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

  1. #2041
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    Quote Originally Posted by Grant Hutchison
    Quote Originally Posted by SelfSim
    Footnote:

    Whilst this explanation may be considered reasonably accurate as far as the SARS-CoV-2 virus is concerned, it certainly cannot be taken as applying for the behaviors of all virus types (as the generalisations made in the above text, imply).
    I made one deliberate omission which I don't think will confuse anyone, but otherwise on rereading I still think it's a reasonable short summary. What concerns you?
    Oh, I’m not concerned or confused.

    The original description doesn’t realise the distinctions of latent, lytic and lysogenic infection .. which are needed to clarify other known virus infection modes.

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    Quote Originally Posted by Selfsim View Post
    Oh, I’m not concerned or confused.
    Good news.

    Grant Hutchison

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    And "no lockdown" Sweden has now transitioned to an estimated reproductive number Re less than one. Lots of estimates involved, but interesting nevertheless.
    In a recent WHO press briefing, Mike Ryan of the WHO Health Emergencies Programme said several useful things to bear in mind about Sweden (starting 00:41:12).
    I think there's a perception out there that Sweden has not put in place control measures and has just allowed the disease to spread. Nothing could be further from the truth. Sweden has put in place a very strong public health policy around physical distancing, around caring and protecting for people in long-term facilities and many other things.
    I think if we are to reach a new normal in many ways Sweden represents a future model of, if we wish to get back to a society in which we don't have lock-downs then society may need to adapt for a medium or potentially a longer period of time in which our physical and social relationships with each other will have to be modulated by the presence of the virus.
    So I think there may be lessons to be learned from our colleagues in Sweden but again I wanted just to emphasise, Sweden has not avoided controlling COVID-19. It's taken a very strong strategic approach to controlling COVID-19 across all of the elements of society. What it has done differently is that it really, really has trusted its own communities to implement that physical distancing and that is something that remains to be seen, whether that will be fully successful or not.
    Grant Hutchison

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    New mutation indicates that coronavirus might be weakening, study says:
    ... Out of the 382 nasal swab samples the researchers examined from coronavirus patients in the state, a single sample was missing a significant chunk of its genome. Eighty-one of the letters were permanently deleted, according to the new study published in the Journal of Virology.

    “One of the reasons why this mutation is of interest is because it mirrors a large deletion that arose in the 2003 SARS outbreak,” Lim said in a statement.
    During the middle and late phases of the 2003 SARS epidemic, the virus accumulated mutations that lessened its strength, according to the researchers.

    Where the deletion occurs in the genome is pretty meaningful because it’s a known immune protein which means it counteracts the host’s antiviral response,” Lim told the Daily Mail.

    A weakened virus that causes less severe symptoms may get a leg up if it is able to spread efficiently through populations by people who don’t know they are infected, the scientists say. However, it’s too soon to say whether the novel coronavirus is beginning to lose its potency, according to the researchers.
    From the paper:
    Like SARS-CoV, the SARS-CoV-2 genome encodes multiple open reading frames in the 3' region. We found that the SARS-CoV-2 AZ-ASU2923 genome has an 81 nucleotide deletion in the ORF7a gene resulting in a 27 amino-acid in-frame deletion (Figure 2B). The SARS-CoV ORF7a ortholog is a viral antagonist of host restriction factor BST-2/Tetherin and induces56 apoptosis (11-14).

    To validate the deletion, we performed RT-PCR using primers spanning the region and verified by Sanger sequencing the amplicons (Figure 2C). Similar deletions in SARS-CoV-2 genomes are emerging, notably in the ORF8 gene that may potentially reduce virus fitness. Hence, further experiments are needed to determine the functional consequences of the ORF7a deletion.
    This is another random aspect impacting virus infectiousness (other than herd immunity). Notice its impact on the spread could go either way, (ie: more or less).
    Last edited by Selfsim; 2020-May-05 at 10:50 PM.

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    Quote Originally Posted by Selfsim View Post
    The original description doesn’t realise the distinctions of latent, lytic and lysogenic infection .. which are needed to clarify other known virus infection modes.
    It appears Selfsim isn't going to explain further.
    If anyone's curious, this refers to the way in which some viruses can become latent within infected cells, producing no virions for years on end, their genetic material either incorporated into the host's nuclear DNA as a provirus, or floating around loose as an episome. The viral genes just hang around without driving virion production, but perhaps expressing some genes to modify the cell's behaviour and protect themselves. They may even reproducing along with the rest of the cell's DNA if the cell divides. The most familiar example is probably the chickenpox virus, varicella zoster, which can become latent in nerve cells and then reactivate decades later as shingles.
    This was the detail I chose to skip over because it doesn't make any difference to the basic narrative--if the latent virus is to cause infection in others, it eventually, at some point, has to trick the host cell into producing and releasing more virions. (Hence the fact that you can catch chickenpox from someone with shingles--the cells in the shingles blisters are shedding infective virions.)

    (The human genome is actually littered with remnants of old latent viruses, which found their way into sperm or egg cells and became inheritable. Search on Endogenous Viral Elements or Endogenous Retroviruses for more information.)

    Grant Hutchison

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    .. and then we get:

    Scientists say a now-dominant strain of the coronavirus appears to be more contagious than original:
    Scientists have identified a new strain of the coronavirus that has become dominant worldwide and appears to be more contagious than the versions that spread in the early days of the COVID-19 pandemic, according to a new study led by scientists at Los Alamos National Laboratory.The new strain appeared in February in Europe, migrated quickly to the East Coast of the United States and has been the dominant strain across the world since mid-March, the scientists wrote.
    ..
    Wherever the new strain appeared, it quickly infected far more people than the earlier strains that came out of Wuhan, China, and within weeks it was the only strain that was prevalent in some nations, according to the report. The new strain’s dominance over its predecessors demonstrates that it is more infectious, according to the report, though exactly why is not yet known.
    ...

    The Los Alamos team, assisted by scientists at Duke University and the University of Sheffield in England, identified 14 mutations. Those mutations occurred among the nearly 30,000 base pairs of RNA that other scientists say make up the coronavirus’s genome. The report authors focused on a mutation called D614G, which is responsible for the change in the virus’ spikes. “The story is worrying, as we see a mutated form of the virus very rapidly emerging, and over the month of March becoming the dominant pandemic form,” study leader Bette Korber, a computational biologist at Los Alamos, wrote on her Facebook page. “When viruses with this mutation enter a population, they rapidly begin to take over the local epidemic, thus they are more transmissible.”

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    Quote Originally Posted by grant hutchison View Post
    It appears Selfsim isn't going to explain further.
    If anyone's curious, this refers to the way in which some viruses can become latent within infected cells, producing no virions for years on end, their genetic material either incorporated into the host's nuclear DNA as a provirus, or floating around loose as an episome. The viral genes just hang around without driving virion production, but perhaps expressing some genes to modify the cell's behaviour and protect themselves. They may even reproducing along with the rest of the cell's DNA if the cell divides. The most familiar example is probably the chickenpox virus, varicella zoster, which can become latent in nerve cells and then reactivate decades later as shingles.
    This was the detail I chose to skip over because it doesn't make any difference to the basic narrative--if the latent virus is to cause infection in others, it eventually, at some point, has to trick the host cell into producing and releasing more virions. (Hence the fact that you can catch chickenpox from someone with shingles--the cells in the shingles blisters are shedding infective virions.)

    (The human genome is actually littered with remnants of old latent viruses, which found their way into sperm or egg cells and became inheritable. Search on Endogenous Viral Elements or Endogenous Retroviruses for more information.)

    Grant Hutchison
    The point is that in the broader virus context, shedding, (even if that is the process detected by PCR tests), is not a good indicator of potential infectiousness, or otherwise.

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    Quote Originally Posted by headrush View Post
    With regard to smoking and under-representation of smokers in covid19 cases. It occurred to me that maybe it is the suppression of the immune system experienced by smokers that is preventing an overreaction to the virus. Prevention of the cytokine storm scenario may lead to a better outcome. I'm not sure how to square that possibility with the danger faced by immune deficient patients. Possibly a reduced but not entirely eliminated immune response. I've not heard of any results from the French nicotine patch trials yet.
    This is just complete speculation, but is it possible that people who smoke tend to keep more distance between themselves and others, perhaps as avoidance for passive smoking? So that they tend to have less close interactions?
    As above, so below

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    Quote Originally Posted by Jens View Post
    This is just complete speculation, but is it possible that people who smoke tend to keep more distance between themselves and others, perhaps as avoidance for passive smoking? So that they tend to have less close interactions?
    I think that while what you say is true, it doesn't play a very important part. Smokers are usually only at a distance while they're smoking. The rest of the time they act in exactly the same ways and are subject to the same influences as non-smokers. In fact, smokers will be worse in some respects, frequently putting their hands to their mouth for example.

    It may turn out that smoking plays no part in the progression or suppression of covid19. My interest is pretty personal as I am a smoker. Well, I was up until 2 weeks ago. We'll see how it turns out this time

    This is why I have been interested in how long the effects of smoking last after quitting. It would be pretty ironic to give up the thing that was protecting me against imminent serious infection, but if the effects are still active then I have to try to stop for the longer term benefit. I am quitting now because I had a prearranged consultation with a stop smoking advisor a few weeks ago which was actually booked in January. They are pretty busy.

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    Not trying to derail this thread, but I really think that the following thread can be useful in saving lives and breathes.
    I quit smoking on December 1, 2006 and never had a smoke since. It was virtually withdrawal-pain-free after smoking 3xpacks-of-25 (Dunhills) a day, for decades.

    https://forum.cosmoquest.org/showthr...than-16-months

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    Quote Originally Posted by a1call View Post
    Not trying to derail this thread, but I really think that the following thread can be useful in saving lives and breathes.
    I quit smoking on December 1, 2006 and never had a smoke since. It was virtually withdrawal-pain-free after smoking 3xpacks-of-25 (Dunhills) a day, for decades.

    https://forum.cosmoquest.org/showthr...than-16-months
    Agree!

    As a life long smoker with no intention of quitting, I feel it's safe to state there zero health benefits to smoking.

    Now if you want to flip this back to science, what are the chances that there is a bias in data collection in regards to smoking? I can think of a couple of possibilities for that. After a smoke, I don't feel real fresh and I am not inclined to let someone stick something in my mouth or nose, even if it was for a medical test. So I would be missed because I'd avoid the test. If someone doesn't observe me smoking, I won't tell them that I do smoke. I've had too many bad experiences with that sudden "reveal". It's more than annoying. When I go to the doctor's office, I won't smoke before hand and change my clothes. I do tend to be up front with my doctor because I personally know them outside of their practice and have no chance of fooling them, but I don't feel it's necessary to draw more attention than necessary to it. As near as I can tell, when I write "I smoke x of pack a day" it really doesn't sink in the same way as if I smell like of fire at tobacco plantation. I am sort of the opinion that there are many reasons why people can't pick out a smoker and equally many reasons not to disclose that information in any meaningful way.

    Some of these studies could either have a threshold that isn't being met - "I smoke 3 cigarettes a day" which doesn't get recorded as a "smoker", or they aren't asking the question because they can't observe a reason to do so or the respondent lies, or the respondent is in the ever quitting mode, so they "I used to smoke" even when they aren't trying to quit. It could be something ridiculous like the question is buried someplace in the paperwork and isn't being focused on or it's in an app that springs up an annoy amount of subsequent questions - how much?, how often?, how long? and the questioner isn't real religious about running down that path.

    I would think that there are all kinds of biases that researchers deal with and this might be one of the trickier ones.
    Solfe

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    Quote Originally Posted by Solfe View Post
    Agree!

    As a life long smoker with no intention of quitting, I feel it's safe to state there zero health benefits to smoking.

    Now if you want to flip this back to science, what are the chances that there is a bias in data collection in regards to smoking? I can think of a couple of possibilities for that. After a smoke, I don't feel real fresh and I am not inclined to let someone stick something in my mouth or nose, even if it was for a medical test. So I would be missed because I'd avoid the test. If someone doesn't observe me smoking, I won't tell them that I do smoke. I've had too many bad experiences with that sudden "reveal". It's more than annoying. When I go to the doctor's office, I won't smoke before hand and change my clothes. I do tend to be up front with my doctor because I personally know them outside of their practice and have no chance of fooling them, but I don't feel it's necessary to draw more attention than necessary to it. As near as I can tell, when I write "I smoke x of pack a day" it really doesn't sink in the same way as if I smell like of fire at tobacco plantation. I am sort of the opinion that there are many reasons why people can't pick out a smoker and equally many reasons not to disclose that information in any meaningful way.

    Some of these studies could either have a threshold that isn't being met - "I smoke 3 cigarettes a day" which doesn't get recorded as a "smoker", or they aren't asking the question because they can't observe a reason to do so or the respondent lies, or the respondent is in the ever quitting mode, so they "I used to smoke" even when they aren't trying to quit. It could be something ridiculous like the question is buried someplace in the paperwork and isn't being focused on or it's in an app that springs up an annoy amount of subsequent questions - how much?, how often?, how long? and the questioner isn't real religious about running down that path.

    I would think that there are all kinds of biases that researchers deal with and this might be one of the trickier ones.
    Firstly, speaking as someone who has recently stopped, smokers smell. I didn't realise how much. Even if you've changed your clothes. It's on your breath when you speak.

    Secondly, the smoking/Covid-19 thing came about because some doctors observed that some patients were suffering less acutely and surviving hospital treatment better. The common aspect between them was that they smoked. I don't think there's much sample bias to be found in chest x-rays. Doesn't matter what the patient says or claims, the physical evidence is there to see. I would assume a hospitalised case of Covid-19 would get xrayed or scanned somehow.

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    Quote Originally Posted by Selfsim View Post
    The point is that in the broader virus context, shedding, (even if that is the process detected by PCR tests), is not a good indicator of potential infectiousness, or otherwise.
    Not shedding detectible viral genetic material is a good test of not being infectious, however. You might start shedding tomorrow, but that's true of all viral infections.
    When people are shedding viral genetic material, the immediate question is whether they are shedding intact virions. Which is what makes PCR results difficult to interpret in convalescent people.

    Grant Hutchison

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    Quote Originally Posted by headrush View Post
    Secondly, the smoking/Covid-19 thing came about because some doctors observed that some patients were suffering less acutely and surviving hospital treatment better. The common aspect between them was that they smoked.
    It's actually an epidemiological thing, rather than a patient-centred thing. What was noticed was that the proportions of hospitalized and critically ill patients who are smokers is lower than the proportion of the general population who are smokers. Something appeared to be reducing the smokers' risk either of catching the disease, or of developing severe problems because of the disease. (This seems like a nitpick, but it becomes relevant below.)

    Quote Originally Posted by headrush View Post
    I don't think there's much sample bias to be found in chest x-rays. Doesn't matter what the patient says or claims, the physical evidence is there to see. I would assume a hospitalised case of Covid-19 would get xrayed or scanned somehow.
    X-rays and CT scans are a pretty blunt instrument when it comes to smoking. Most smokers have normal chest X-rays until they develop chronic obstructive pulmonary disease, at which point it's impossible to say whether the disease is smoking-related or not. Probably the best way to detect current smokers is to measure carboxyhaemoglobin levels, which are higher in smokers. These are routinely reported by modern blood gas analysers, and a blood gas test would be routine for someone with severe COVID, requiring ventilatory support, but maybe not with milder disease needing just a little supplementary oxygen.

    But I'd say that the salient fact here is that smokers may well lie to their doctors when they're feeling well and consulting about something minor, but when they're admitted to hospital with breathing difficulties, they (and their relatives) are keen to share every little fact that might contribute to their care (just like the rest of us). So in epidemiological terms, hospitalized smokers are more likely to confess to smoking than they would be in routine interviews in the community. Which means our community figures are more of an underestimate than our hospitalized figures, and makes the relative absence of hospitalized COVID patients who admit to smoking even more striking.

    Grant Hutchison

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    I haven’t been following carefully. I recall that the smoker situation was reported early-on. Has the reduced proportion of smokers carried throughout the pandemic?


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    I may have many faults, but being wrong ain't one of them. - Jimmy Hoffa

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    Quote Originally Posted by Extravoice View Post
    I haven’t been following carefully. I recall that the smoker situation was reported early-on. Has the reduced proportion of smokers carried throughout the pandemic?
    The pattern's still there, and is now established across multiple studies (which is a good test that it's a real signal). Here is a recent report from France, for example:
    Conclusions and relevance: Our cross sectional study in both COVID-19 out- and inpatients strongly suggests that daily smokers have a very much lower probability of developing symptomatic or severe SARS-CoV-2 infection as compared to the general population.
    Grant Hutchison

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    I guess that could tie in with the anecdotal evidence that there were several atypical cases of pneumonia and other respiratory problems in Italy in November and December, and the recent confirmation of a case of Covid-19 in France from December.

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    The problem for us non smokers is that just wearing a nicotine patch is not necessarily recommended even if the nicotine hypothesis is demonstrated. Nicotine is a poison and is addictive. The good part of the story is that patches might reduce worsening once the later phase kicks in, maybe?
    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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    I found this:
    A https://onlinelibrary.wiley.com/doi/...6.2012.04772.x
    Which tells that venous thromboembolism VTE is 1.8 times worse in smokers with blood groups AB compared to O. The role of blood group in severe symptoms has been mentioned on this thread before.
    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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    The statistical bias for smokers relative to Covid-19 is scientifically intriguing. But to reason that smoking is a tool against the pandemic is as idiotic as suggesting that bleach injection will protect you against the pandemic. Bleach will kill you instantly and it should be easy to show that an average person has greater chance of suffocating to death in the long run from smoking than COVID-19. I have seen what smoking can do people.
    Just my 2 cents.

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    Quote Originally Posted by headrush View Post
    Secondly, the smoking/Covid-19 thing came about because some doctors observed that some patients were suffering less acutely and surviving hospital treatment better. The common aspect between them was that they smoked. I don't think there's much sample bias to be found in chest x-rays. Doesn't matter what the patient says or claims, the physical evidence is there to see. I would assume a hospitalised case of Covid-19 would get xrayed or scanned somehow.
    Locally, we've been having mobile testing centers checking people (We also are getting used to the idea that a grocery store is not "random sampling" for a lot of reasons). I was thinking of the smoking issue against a swab and questionnaire style test. But you are right, an X-ray doesn't' lie.
    Solfe

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    Quote Originally Posted by a1call View Post
    ... it should be easy to show that an average person has greater chance of suffocating to death in the long run from smoking than COVID-19.
    Quite difficult to show, actually, and I wouldn't bet on the outcome.
    1) We don't have all the data. The longer this goes on, and the more cases and deaths we have, the greater the number of smokers who are going to have been "protected" from death or life-changing illness.
    2) There's a lifetime dose-response curve to smoking risk, and quite probably to smoking benefit in COVID. There's no particular reason to assume these will be the same shape, so it's possible there may be a smoking minimax "sweet spot"--a daily consumption that minimizes long term risk while maximizing short term benefit. It's pretty likely that we won't be able to naively sort the problem into "smokers" and "non-smokers".
    3) If you could choose an intervention now, that increased your chance of surviving a disease this year, but also will shortened your life in the long term if you survive the disease, what would you do? These are difficult problems, and epidemiologists address them with the concept of the Quality Adjusted Life Year (QALY). How many years of extra life (on average) could a smoker exposed to COVID expect compared to an age-and-sex-matched non-smoker? How many of those years would carry a disease burden that limited quality of life? Again, there might be a sweet spot, an age band in which your risk of immediate death is offset enough to justify the reduced QALYs you can expect to have because you're a smoker.
    4) Finally, there's the cost to society of the disease burden associated with smoking. Are smokers providing a public service, at present, by keeping themselves out of hospital and reducing pressure on scarce resources? But if they survive, they'll consume a disproportionate amount of health-care resource in later life. How do we balance those burdens? That's going to depend on the prevalence of smoking in your society.

    None of this is a recommendation for people to start smoking--the fact that we don't have data should be enough to dissuade anyone from embarking on a course that we know is likely to both shorten their lives and cripple them in the long term. But we should also avoid the sort of moral panic that I keep seeing with regard to these data--"OMG, here's something that is good for smokers! But smoking is bad, bad, bad! We all know that! We've got to stop smokers feeling happy about this! For their own good!"

    Grant Hutchison

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    Quote Originally Posted by grant hutchison View Post
    Quite difficult to show, actually, and I wouldn't bet on the outcome.
    1) We don't have all the data. The longer this goes on, and the more cases and deaths we have, the greater the number of smokers who are going to have been "protected" from death or life-changing illness.
    2) There's a lifetime dose-response curve to smoking risk, and quite probably to smoking benefit in COVID. There's no particular reason to assume these will be the same shape, so it's possible there may be a smoking minimax "sweet spot"--a daily consumption that minimizes long term risk while maximizing short term benefit. It's pretty likely that we won't be able to naively sort the problem into "smokers" and "non-smokers".
    3) If you could choose an intervention now, that increased your chance of surviving a disease this year, but also will shortened your life in the long term if you survive the disease, what would you do? These are difficult problems, and epidemiologists address them with the concept of the Quality Adjusted Life Year (QALY). How many years of extra life (on average) could a smoker exposed to COVID expect compared to an age-and-sex-matched non-smoker? How many of those years would carry a disease burden that limited quality of life? Again, there might be a sweet spot, an age band in which your risk of immediate death is offset enough to justify the reduced QALYs you can expect to have because you're a smoker.
    4) Finally, there's the cost to society of the disease burden associated with smoking. Are smokers providing a public service, at present, by keeping themselves out of hospital and reducing pressure on scarce resources? But if they survive, they'll consume a disproportionate amount of health-care resource in later life. How do we balance those burdens? That's going to depend on the prevalence of smoking in your society.

    None of this is a recommendation for people to start smoking--the fact that we don't have data should be enough to dissuade anyone from embarking on a course that we know is likely to both shorten their lives and cripple them in the long term. But we should also avoid the sort of moral panic that I keep seeing with regard to these data--"OMG, here's something that is good for smokers! But smoking is bad, bad, bad! We all know that! We've got to stop smokers feeling happy about this! For their own good!"

    Grant Hutchison
    Thanks Grant, a lot of useful information there.
    For myself, I'm just hoping the beneficial effect of smoking doesn't wear off too quickly so I can continue to quit without dying of the virus. Otherwise I may as well keep smoking until its all over.

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    Quote Originally Posted by grant hutchison View Post
    But I'd say that the salient fact here is that smokers may well lie to their doctors when they're feeling well and consulting about something minor, but when they're admitted to hospital with breathing difficulties, they (and their relatives) are keen to share every little fact that might contribute to their care (just like the rest of us). So in epidemiological terms, hospitalized smokers are more likely to confess to smoking than they would be in routine interviews in the community.
    But that doesn't square with the reported data, which claims that roughly 25% of the French population in general smoke (but roughly only 5% of covid-19 hospitalizations are smokers). I'm not sure where the 25% figure comes from, but it seems to be from prior surveys, independent of the pandemic.
    Everyone is entitled to his own opinion, but not his own facts.

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    Quote Originally Posted by profloater View Post
    The problem for us non smokers is that just wearing a nicotine patch is not necessarily recommended even if the nicotine hypothesis is demonstrated.
    Yes, with patches, even "Step 3" at 7 mg can be an overdose if you're not already hooked to some degree. And cutting patches in half releases all the nicotine at once, which would be a massive overdose.
    Everyone is entitled to his own opinion, but not his own facts.

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    Quote Originally Posted by grant hutchison View Post
    Quote Originally Posted by SelfSim
    The point is that in the broader virus context, shedding, (even if that is the process detected by PCR tests), is not a good indicator of potential infectiousness, or otherwise.
    ... When people are shedding viral genetic material, the immediate question is whether they are shedding intact virions.
    See, the issue here is that question is biased purely from concerns of a hypothesised community spread transmission method (and a admittedly a well-evidenced one), but it is also a singular focus.

    The fact is that a virus genome, in isolation, is the blueprint for generating a virion. Any such intact viral genome has the potential of (re)generating infection on a planet of living organisms. The potential of infection still exists regardless of the immediate form in which it is 'shed', (or the particular concerns/biases of the observer .. aka: community spread).
    This is the current explanation for how SARS-2 became a 'novel' infection in the first place!

    This matter serves as a distinction between a scientific focus, and a purely epidemological one.

    The heavy emphasis on epidemiology, will only ever inform scientific enquiry .. which is what I believe was missed (and extinguished by) matters occurring in this thread earlier on.

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    The effects of smoking on up- or down-regulation of ACE-2 receptors is an aside issue because infection still occurs in all non-smoking humans.

    The main causes of death still point towards viral infection (and functional breakdowns) of other organs also lined with ACE-2 receptors, regardless of smoking/non smoking behaviors.

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    Quote Originally Posted by Cougar View Post
    But that doesn't square with the reported data, which claims that roughly 25% of the French population in general smoke (but roughly only 5% of covid-19 hospitalizations are smokers). I'm not sure where the 25% figure comes from, but it seems to be from prior surveys, independent of the pandemic.
    The point is not trying to square it with the data, but trying to tease out the effect of bias in the data. We can assume that both figures (25% community, 5% hospital) are underestimates, because people tend to conceal their smoking status, not pretend to smoke when they don't. Is it possible, then, that the effect we see is due entirely to people lying about their smoking status, with more liars in the hospital group than the community group? I'm saying that's extremely unlikely, because smokers may well blithely conceal their smoking status when having health checks or consulting about an ingrown toenail, but smokers hospitalized because of breathing difficulties are highly motivated to declare their real status.
    It was a response to Solfe's point about smokers concealing their smoking habit, which while certainly true is very unlikely to account for the underrepresentation of smokers among those hospitalized with COVID.

    Grant Hutchison

  29. #2069
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    Quote Originally Posted by Selfsim View Post
    The fact is that a virus genome, in isolation, is the blueprint for generating a virion. Any such intact viral genome has the potential of (re)generating infection on a planet of living organisms. The potential of infection still exists regardless of the immediate form in which it is 'shed', (or the particular concerns/biases of the observer .. aka: community spread).
    This is the current explanation for how SARS-2 became a 'novel' infection in the first place!
    I'm sorry, I can't make head nor tail of that. Viral RNA can't make virions unless it can get its whole genome inside a cell and subvert the cellular machinery; so describing shed debris of viral RNA as being "potentially infectious" is like describing scattered bits of a car engine as being "potentially driveable".

    Nor do I understand your idea of the "current explanation" for the origin of SARS-CoV-2. Are you suggesting it arose from bits of naked viral RNA? If so, can you provide a reference?

    Grant Hutchison

  30. #2070
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    Quote Originally Posted by headrush View Post
    Firstly, speaking as someone who has recently stopped, smokers smell. I didn't realise how much. Even if you've changed your clothes. It's on your breath when you speak.
    Yes, I didn't write that directly because I was trying to be polite. I sort of meant that, in the sense: if I am on a train and there is somebody who smells like cigarettes, I will tend to avoid sitting next to them. So it is possible that they maintain more distance, perhaps passively rather than actively. And hence are less prone to being infected. But is just one confounding factor to the idea that smoking may protect you from COVID.
    As above, so below

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