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Coronavirus

Discussion in 'Off Topic' started by Wenche, Jan 27, 2020.

  1. bkp_duke

    bkp_duke Active Member

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    As a physician you should know that the mucous membranes of your eyes can express the proper receptors for some viruses to bind.

    The classic example of this type of virus is adenovirus:
    mucous membranes of the eyes - causes pink eye
    mucous membranes of the respiratory tract - causes URI symptoms

    The same virus sub-type can infect through multiple mechanisms, although I do agree that the rate / risk of infection via the eyes is much much lower than through the respiratory tract.


    EDIT - for the record, I do now know if COVID-19 has the proper protein structure on the surface for infections via the eye. My point was you were making a very broad, yet incorrect statement regarding infections via the eye.
     
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  2. Cosmacelf

    Cosmacelf Well-Known Member

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    The Washington Post recently posted a fact check on a recent Biden ad that had deceptively edited what I think is the source of all these "Trump called coronavirus a hoax" posts. On February 28, during a rally, Trump, in his rambling style, said that his political opponents were ginning up the coronavirus response or lack of response as the next crisis to attack him. He liken it to the Russia conspiracy theories, and the failed impeachment trial. Since he called all these previous political hits "hoaxes", he was calling the attempt to hurt him politically about coronavirus a hoax. He WASN'T calling the virus or the threat of the virus itself a hoax. He was calling the attempt to use the crisis as a political weapon a hoax (ie. in his eyes, the criticism of his response isn't valid).

    The Washington Post article: https://www.washingtonpost.com/politics/2020/03/13/biden-ad-manipulates-video-slam-trump/

    I'm well aware that the article criticizes Trump for other things, like similarly deceptively edited video, lack of response, etc. But saying that Trump called the coronavirus outbreak a hoax is simply not true. And I do understand there is a certain amount of sarcastic mocking in some of the comments above, but it can perpetuate a myth.
     
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  3. bkp_duke

    bkp_duke Active Member

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  4. Snapdragon III

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    Quick update to my personal situation. I woke up this morning and felt significantly better. Much less fatigued than I have for the last 7 days. My wife is also starting to feel better. I am feeling very confident at this point that our Covid cases were very mild ones, and are going to stay that way. It is a great feeling. The worst part for us has been the worry and uncertainty that it would get much worse. The actual symptoms were not that terrible for us. Fatigue, sore throats, mild fever, itchy but dry noses, shortness of breath with almost any physical activity. Our 11 year old daughter did not have any symptoms at all.
     
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  5. dfwatt

    dfwatt Active Member

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    #3265 dfwatt, Mar 15, 2020
    Last edited: Mar 15, 2020
    Although there's a lot about multiple organ failure in sepsis that still remains to be mapped out don't you think there's increasing evidence for a cytokine basis to this? I believe the evidence base is compelling that cytokines cause confusional states and delirium in sepsis. That's kind of my area so I feel pretty conversant with the literature on that.

    Additionally there's the very interesting and provocative review available on Medline about how prior immunization with anything except the S protein fragment of the prior Coronavirus creates animals that show immunopathology of the lung when rechallenged with respiratory viruses to which they have been inoculated. I think this duplicates experience in children as well who were inoculated against a common respiratory cold virus who showed similar immunopathology of the lung when rechallenged.

    I certainly defer to your greater expertise in this but don't you think there's a decent evidence base already to conclude that in some forms of severe pneumonia the problem is the immune system at least as much as the pathogen, although of course that distinction is always tricky because the pathogen is driving immune activation through various DAMP and other aspects of the inflammasome.
     
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  6. bkp_duke

    bkp_duke Active Member

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    #3266 bkp_duke, Mar 15, 2020
    Last edited: Mar 15, 2020
    I do think that is a possibility.

    I would LOVE to see at least a case series reported on the autopsies of those that have died from this. Tissue analysis specifically. It would help tease out the specifics of the ARDS cases that caused the patients to expire.

    A great follow up study, but one that would be much harder to collect, would be biopsy analysis of patients with milder symptoms (I know the ethical ramifications for asking for this kind of data).
     
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  7. Unpilot

    Unpilot Sell order in at $5999.99

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  8. Sanny

    Sanny Member

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    Looking for ton of dislikes. Disproportionally many people here (and the ones that are writing those excellent touching medium posts) are in IT, marketing, etc, or employed by gov/large corporations that will be bailed out. In my view remote work is bullshit and doesn't work outside of those professions that employ it widely regardless. For others its means tons of people will just stop working or just will pretend to be working (still accounting for a paycheck that someone will provide for them on time).
    I do not see a debate on the very important moral topic: what if do whatever we all can and then we think that we managed to save that unknown % of folks and we all feel so good about it. But after the victory we see that let's say 30% of us will lose jobs this year without an option to find another one? Will you support those harsh measures with unknown outcome if there is a certain chance that your job is lost as a result?
     
  9. bkp_duke

    bkp_duke Active Member

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    The CFR (case fatality rate) is much higher than with H1N1. Also, there was debate among infectious disease docs and immunologists at the time that previous influenza exposure or vaccines might have given partial immunity to the H1N1 influenza virus, where that does not exist in this case.
     
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  10. Doggydogworld

    Doggydogworld Active Member

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    Interesting graph. South Korea's rate is roughly half of Wuhan's rate for each age bracket. But their overall rate is ~1/4th of Wuhan's. South Korea's confirmed cases clearly skewed younger, by about a dozen years on average. I'd say that's mostly due to testing differences, i.e. tracing and testing every known contact vs. only testing those who come to the hospital with symptoms.
    Nice list of actual testing capacity shows 34k as of today. Utilization and geographic coverage are still spotty, but improving.
    Those early 33% growth rates reflect ~33% daily growth in test capacity. Italy went from 4 cases on February 20 to 655 a week later. That 107% daily growth rate was clearly testing catch-up, not virus spread. Switzerland case count grew 62% yesterday - another incidence of testing catch-up. The US is slowly catching up as testing becomes more available.

    New cases were flat in Italy yesterday. That could be a sign they've caught up, but it's way too early to tell. The situation is so grim in some badly afflicted areas that they may lack the human resources to maintain testing rates.
    You believe Shanghai's data? I don't think it's running rampant there, but total eradication sounds a little Dear Leader-ish.
     
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  11. SageBrush

    SageBrush REJECT Fascism

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    Glad to hear, but do your community a favor and wear a mask in public places until you test (in about a week) negative.

    My wife woke up with a sore throat and a headache yesterday. She is spending most of her time in the guest room now and when she leaves it she wears a mask. If she has any progression of symptoms I'll try to get her tested but tests are a new thing to NM so this may have to handled clinically. And as is, we both wear masks in public spaces so the practical difference of being testing or not is limited.
     
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  12. dfwatt

    dfwatt Active Member

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    I'll see what I can dig out in terms of preliminary reports because I think I've seen a couple of things but I don't know how detailed or methodologically careful they were.

    I think it's worth remembering that immune activation is an "emergency defense mode" in a sense and therefore by definition it may potentially sacrifice other modes or functional vectors or adaptive programs built into the organism. You can't optimize for everything. And although it seems contradictory, at some point, immune activation may even jeopardize life.
     
  13. KarenRei

    KarenRei ᴉǝɹuǝɹɐʞ

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    There's enough cases out there that with sufficient effort you could surely find people who died from unrelated causes while sick (for example, car/motorcycle accidents)
     
  14. traxila

    traxila Supporting Member

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    Great news! Very happy to hear!

    Did you take any medications?

    Zinc? Hydroxychloroquine? Quercetin?

    Finish your recoveries and get out into the world and calm people down! Not to mention have a blast!

    All the best!
     
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  15. bkp_duke

    bkp_duke Active Member

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    Actually, the best comparison would be from mild cases of coronavirus that did not exhibit signs / symptoms of cytokine storm. That would account for a variable matching dataset far better than uninfected individuals that died of an unrelated cause.
     
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  16. bkp_duke

    bkp_duke Active Member

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    Reading this now, it appears to be the article that got all the attention.
    Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China

    Only part way through, but two significant confounding factors so far are:

    1) the ages of the populations do not match (not unexpected, but it makes data analysis much harder)
    2) I have yet to see if they accounted for secondary infections as a cause for their conclusions
     
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  17. traxila

    traxila Supporting Member

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    This is a fair point. I will not try to minimize the hardships that can visit people in their economic situation. But in the end the best way to preserve the economy will be to minimize the body count. An overwhelmed health care system can be the first step to chaos. Not saying that is happening here, but it is something to consider.
     
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  18. bkp_duke

    bkp_duke Active Member

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    OK, finished reading that study.

    It's an early study, so I'm not going to nit-pick it to death. Better data will come out over time, but if I were reviewing that paper, I would have serious issue with the last line (which is the line getting all the publicity):
    "The results obtained from this study also suggest that COVID-19 mortality might be due to virus-activated “cytokine storm syndrome” or fulminant myocarditis."

    The authors base this conclusion upon the following inflammatory markers being higher in those patients that died:
    Cardiac Troponin, Myoglobin, C-reactive Protein, Interleukin-6

    The above are all general markers of inflammation. And there in lies the rub and my concern with their conclusion. By definition, the more severe patients are those at greatest risk of dying. And in patients that die from other respiratory illnesses, by definition, they have higher levels of inflammation.

    Basically, there is a correlation in the data, but the authors do not present a sufficient case for causation. It cannot be concluded from the presented data set that cytokine storm is the cause of death, or simply a byproduct of having a more severe case (which results in death).

    Just my 0.02. Feel free to disagree.
     
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  19. Dr. J

    Dr. J Active Member

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    I believe this is the same gentleman who said, in a visit to the CDC, that he preferred people remain quarantined on a cruise ship rather than be taken off and counted in the US infection numbers: "I like the numbers where they are."

    Trump doesn't think the coronavirus pandemic is a hoax--he wants his base to think it's a hoax.
    Trump’s Dangerously Effective Coronavirus Propaganda
     
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  20. dfwatt

    dfwatt Active Member

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    I completely agree that causal attribution based on what's in that article is very difficult. What is clear is that there is something extremely undesirable about the intersection between aging immune systems and this pathogen. I don't know what that is, but I have to wonder if it's a function of a kind of 'partial recognition' of the pathogen driving some kind of sensitivity to it but without any increased effectiveness. I really don't know. And I'm just thinking out loud and trying to do hypothesis testing.

    But it's worth remembering that this kind of very steep mortality gradient in relationship to age is not universal by any means in relationship to viruses. Indeed some viruses are more deadly in the Young. But I just wonder if aging immune systems show a more potentiated pro-inflammatory state with subsequent risk to both lung and heart due to some partial recognition of some components of the virus without an effective antibody mediated response. Again just my thinking out loud.
     

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