that has got on to people's hands. Respiratory viruses will rapidly penetrate mucous membranes and get into the circulation.
    Food-borne virus infections are generally those transmitted by the "faecal-oral" route, which are adapted to get through the stomach and infect the gut. Virus shed from the infected gut then gets on to people's hands, and on to other people's food.
    So it's two different areas of viral endeavour, in which different viruses largely specialize. There's occasional evidence of faecal-oral virus being spread by mucous membrane contact (a supposedly airborne norovirus outbreak, for instance), and occasional evidence of respiratory viruses being spread by the faecal oral route (a SARS outbreak in Hong Kong that seemed to be related to sewage).

    Grant Hutchison

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    Some nice drops in rates, though I noticed that Sunday reports (last 3 weeks) suggest light reporting rather than a physical reduction on both rates.

    World rates thru Apr 5.jpg
    7 Cntry thru Apr 5.jpg
    US dual thru Apr 5.jpg

    [The 7-Country graph has a corrected heading. I failed to catch the header stating it was an "average" of rates, but the averaging of the rates themselves was discontinued.]
    Attached Images Attached Images
    Last edited by George; 2020-Apr-06 at 06:58 PM.
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    Whoa, whoa, what's going on with the Boris J man over there; no politics, but he's in the ICU. That's doubleplus ungood.
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    Quote Originally Posted by grant hutchison View Post
    So it's two different areas of viral endeavour, in which different viruses largely specialize.
    But what I don't understand is, if there is a virus on a food, and you eat it, will that not contact mucous membranes on its way down the throat? Or do they expect the saliva to wash it all the way down? Also, if the virus on the food touches the lips on the way in, then presumably saliva won't wash the lips. So I wondered why they flat out stated that you could not get COVID-19 from eating food. (Even now the CDC website says "Currently, there is no evidence to support transmission of COVID-19 associated with food. " and "In general, because of poor survivability of these coronaviruses on surfaces, there is likely very low risk of spread from food products or packaging.") It sounds like you would be skeptical of these claims, as would I. (Indeed, today I actually washed my face with soap after eating take-out food, something I have never seen recommended anywhere.) I feel like so much energy goes into trying to keep people from over-reacting, but so far I see very little danger that over-reaction is where the danger lies. Though we do see some strange forms of reaction-- in the US now, we typically see restaurant personnel wearing gloves at all stages of the proces, though of course that's not by itself much protection and as you said before, might make people think handwashing is unnecessary because they are wearing gloves. I don't know if the cooks always wore gloves, that might protect against dirt under the nails and so forth but it's hard to see how gloves help with COVID-19. Not reassuring when it comes to take-out food.
    Last edited by Ken G; 2020-Apr-06 at 10:07 PM.

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    Quote Originally Posted by headrush View Post
    Quote Originally Posted by Grant Hutchison
    grant hutchisonI looked around for this information recently, and couldn't find anything specific. People started to investigate in the aftermath of SARS, but I suspect research funding dried up when SARS came quickly under control. Also, sampling cells from deep in the lungs is quite invasive--it's not something you'd want to subject a person to repeatedly while they were giving up smoking.
    The minimum timescale would have to be the turnover time of surface receptors (days) or of the pneumocyte cells (a week).

    But ACE-2 is perhaps not actually the issue here. People who smoke are more susceptible to respiratory viruses generally, including those like flu with no ACE-2 affinity. And the general protective mechanism in the lung take months to recover when a person gives up smoking. Also, the biology and epidemiology remain unclear:
    Thanks Grant, that's helpful even if the results are unclear.
    Slightly misleading way to end such a conversation.
    Quote Originally Posted by Farsalinos etal
    However, it is well-established that smokers are more likely than non-smokers to suffer from comorbidities, such as cardiovascular disease, which are risk factors for adverse COVID-19 outcomes.
    Risk of death outcomes for the elderly infected with Covid-19 still appear to outweigh the same in younger infected groupings. Smoking in older populations was way more prevalent in the past. The chances of already existing comorbidities in this group, is thus more likely in comparison with the younger group.

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    Quote Originally Posted by Ken G View Post
    .. Not reassuring when it comes to take-out food.
    We still have to eat!
    I guess the risk of infection depends on the count of human contacts with the food item(s) as it is prepared. Certain cooking techniques (eg: flame grilled) probably doesn't help the virus' lipid coating survival likelihood .. but the container the final product goes into, would be a different matter, I guess.

    I personally think stating that one cannot not get COVID-19 from eating food, must be incorrect .. given that the human body already contains many potentially dangerous viruses(?)

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    Interesting animated model (containing some hypotheses) which shows the virus mutation characteristics and geographical spread over time.

    Estimated mutation rate for novel coronavirus looks to be about 26 mutations per year.

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