5 ms·

Why is that the most preposterous hypothesis that doesn't warrant any review? We have no reliable antibody tests, and then won't give the unreliable ones peopl

Why is that the most preposterous hypothesis that doesn't warrant any review? We have no reliable antibody tests, and then won't give the unreliable ones people because they are so rare. So where does the confidence come from that we can rule out this possibility? What if this is already the "second wave". Something with lower symptoms wouldn't have warranted checking for a new strain, complications and deaths would fit into the normal distribution of last fall's flu season with no outlier spikes. We would then be deep into the second wave and can't even test most for people currently exposed to it, much less having already been exposed. This is enough not to dismiss the hypothesis.

MaulingMonkey 6y ago
> Why is that the most preposterous hypothesis that doesn't warrant any review? It's not. What is preposterous is advancing the hypothesis without any meaningful evidence, to the detrement of more useful topics, or even useful discussion of the same topic. It's one thing to be an epidemiologist saying "hey, let's see how we can double check the exact origins of this", which is a potentially useful line of inquery. It's another to take some hypochondriac's third hand retelling of someone else's flu symptoms back in December and jump to the same untested unproven unscientific fear-driven conclusions they did on little more than their wild speculation. Even if they do somehow end up being right, they'll be right in the "broken clock is right twice a day" sense rather than a bringing anything useful to the table sense. So far, alternative suggestions as to the virus's origins have looked more similar to the latter - with perhaps some undertones of (completely understandable and expected) attempted political diversion (I sure wouldn't want fault for this mess hanging on my neck!) If you have some epidemiologist's proposed study that you're trying to drive funding towards - something that even remotely looks like the former - it'd be a welcome breath of fresh air on the topic, and I'd suggest sharing that as a far more useful and constructive way of advancing the hypothesis.
- pm_me_ur_fullz 6y ago
  People don't advance a hypothesis without enough anecdotes to say "look over there" People like you can help fill gaps of savants saying "this isn't a constructive methodology but it isn't inherently without merit" versus "I don't want to believe that because thats not consensus right now" versus "hm thats interesting maybe worth a look sometime before the 2022 congressional committee to fund the epidemiologists?"
  - sjg007 6y ago
    We would have seen a higher death rate if the virus was here earlier. As for hiding within the flu statistics, we test for influenza so these deaths would not have been classified as flu related. It's possible to have flu and covid-19 but early on it would have been rare. It's probably still somewhat rare. I am sure flu surveillance samples will be retroactively tested for the virus that causes covid-19. Stanford did this and they have mid to late Feb.
    - pm_me_ur_fullz 6y ago
      > We would have seen a higher death rate if the virus was here earlier. > What if this is already the "second wave". Something with lower symptoms wouldn't have warranted checking for a new strain, complications and deaths would fit into the normal distribution of last fall's flu season with no outlier spikes. I think you are misunderstanding what wave means here. It means an earlier not as deadly strain/conditions had already occurred, just like in the Spanish Flu in the spring versus the fall deadly resurgance, but at lower orders of magnitude. The strain itself doesn't have to be different if the co-morbidities were different - such as different opportunistic viruses or bacterias being present.
      - sjg007 6y ago
        We know this is not true because the mutation rate is too low.
        pm_me_ur_fullz 6y ago
        I specifically wrote "/conditions" to predict that specific rebuttal. The virus could be the same, the opportunistic additional virus/bacteria could be different. just like HIV causes no symptoms, until your immune system is down and a different infection (caused by bacteria or virus) kills you. Maybe even a normal "gut" bacteria, or something in your body usually present, is what kills you. There is research pointing to Sars-Cov-2 attacking T cells directly. Instant AIDS. In the fall and early winter, there could have been different variables that made it less debilitating and deadly than the spring variables. And in that case the fall and early winter deaths and pneumonia would have blended in to normal distribution.

MaulingMonkey 6y ago

> Why is that the most preposterous hypothesis that doesn't warrant any review? It's not. What is preposterous is advancing the hypothesis without any meaningful evidence, to the detrement of more useful topics, or even useful discussion of the same topic. It's one thing to be an epidemiologist saying "hey, let's see how we can double check the exact origins of this", which is a potentially useful line of inquery. It's another to take some hypochondriac's third hand retelling of someone else's flu symptoms back in December and jump to the same untested unproven unscientific fear-driven conclusions they did on little more than their wild speculation. Even if they do somehow end up being right, they'll be right in the "broken clock is right twice a day" sense rather than a bringing anything useful to the table sense. So far, alternative suggestions as to the virus's origins have looked more similar to the latter - with perhaps some undertones of (completely understandable and expected) attempted political diversion (I sure wouldn't want fault for this mess hanging on my neck!) If you have some epidemiologist's proposed study that you're trying to drive funding towards - something that even remotely looks like the former - it'd be a welcome breath of fresh air on the topic, and I'd suggest sharing that as a far more useful and constructive way of advancing the hypothesis.

pm_me_ur_fullz 6y ago
People don't advance a hypothesis without enough anecdotes to say "look over there" People like you can help fill gaps of savants saying "this isn't a constructive methodology but it isn't inherently without merit" versus "I don't want to believe that because thats not consensus right now" versus "hm thats interesting maybe worth a look sometime before the 2022 congressional committee to fund the epidemiologists?"
- sjg007 6y ago
  We would have seen a higher death rate if the virus was here earlier. As for hiding within the flu statistics, we test for influenza so these deaths would not have been classified as flu related. It's possible to have flu and covid-19 but early on it would have been rare. It's probably still somewhat rare. I am sure flu surveillance samples will be retroactively tested for the virus that causes covid-19. Stanford did this and they have mid to late Feb.
  - pm_me_ur_fullz 6y ago
    > We would have seen a higher death rate if the virus was here earlier. > What if this is already the "second wave". Something with lower symptoms wouldn't have warranted checking for a new strain, complications and deaths would fit into the normal distribution of last fall's flu season with no outlier spikes. I think you are misunderstanding what wave means here. It means an earlier not as deadly strain/conditions had already occurred, just like in the Spanish Flu in the spring versus the fall deadly resurgance, but at lower orders of magnitude. The strain itself doesn't have to be different if the co-morbidities were different - such as different opportunistic viruses or bacterias being present.
    - sjg007 6y ago
      We know this is not true because the mutation rate is too low.
      - pm_me_ur_fullz 6y ago
        I specifically wrote "/conditions" to predict that specific rebuttal. The virus could be the same, the opportunistic additional virus/bacteria could be different. just like HIV causes no symptoms, until your immune system is down and a different infection (caused by bacteria or virus) kills you. Maybe even a normal "gut" bacteria, or something in your body usually present, is what kills you. There is research pointing to Sars-Cov-2 attacking T cells directly. Instant AIDS. In the fall and early winter, there could have been different variables that made it less debilitating and deadly than the spring variables. And in that case the fall and early winter deaths and pneumonia would have blended in to normal distribution.