Day 121: COVID-19 Why Are States Obscuring the Data?

 

The screengrab above is from the Vermont Department of Health Weekly Summary of Vermont COVID-19 Data. It makes quite clear how residents of long-term care facilities are the majority of deaths from COVID-19 in that state. Similarly, the following chart illustrates the same thing, just adding that “Health Settings” include not only hospitals and long-term care, but therapeutic centers and behavioral health institutions as well.

Contrast Vermont’s data clarity with that of Minnesota. Although it is reported that 81% of Minnesota’s deaths occurred among residents of long-term care facilities, that is not easily demonstrated by the Minnesota Department of Health’s Stay Safe MN website. First, the only data that mention long-term care facilities is “case data,” not “death data.” Second, what death data there is is only disaggregated by race and ethnicity, not any other factors:

Congregant living?

Are LTC and Residential Behavioral Health “Non-Hospitalized?”

No correlation of deaths to anything other than race and ethnicity. Why is it important to correlate death to race and ethnicity, but not to residence in long-term care?

Of course, Minnesota is not alone in obscuring the relationship between infections in long-term care facilities and death. But why? When the data suggests that just getting your long-term care facilities infection control protocols in place would have reduced your deaths from COVID-19 by 80%, why wouldn’t you focus your energy there rather than house arrest for all residents? I get it that if you have a lot of infected but asymptomatic or minimally ill people going about, there is a greater challenge in protecting the residents of the long-term care facilities. But how is it less costly to impact the livelihoods of tens of millions rather than treat long-term care facilities more like Level 4 Bio labs?

The New York and Florida situations have been contrasted with regard to, in the one case, introducing infections into long-term care facilities, and in the other, putting emphasis on protecting residents of long-term care facilities as compared to other broader societal restrictions. As Texas Governor Greg Abbott tweeted, there does seem to be some correlation between the governing philosophies and the epidemic outcomes:

The first thing is focusing your efforts on the vulnerable, not controlling the whole of your society. Maybe you are obscuring the data so that it doesn’t make clear the consequences of your governing philosophy?

[Note: Links to all my COVID-19 posts can be found here.]

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  1. Jack Shepherd Inactive
    Jack Shepherd
    @dnewlander

    Hammer, The (View Comment):

    Please excuse what may be a dumb question, but could someone point me to the actual studies that determined not just that asymptomatic spread is possible, but that it is common, and that it is a statistically significant contributing factor with respect to transmission?

    This seems to be taken for granted to the point that I virtually never see it actually discussed.

    I don’t have a link to hand, but just the other day I saw a report that asymptomatic spread is very unlikely.

    Someone needs to tell America’s Democratic governors.

    Oh, wait. They don’t care. Since this is now political.

    • #31
  2. Hammer, The Inactive
    Hammer, The
    @RyanM

    Jack Shepherd (View Comment):

    Hammer, The (View Comment):

    Please excuse what may be a dumb question, but could someone point me to the actual studies that determined not just that asymptomatic spread is possible, but that it is common, and that it is a statistically significant contributing factor with respect to transmission?

    This seems to be taken for granted to the point that I virtually never see it actually discussed.

    I don’t have a link to hand, but just the other day I saw a report that asymptomatic spread is very unlikely.

    Someone needs to tell America’s Democratic governors.

    Oh, wait. They don’t care. Since this is now political.

    It seems to me that all of these measures that people insist we must take – masking and socially distancing and so forth – are based entirely on the premise of asymptomatic spread. Wouldn’t it behoove us to determine the extent to which it exists?

    • #32
  3. MISTER BITCOIN Inactive
    MISTER BITCOIN
    @MISTERBITCOIN

    Gumby Mark (R-Meth Lab of Demo… (View Comment):

    In AZ the state data site, which is otherwise excellent, does not allow you to find long-term care information separately. However, Maricopa County (Phoenix metro) with 60% of the state population not only breaks out long-term resident cases and deaths but separately accounts for long-term staff cases and deaths. As of today, 73% of fatalities are in long-term care and the % has been increasing over the past month. Some of the worst outbreaks have been in assisted living, not nursing homes, so relatively speaking healthier people in these facilities.

    Unfortunately, Gov Abbott’s tweet, by avoiding per capita analysis, utilizes the same trick that CNN and the NY Times deploy. On a per capita basis, California is almost identical to Florida and much, much closer to Texas than it is to NY.

    DO YOU live in a long term care facility or nursing home?

     

    • #33
  4. MarciN Member
    MarciN
    @MarciN

    Hammer, The (View Comment):

    Jack Shepherd (View Comment):

    Hammer, The (View Comment):

    Please excuse what may be a dumb question, but could someone point me to the actual studies that determined not just that asymptomatic spread is possible, but that it is common, and that it is a statistically significant contributing factor with respect to transmission?

    This seems to be taken for granted to the point that I virtually never see it actually discussed.

    I don’t have a link to hand, but just the other day I saw a report that asymptomatic spread is very unlikely.

    Someone needs to tell America’s Democratic governors.

    Oh, wait. They don’t care. Since this is now political.

    It seems to me that all of these measures that people insist we must take – masking and socially distancing and so forth – are based entirely on the premise of asymptomatic spread. Wouldn’t it behoove us to determine the extent to which it exists?

    Asymptomatic spread occurs with all upper respiratory viruses. People who don’t have symptoms yet, or may never have them, cough and the virus travels in their droplets.

    The question with this virus is whether people who have recovered are still contagious. Are asymptomatic carriers developing immunity and thus are they not spreading the disease after a two-week period during which their body develops antibodies? That varies from virus to virus. They have just learned this past week the answer to this question, which is extremely big news. Those who have recovered, with or without symptoms, are spreading (or “shedding”) the virus, but it’s dead.

    This should be on the front page of every paper in the world right now.

    Okay, I can’t find that article that I saw two days ago, but as I was looking for it, I found this, which is also important news: “New Data Suggest People Aren’t Getting Reinfected with the Coronavirus.” That is a breakthrough announcement.

    Good grief, this is also breathtakingly good news: 

    This one could be big. Researchers from the University of Washington School of Medicine and Vir Biotechnology say that the antibody they’ve identified, known as S309, “likely covers the entire family of related coronaviruses.” One of the chief obstacles to the development of a SARS-CoV-2 vaccine — or potent antiviral — is that the virus is perpetually mutating. But the Vir Biotechnology study suggests that S309 targets and disables the spike proteins that all known coronaviruses use to enter human cells. Which would mean that, no matter how the novel coronavirus evolves, it would “be quite challenging for [the virus] to become resistant to the neutralizing activity of S309.”

    For now, S309 has only proven itself to be an effective COVID-19 slayer in lab cultures, and still needs to be tested in people.

    What a week! And Moderna’s good vaccine news!

    Ring the church bells!

    And I’ll find that other story about the dead virus later. :-) I have to go celebrate. :-)

    • #34
  5. MarciN Member
    MarciN
    @MarciN

    All four of those announcements in the last week are game changers

    If I were Donald Trump, I would be on the news today with a smile and say, “We’ve got hope and we’ve finally got answers. Hallelujah!” 

    At Davos two years ago, I heard him say something to the effect of, “The United States is open for business.” He should replay that speech and say, “The United States is Reopened for business!” :-) :-)

    • #35
  6. Mendel Inactive
    Mendel
    @Mendel

    Hammer, The (View Comment):
    I have a really difficult time believing that there are not very smart people out there pursuing that very line. With Sars1, from which we are apparently choosing to learn no lessons, and which died out with far less infection than the 70% cited by most people, somebody found that there was a correlation between infection and standing water in drains… that means somebody was taking a look at cases and attempting to connect threads, in the classic Sherlock Holmes method of problem solving.

    I’ve also been banging this drum since the very beginning. EVERY virus (or other infectious disease) has a unique set of transmission characteristics that include Achilles’ heels that allow transmission to be greatly reduced using fairly simple measures. Even though I never specialized in epidemiology, we were still taught the example of the Amboy Gardens in SARS-1 at an early point in our virology training as a stark lesson: there’s no substitute for old-fashioned, gumshoe detective work.

    There are three parts to the answer to the question of “why isn’t anyone pursuing this strategy for Covid?”

    1) The virus itself: due to so many asymptomatic cases, when it enters a community it usually goes unnoticed. Then, at some point, it often explodes. That makes it difficult for epidemiologists to track it on the pavement level: they need a situation with so few cases that they can clearly link one single case to another single case. By the time the virus explodes, that becomes too difficult (too many people in contact with multiple infected individuals), and by that point the experts are usually overwhelmed with more urgent duties.

    2) The lockdowns: because we’ve forcefully stopped the spread of the virus in most places (often before it could ever take root), we’ve robbed ourselves of countless opportunities to study the virus within the optimal window for epidemiological sleuth-work.

    3) Us: despite the hurdles of 1) and 2), there actually have been a decent number of studies about the real-world transmission characteristics of SARS-2, especially over the past month. While too many questions still remain unanswered, in my opinion we have enough reasonably solid data to take actionable consequences. The remaining hurdle? Almost nobody is interested in partial measures. The majority of the population is so terrified of this virus that they seem content to stay home until their state has developed a robust test/trace/isolate program to completely suppress viral transmission – even though that could still take a month or longer. Meanwhile, most of the people who find that timeline intolerable are also convinced that SARS-2 is not meaningfully more dangerous than the common flu, and therefore tend to reject any measures that inconvenience their own lives.

    • #36
  7. Mendel Inactive
    Mendel
    @Mendel

    Hammer, The (View Comment):
    Please excuse what may be a dumb question, but could someone point me to the actual studies that determined not just that asymptomatic spread is possible, but that it is common, and that it is a statistically significant contributing factor with respect to transmission?

    There aren’t many real-world studies that conclusively show asymptomatic transmission. But there is enough indirect evidence suggesting a major impact of asymptomatic transmission that it also can’t be ruled out (yet).

    Asymptomatic transmission is difficult to prove for several rasons. All of the hurdles in my last comment obviously apply. There’s also the issue that many of the initial symptoms of Covid can be so mild or unremarkable (like coughing, which everyone does everyday) that the defining line between symptomatic and asymptomatic is murky and arbitrary. Add to that people’s often-inaccurate memories of such details several weeks or months after the event. There’s also the possibility of presymptomatic infections – i.e. people are not symptomatic when they transmit the virus, but start getting symptoms a day or two later. Those people will still likely be classified as “symptomatic” in any studies, even though they did not experience any symptoms when they were contagious.

    In terms of the indirect data, one of the key indicators of asymptomatic/presymptomatic contagion is the fact that asymptomatic patients have just as much viral replication in their upper respiratory tract as symptomatic patients, and those viruses are just as viable as in symptomatic patients. Even in symptomatic patients, the viral load in the upper respiratory tract reaches its peak right before symptoms start.

    The other major piece of evidence is from population-wide calculations of transmission. Basically, taking the number of people with symptomatic infections and multiplying that by our estimates of how contagious the virus is can’t account for the actual number of people who end up becoming infected. It’s like dark matter: the final results can’t be explained by the infections we “see”, so there must be some missing element. Asymptomatic/presymptomatic infection is the most likely culprit, although not the only one.

    • #37
  8. Stad Coolidge
    Stad
    @Stad

    CarolJoy, Above Top Secret (View Comment):
    Why is there no punishment for the hospital admins who ignored the Navy hospital ship Trump sent to NYC harbor, so infected elderly could be housed and treated separately from those who were uninfected?

    Good question.  Even if the governor directed them to put the patients in nursing homes, did not a single hospital manager say, “Governor, why not use the hospital ship?”

    I know why the ship wasn’t used, and the answer is in your sentence – the words “Trump sent” . . .

    • #38
  9. Ontheleftcoast Inactive
    Ontheleftcoast
    @Ontheleftcoast

    MarciN (View Comment):
    The question with this virus is whether people who have recovered are still contagious. Are asymptomatic carriers developing immunity and thus are they not spreading the disease after a two-week period during which their body develops antibodies? That varies from virus to virus. They have just learned this past week the answer to this question, which is extremely big news. Those who have recovered, with or without symptoms, are spreading (or “shedding”) the virus, but it’s dead. 

    That’s not all they’re learning!

    Big Pharma drug development scientist Derek Lowe’s excellent In the Pipeline blog discusses a recent paper; (to get to the point where it makes some sense he also provides as clear an introduction to the underlying immunology as I’ve seen):

    First of all, patients exposed to SARS-CoV-2 were mounting an antibody response that is consistent with our understanding of what “immune to a disease you’ve recovered from” looks like. Not yet proven to confer immunity, but it looks like it ought to. But wait, there’s more!

    …in the unexposed patients, 40 to 60% had CD4+ cells that already respond to the new coronavirus. This doesn’t mean that people have already been exposed to it per se, of course – immune crossreactivity is very much a thing, and it would appear that many people have already raised a response to other antigens that could be partially protective against this new virus. What antigens those are, how protective this response is, and whether it helps to account for the different severity of the disease in various patients (and populations) are important questions that a lot of effort will be spent answering. As the paper notes, such cross-reactivity seems to have been a big factor in making the H1N1 flu epidemic less severe than had been initially feared – the population already had more of an immunological head start than thought.

    So overall, this paper makes the prospects for a vaccine look good: there is indeed a robust response by the adaptive immune system, to several coronavirus proteins.

    You can be as suspicious of the vaccine establishment and Bill Gates as seems appropriate to you, but one underlying meaning of that last sentence is also that because the adaptive immune system has responded to this coronavirus in patients who have recovered it’s worth trying to develop a vaccine in the first place. In the absence of this response, about which there has been considerable uncertainty, there would be little point in trying. Vaccine or no, that’s good news.

    • #39
  10. Ontheleftcoast Inactive
    Ontheleftcoast
    @Ontheleftcoast

    Regarding the title of the OP, it’s not just the states. This is one more example that it ain’t glory the CDC has been covering itself with:

    The Centers for Disease Control and Prevention is conflating the results of two different types of coronavirus tests, distorting several important metrics and providing the country with an inaccurate picture of the state of the pandemic. We’ve learned that the CDC is making, at best, a debilitating mistake: combining test results that diagnose current coronavirus infections with test results that measure whether someone has ever had the virus. The upshot is that the government’s disease-fighting agency is overstating the country’s ability to test people who are sick with COVID-19. The agency confirmed to The Atlantic on Wednesday that it is mixing the results of viral and antibody tests, even though the two tests reveal different information and are used for different reasons.

    This is not merely a technical error. States have set quantitative guidelines for reopening their economies based on these flawed data points.

    Several states—including Pennsylvania, the site of one of the country’s largest outbreaks, as well as Texas, Georgia, and Vermont—are blending the data in the same way. Virginia likewise mixed viral and antibody test results until last week, but it reversed course and the governor apologized for the practice after it was covered by the Richmond Times-Dispatch and The Atlantic. Maine similarly separated its data on Wednesday; Vermont authorities claimed they didn’t even know they were doing this. 

    The widespread use of the practice means that it remains difficult to know exactly how much the country’s ability to test people who are actively sick with COVID-19 has improved.

    “’You’ve got to be kidding me,” Ashish Jha, the K. T. Li Professor of Global Health at Harvard and the director of the Harvard Global Health Institute, told us when we described what the CDC was doing. “How could the CDC make that mistake? This is a mess.”

    • #40
  11. MarciN Member
    MarciN
    @MarciN

    Ontheleftcoast (View Comment):
    You can be as suspicious of the vaccine establishment and Bill Gates as seems appropriate to you, but one underlying meaning of that last sentence is also that because the adaptive immune system has responded to this coronavirus in patients who have recovered it’s worth trying to develop a vaccine in the first place. In the absence of this response, about which there has been considerable uncertainty, there would be little point in trying. Vaccine or no, that’s good news.

    Wow. Very exciting. 

    The whole point of what Moderna is doing is to enable the world to develop vaccines fast. The owners of the company are starting with mRNA rather than DNA. The guys who built this new company have sunk an enormous amount of capital into this theory. I hope they are right for the world’s sake and for their investors and scientists. 

    Having this fast response to new viruses will enable people to travel again around the world. 

    The company is right on schedule in their covid-19 response. 

    I am a long-time fan of Bill Gates, and I admire everything he’s done, especially his philanthropy. I’m sorry he has attracted so much mistrust on Ricochet,and I’m not bothering to argue with people here about him. But I haven’t changed my high opinion of him. I am an admirer. :-) But for those who don’t trust Bill Gates, I don’t think he’s actually involved except peripherally in the Moderna startup. However, I wouldn’t say that for sure. It took an unbelievable amount of investment money to get that company off the ground. He may be one of the investors. Where Gates is going to help here is that he’s working on the production and distribution side. The minute someone has a vaccine ready to go, his production facilities can get to work. 

    • #41
  12. MarciN Member
    MarciN
    @MarciN

    Ontheleftcoast (View Comment):

    Regarding the title of the OP, it’s not just the states. This is one more example that it ain’t glory the CDC has been covering itself with:

    The Centers for Disease Control and Prevention is conflating the results of two different types of coronavirus tests, distorting several important metrics and providing the country with an inaccurate picture of the state of the pandemic. We’ve learned that the CDC is making, at best, a debilitating mistake: combining test results that diagnose current coronavirus infections with test results that measure whether someone has ever had the virus. The upshot is that the government’s disease-fighting agency is overstating the country’s ability to test people who are sick with COVID-19. The agency confirmed to The Atlantic on Wednesday that it is mixing the results of viral and antibody tests, even though the two tests reveal different information and are used for different reasons.

    This is not merely a technical error. States have set quantitative guidelines for reopening their economies based on these flawed data points.

    Several states—including Pennsylvania, the site of one of the country’s largest outbreaks, as well as Texas, Georgia, and Vermont—are blending the data in the same way. Virginia likewise mixed viral and antibody test results until last week, but it reversed course and the governor apologized for the practice after it was covered by the Richmond Times-Dispatch and The Atlantic. Maine similarly separated its data on Wednesday; Vermont authorities claimed they didn’t even know they were doing this.

    The widespread use of the practice means that it remains difficult to know exactly how much the country’s ability to test people who are actively sick with COVID-19 has improved.

    “’You’ve got to be kidding me,” Ashish Jha, the K. T. Li Professor of Global Health at Harvard and the director of the Harvard Global Health Institute, told us when we described what the CDC was doing. “How could the CDC make that mistake? This is a mess.”

    It is heartbreaking to see the CDC’s poor functioning. The private sector and universities have really left them behind in this crisis.

    I don’t know what’s going on with them.

    There’s probably a money issue involved. They are probably spread pretty thin as the catalog of diseases grows. They will need to push more off their plate to the private sector and universities now.

    Marriott has said they will have a microbiologist in their boardroom from now on. That will be true for all event sponsors too and most especially the airlines. If I were a young person right now, I’d be looking into a career in microbiology. :-)

    Things are changing. And the CDC will fix itself. I say that assuming that we will have a Republican administration for four more years. The Democrats don’t know how to fix organizations. Trump’s losing would be a global disaster.

    • #42
  13. The Reticulator Member
    The Reticulator
    @TheReticulator

    Hammer, The (View Comment):
    It seems to me that all of these measures that people insist we must take – masking and socially distancing and so forth – are based entirely on the premise of asymptomatic spread. Wouldn’t it behoove us to determine the extent to which it exists?

    I don’t think they’re entirely based on that premise. Back at the beginning there was a report of asymptomatic analysis that was based on sloppy (i.e. lazy) analysis and an overly hasty jumping to conclusions. I haven’t heard of any reports that show it’s a thing, and I’ve been trying to pay attention. But there is still such a thing as presymptomatic spread, and that can be a good reason for pre-emptive social distancing and isolation. Whether it’s a good enough reason to continue the lockdowns we’ve had in place is not nearly so certain.  I’m in favor of opening up, and of not being quite so balky about it as some of our governors. 

    • #43
  14. The Reticulator Member
    The Reticulator
    @TheReticulator

    MarciN (View Comment):

    The question with this virus is whether people who have recovered are still contagious. Are asymptomatic carriers developing immunity and thus are they not spreading the disease after a two-week period during which their body develops antibodies? That varies from virus to virus. They have just learned this past week the answer to this question, which is extremely big news. Those who have recovered, with or without symptoms, are spreading (or “shedding”) the virus, but it’s dead. 

    This should be on the front page of every paper in the world right now. 

    Okay, I can’t find that article that I saw two days ago, but as I was looking for it, I found this, which is also important news: “New Data Suggest People Aren’t Getting Reinfected with the Coronavirus.” That is a breakthrough announcement.

    I haven’t followed your links yet, but yesterday’s MedCram update (#73, Relapse, Re-Infections, & Re-Positives – The Likely Explanation) discussed a new report on this topic. It shows how testing for the presence of the virus can result in false positives, and how we can know.  The conclusion of the study that is discussed was based on contact tracing. 

    • #44
  15. MarciN Member
    MarciN
    @MarciN

    The Reticulator (View Comment):

    MarciN (View Comment):

    The question with this virus is whether people who have recovered are still contagious. Are asymptomatic carriers developing immunity and thus are they not spreading the disease after a two-week period during which their body develops antibodies? That varies from virus to virus. They have just learned this past week the answer to this question, which is extremely big news. Those who have recovered, with or without symptoms, are spreading (or “shedding”) the virus, but it’s dead.

    This should be on the front page of every paper in the world right now.

    Okay, I can’t find that article that I saw two days ago, but as I was looking for it, I found this, which is also important news: “New Data Suggest People Aren’t Getting Reinfected with the Coronavirus.” That is a breakthrough announcement.

    I haven’t followed your links yet, but yesterday’s MedCram update (#73, Relapse, Re-Infections, & Re-Positives – The Likely Explanation) discussed a new report on this topic. It shows how testing for the presence of the virus can result in false positives, and how we can know. The conclusion of the study that is discussed was based on contact tracing.

    Wow. Again, news we need to know. 

    The answers are coming steadily every day now. Thank you, God. 

    This is looking more and more manageable every single day. 

     

    • #45
  16. Hammer, The Inactive
    Hammer, The
    @RyanM

    Mendel (View Comment):

    Hammer, The (View Comment):
    Please excuse what may be a dumb question, but could someone point me to the actual studies that determined not just that asymptomatic spread is possible, but that it is common, and that it is a statistically significant contributing factor with respect to transmission?

    There aren’t many real-world studies that conclusively show asymptomatic transmission. But there is enough indirect evidence suggesting a major impact of asymptomatic transmission that it also can’t be ruled out (yet).

    Asymptomatic transmission is difficult to prove for several rasons. All of the hurdles in my last comment obviously apply. There’s also the issue that many of the initial symptoms of Covid can be so mild or unremarkable (like coughing, which everyone does everyday) that the defining line between symptomatic and asymptomatic is murky and arbitrary. Add to that people’s often-inaccurate memories of such details several weeks or months after the event. There’s also the possibility of presymptomatic infections – i.e. people are not symptomatic when they transmit the virus, but start getting symptoms a day or two later. Those people will still likely be classified as “symptomatic” in any studies, even though they did not experience any symptoms when they were contagious.

    In terms of the indirect data, one of the key indicators of asymptomatic/presymptomatic contagion is the fact that asymptomatic patients have just as much viral replication in their upper respiratory tract as symptomatic patients, and those viruses are just as viable as in symptomatic patients. Even in symptomatic patients, the viral load in the upper respiratory tract reaches its peak right before symptoms start.

    The other major piece of evidence is from population-wide calculations of transmission. Basically, taking the number of people with symptomatic infections and multiplying that by our estimates of how contagious the virus is can’t account for the actual number of people who end up becoming infected. It’s like dark matter: the final results can’t be explained by the infections we “see”, so there must be some missing element. Asymptomatic/presymptomatic infection is the most likely culprit, although not the only one.

    It is very frustrating, because people still make (or force) major changes in our lives, and we really have no idea that what they’re doing is in any way helpful.  In this morning’s “Morning Jolt,” Jim Geraghty says that the CDC just changed its guidelines, again, now saying that the touching of infected objects is not an important mode of transmission – Jim concludes that subway rails wasn’t important, but coming within six feet of each other is.  Well… until they say it isn’t.  I have a feeling that virtually all of this stuff is just working around the very margins.  Outbreaks do occur, and people do get sick, but we haven’t been doing a good job of figuring out why – and we’ve been too focused on enforcing actions based on guesses.

    • #46
  17. Ontheleftcoast Inactive
    Ontheleftcoast
    @Ontheleftcoast

    Mendel (View Comment):

    Hammer, The (View Comment):
    Please excuse what may be a dumb question, but could someone point me to the actual studies that determined not just that asymptomatic spread is possible, but that it is common, and that it is a statistically significant contributing factor with respect to transmission?

    There aren’t many real-world studies that conclusively show asymptomatic transmission. But there is enough indirect evidence suggesting a major impact of asymptomatic transmission that it also can’t be ruled out (yet).

    Asymptomatic transmission is difficult to prove for several rasons. All of the hurdles in my last comment obviously apply. There’s also the issue that many of the initial symptoms of Covid can be so mild or unremarkable (like coughing, which everyone does everyday) that the defining line between symptomatic and asymptomatic is murky and arbitrary. Add to that people’s often-inaccurate memories of such details several weeks or months after the event. There’s also the possibility of presymptomatic infections – i.e. people are not symptomatic when they transmit the virus, but start getting symptoms a day or two later. Those people will still likely be classified as “symptomatic” in any studies, even though they did not experience any symptoms when they were contagious.

    In terms of the indirect data, one of the key indicators of asymptomatic/presymptomatic contagion is the fact that asymptomatic patients have just as much viral replication in their upper respiratory tract as symptomatic patients, and those viruses are just as viable as in symptomatic patients. Even in symptomatic patients, the viral load in the upper respiratory tract reaches its peak right before symptoms start.

    The other major piece of evidence is from population-wide calculations of transmission. Basically, taking the number of people with symptomatic infections and multiplying that by our estimates of how contagious the virus is can’t account for the actual number of people who end up becoming infected. It’s like dark matter: the final results can’t be explained by the infections we “see”, so there must be some missing element. Asymptomatic/presymptomatic infection is the most likely culprit, although not the only one.

    It’s looking like there may be some crossover immunity from other coronaviruses. This is of course not a binary ” I won’t get it since I’m immune” vs “OMG I’m gonna get it for sure.” Crossover immunity can blunt the impact of the infection, making the resulting illness milder or perhapse even producing the legendary “asymptomatic infections.”

     

    • #47
  18. Hammer, The Inactive
    Hammer, The
    @RyanM

    MarciN (View Comment):

    Good grief, this is also breathtakingly good news:

    This one could be big. Researchers from the University of Washington School of Medicine and Vir Biotechnology say that the antibody they’ve identified, known as S309, “likely covers the entire family of related coronaviruses.” One of the chief obstacles to the development of a SARS-CoV-2 vaccine — or potent antiviral — is that the virus is perpetually mutating. But the Vir Biotechnology study suggests that S309 targets and disables the spike proteins that all known coronaviruses use to enter human cells. Which would mean that, no matter how the novel coronavirus evolves, it would “be quite challenging for [the virus] to become resistant to the neutralizing activity of S309.”

    For now, S309 has only proven itself to be an effective COVID-19 slayer in lab cultures, and still needs to be tested in people.

    What a week! And Moderna’s good vaccine news!

    Ring the church bells!

    And I’ll find that other story about the dead virus later. :-) I have to go celebrate. :-)

    Interesting thing about that article – they found that people exposed to sars1 had some level of immunity to sars2.  This is why I hate it when we have guesses and hunches and just run with them.  People say “Asia did really well.  Why?  Because they all wear masks!  We all need to wear masks!”  Well… maybe, maybe not.  Maybe Asian countries have done really well because they were previously exposed to sars1.  Or, maybe something else.  Just seems terribly hasty to go from one observation straight to legally mandated adoption of the strategies that observation leads to…

    • #48
  19. Hammer, The Inactive
    Hammer, The
    @RyanM

    MarciN (View Comment):

    Good grief, this is also breathtakingly good news: 

    This one could be big. Researchers from the University of Washington School of Medicine and Vir Biotechnology say that the antibody they’ve identified, known as S309, “likely covers the entire family of related coronaviruses.” One of the chief obstacles to the development of a SARS-CoV-2 vaccine — or potent antiviral — is that the virus is perpetually mutating. But the Vir Biotechnology study suggests that S309 targets and disables the spike proteins that all known coronaviruses use to enter human cells. Which would mean that, no matter how the novel coronavirus evolves, it would “be quite challenging for [the virus] to become resistant to the neutralizing activity of S309.”

    For now, S309 has only proven itself to be an effective COVID-19 slayer in lab cultures, and still needs

    And lastly – while the moderna trials may be good news…  I hesitate to put much stock in the article you cited.  It has a bullet list of good and bad news, and a lot of what it talks about is just garbage.  Especially in the bad news section, it takes possible implications of a single study and then runs with it, and it does this in many places…  so that leads me to think that it’s good news section is equally faulty.

    • #49
  20. Hammer, The Inactive
    Hammer, The
    @RyanM

    Mendel (View Comment):
    Meanwhile, most of the people who find that timeline intolerable are also convinced that SARS-2 is not meaningfully more dangerous than the common flu, and therefore tend to reject any measures that inconvenience their own lives.

    @mendel; I think this is in need of some elaboration.  It seems to me that canceling sports, closing schools, asking everyone to wear masks and stay six feet apart – all of those things appear to be clumsy approaches to a problem that can be solved with better techniques.  We know that more than 60% of deaths occur in nursing homes, and something approaching 98% of deaths occur with people who have some pretty serious underlying conditions.  If we eliminated just the nursing home deaths, the death-rate of this thing goes down way below the flu.  Now, I’m assuming that many flu deaths also occur in nursing homes, so maybe that isn’t as big as it sounds.  But you talk about people being unwilling to take measures…  it seems to me that we need to recognize that different people should be taking different measures.

    I am 38 years old and pretty healthy.  I’m not willing to wear a mask, and I’m in no hurry to practice “social distancing.”  I have no desire to stay home from work, and I’d rather have my kids acting like normal kids, playing with friends, going to school, doing sports.

    But I am sure as heck not going to walk around in a hospital or in a nursing home as if there’s no problem, and I’m going to be super careful about what to do with the elderly.  I’m actually torn about that, because I have no intention of simply not seeing my own parents until a vaccine comes along – but I am still trying to exercise some caution.

    The problem with this group of people – and we are now just being labeled “deniers,” as with climate change – is not that we don’t think there is any pandemic that is causing problems, it is more that we believe the responses to the pandemic are ridiculous overreactions and likely to do more harm than good.  If we were honest about what are truly at-risk groups, and if we were honest about what our actions need to be to protect those groups, I think more people like me would willingly get on board.  But we’re acting like a nation of germaphobes and hypochondriacs, and the media and politicians are doing their best to keep everyone absolutely terrified because they don’t believe the truth will cause people to react how they should.  That results in a hell of a lot of distrust, especially when so many of these numbers are right out there for us to see.

    Also – if covid is 2X or 5X or even 10X “more deadly” than the flu – what does that really mean in practical terms?  Not as much as is implied.

    • #50
  21. Gumby Mark (R-Meth Lab of Demo… Coolidge
    Gumby Mark (R-Meth Lab of Demo…
    @GumbyMark

    Mendel (View Comment):

     

    In terms of the indirect data, one of the key indicators of asymptomatic/presymptomatic contagion is the fact that asymptomatic patients have just as much viral replication in their upper respiratory tract as symptomatic patients, and those viruses are just as viable as in symptomatic patients. Even in symptomatic patients, the viral load in the upper respiratory tract reaches its peak right before symptoms start.

    The other major piece of evidence is from population-wide calculations of transmission. Basically, taking the number of people with symptomatic infections and multiplying that by our estimates of how contagious the virus is can’t account for the actual number of people who end up becoming infected. It’s like dark matter: the final results can’t be explained by the infections we “see”, so there must be some missing element. Asymptomatic/presymptomatic infection is the most likely culprit, although not the only one.

    I’ve seen the same data re viral load in presymptomatic people.  Which raises a couple of questions.

    Is presymptomatic and asymptomatic just a differentiation between those who eventually develop some of the known Covid symptoms and those who do not, but means nothing in terms of relative ability to transmit the virus?

    When I started looking at how the CDC does its flu case counts, I realized it does not include asymptomatic cases.  However, on looking further it turns out that asymptomatic includes those who thought their allergies were acting up for a couple of days, had a scratchy throat for a day or two, or even thought they had a slight cold.  In other words they had symptoms of something but didn’t realize it was the flu, however mild.  Does this mean asymptomatic but positive covid people can range from never noticing anything to thinking they have something else but having some symptoms that happen to be common to many disorders? 

    Seems like a lot more gray area than I realized on this subject.

    • #51
  22. Hammer, The Inactive
    Hammer, The
    @RyanM

    Gumby Mark (R-Meth Lab of Demo… (View Comment):

    Mendel (View Comment):

     

    In terms of the indirect data, one of the key indicators of asymptomatic/presymptomatic contagion is the fact that asymptomatic patients have just as much viral replication in their upper respiratory tract as symptomatic patients, and those viruses are just as viable as in symptomatic patients. Even in symptomatic patients, the viral load in the upper respiratory tract reaches its peak right before symptoms start.

    The other major piece of evidence is from population-wide calculations of transmission. Basically, taking the number of people with symptomatic infections and multiplying that by our estimates of how contagious the virus is can’t account for the actual number of people who end up becoming infected. It’s like dark matter: the final results can’t be explained by the infections we “see”, so there must be some missing element. Asymptomatic/presymptomatic infection is the most likely culprit, although not the only one.

    I’ve seen the same data re viral load in presymptomatic people. Which raises a couple of questions.

    Is presymptomatic and asymptomatic just a differentiation between those who eventually develop some of the known Covid symptoms and those who do not, but means nothing in terms of relative ability to transmit the virus?

    When I started looking at how the CDC does its flu case counts, I realized it does not include asymptomatic cases. However, on looking further it turns out that asymptomatic includes those who thought their allergies were acting up for a couple of days, had a scratchy throat for a day or two, or even thought they had a slight cold. In other words they had symptoms of something but didn’t realize it was the flu, however mild. Does this mean asymptomatic but positive covid people can range from never noticing anything to thinking they have something else but having some symptoms that happen to be common to many disorders?

    Seems like a lot more gray area than I realized on this subject.

    How could the flu counts not include asymptomatic cases when the numbers are all basically educated guesses?  When we went to the pediatrician w/ flu back in December, the doctor said “well, flu is going around.  We test a few random cases to determine that’s what’s going around, then just assume that’s what you have.  Besides, the flu tests aren’t reliable, anyway.”

    • #52
  23. Mendel Inactive
    Mendel
    @Mendel

    Gumby Mark (R-Meth Lab of Demo… (View Comment):
    Is presymptomatic and asymptomatic just a differentiation between those who eventually develop some of the known Covid symptoms and those who do not, but means nothing in terms of relative ability to transmit the virus?

    The first part is correct, the second part is exactly where we’re not sure yet. It’s also not 100% established that pre-symptomatic people transmit during their presymptomatic phase.

    Gumby Mark (R-Meth Lab of Demo… (View Comment):
    Seems like a lot more gray area than I realized on this subject.

    Indeed. To extend your example, imagine if an epidemiologist interviewed three people, all of whom had experienced the exact same mild symptoms about a month back, whether they remembered being sick in the past month. It’s reasonable to think that one would self-answer no, one would say yes, and the third would say “I wasn’t sick but my allergies did act up for a few days”. Had they been seen by a doctor at the time, all three would probably be classified as symptomatic, but if self-responding (as is usually the case in such surveys), only one of three would be a “yes”.

    There’s also the case of supposedly asymptomatic people actually being “presymptomatic”. For example, there was a big news story a few weeks ago when a Boston homeless shelter tested all of their residents and 40% came back positive, all “asymptomatic”. But since symptoms take a few days to kick in (even after virus is detectable by PCR), you can’t declare somebody asymptomatic until at least a week after the positive test – but 9 times out of 10, nobody follows up on these individuals because the epidemiologists have more pressing responsibilities.

    The question is also of limited utility at the present moment. If it’s a question of who needs to wear masks, I’m fully of the opinion that if a community decides mask wearing is appropriate, then everyone should wear the stupid mask until science has more information. When it comes to the question of how widespread the pandemic already is, antibody studies are filling in the gaps much faster and more precisely than modeling based on guesses of asymptomatic transmission ever could.

    So for the moment, the question is more academic. It may become useful again later.

    • #53
  24. Gumby Mark (R-Meth Lab of Demo… Coolidge
    Gumby Mark (R-Meth Lab of Demo…
    @GumbyMark

    Hammer, The (View Comment):

    Gumby Mark (R-Meth Lab of Demo… (View Comment):

    Mendel (View Comment):

     

    In terms of the indirect data, one of the key indicators of asymptomatic/presymptomatic contagion is the fact that asymptomatic patients have just as much viral replication in their upper respiratory tract as symptomatic patients, and those viruses are just as viable as in symptomatic patients. Even in symptomatic patients, the viral load in the upper respiratory tract reaches its peak right before symptoms start.

    The other major piece of evidence is from population-wide calculations of transmission. Basically, taking the number of people with symptomatic infections and multiplying that by our estimates of how contagious the virus is can’t account for the actual number of people who end up becoming infected. It’s like dark matter: the final results can’t be explained by the infections we “see”, so there must be some missing element. Asymptomatic/presymptomatic infection is the most likely culprit, although not the only one.

    I’ve seen the same data re viral load in presymptomatic people. Which raises a couple of questions.

    Is presymptomatic and asymptomatic just a differentiation between those who eventually develop some of the known Covid symptoms and those who do not, but means nothing in terms of relative ability to transmit the virus?

    When I started looking at how the CDC does its flu case counts, I realized it does not include asymptomatic cases. However, on looking further it turns out that asymptomatic includes those who thought their allergies were acting up for a couple of days, had a scratchy throat for a day or two, or even thought they had a slight cold. In other words they had symptoms of something but didn’t realize it was the flu, however mild. Does this mean asymptomatic but positive covid people can range from never noticing anything to thinking they have something else but having some symptoms that happen to be common to many disorders?

    Seems like a lot more gray area than I realized on this subject.

    How could the flu counts not include asymptomatic cases when the numbers are all basically educated guesses? When we went to the pediatrician w/ flu back in December, the doctor said “well, flu is going around. We test a few random cases to determine that’s what’s going around, then just assume that’s what you have. Besides, the flu tests aren’t reliable, anyway.”

    All I know is what the CDC says it does.  It explicitly does not count asymptomatic cases and it estimates 50% of flu cases may be asymptomatic.  If you were to compare flu mortality rates with any covid rate that includes asymptomatic cases you need to cut the flu mortality rate in half to be comparing apples to apples.  I didn’t realize that’s what the CDC was doing until a few weeks ago when I dove into its website to get more detail on how it did its calculations.  And yes, it is all educated guesses.  In fact, once I looked at the methodology I realized the covid case and mortality data, for all of its many flaws, is probably more accurate than the flu estimates.

    • #54
  25. Mendel Inactive
    Mendel
    @Mendel

    Hammer, The (View Comment):
    It is very frustrating, because people still make (or force) major changes in our lives, and we really have no idea that what they’re doing is in any way helpful.

    I agree, and I also agree that too many drastic measures have been taken (and for far too long) without enough scientific confidence. I could accept full lockdowns in some regions and limited/brief lockdowns in some others, but the blanket policies that have been enforced are ridiculous and have led to a real problem with decision paralysis.

    That being said, though, there is still an underappreciation of how difficult biomedical science really is. As with so many industries/fields, most people just see the shiny final product and have no idea how much messiness is involved in making the sausage. The debates and uncertainty are 100% par for the course, it’s just that the public usually doesn’t have a front-row view of this process.

    One of the major drivers of our current uncertainty is an unwillingness to take calculated risks for the sake of scientific knowledge. There’s a reason we still perform large-scale clinical trials even for drugs that treat diseases we know a lot about: the human body remains so complex and poorly understood that there are many things we can’t know without trying them out in actual humans. And that means exposing humans to a risk, and possibly harming some people in a (theoretically) preventable manner.

    That’s why I was calling for human experiments in healthy young people months ago. If we had had the courage to subject college student volunteers to a miniscule risk, we could have gathered a treasure trove of data about whether asymptomatic/presymptomatic transmission is possible, whether transmission is more droplets or aerosols, whether masks actually help, indoor vs. outdoor transmission, and so much more. Now we’re almost 6 months into this thing and only a little bit wiser.

    And the longer we keep most things shut down, the longer until we can start gathering the data about transmission that would teach us how to safely re-open most of society.

    • #55
  26. Mendel Inactive
    Mendel
    @Mendel

    Hammer, The (View Comment):
    How could the flu counts not include asymptomatic cases when the numbers are all basically educated guesses?

    Because it takes a lot of effort to determine how many asymptomatic cases there are and the extra information is nearly useless – especially in the case of the flu.

    It’s especially difficult to measure asymptomatic cases for the flu, since antibody tests aren’t useful at distinguishing whether somebody had the flu this year, last year, or four years ago.

    And the information is nearly useless because the seasonal flu isn’t much of a public health threat, so why go to the effort?

    So @gumbymark is correct, the 0.1% infection fatality rate everyone has been throwing around for seasonal influenza is probably about twice as high as the presumable rate if asymptomatic cases were to be included. A more apples-to-apples comparison would be to compare that 0.1% rate to the fatality rate of symptomatic Covid-19 infections, which presently is still believed to be somewhere north of 1%.

    • #56
  27. Mendel Inactive
    Mendel
    @Mendel

    Hammer, The (View Comment):
    @mendel; I think this is in need of some elaboration.

    A lot to unpack in that comment.

    First, we actually have a lot of data that Covid-19 is much worse than seasonal flu when it comes to people not in nursing homes. It just doesn’t appear that way in states/counties that have barely been touched by the virus, since nursing homes are usually the first places to get hit, which skews the data early on. Severe cases and mortality are still limited almost exclusively to people over 60, but among that population, Covid-19 actually seems to be much more deadly in otherwise healthy(ish) people than seasonal flu. It’s also important to keep in mind that “comorbidity” doesn’t mean “seriously ill”. Lots of Americans have the Covid comorbidities and live very active, healthy lives.

    Second is the notion of taking “simple measures” like protecting the elderly and the vulnerable. Every ounce of experience we have so far suggests that this is nearly impossible on a practical level. Take your own observation about places that have nearly no virus transmission and where all the deaths have been restricted to nursing homes. Consider the implication: even when the prevalence of the virus is near 0% and nursing homes are already on high alert about the virus, some of them still get hit hard.

    If nursing homes are so vulnerable when viral transmission is near zero and they are on high alert, can they realistically be protected if the virus is actively circulating at natural levels? The experience from every single country where the virus has run free for even a few weeks has been an emphatic no. Even Sweden, whose explicit strategy was to allow the virus to spread at considerably lower levels while specifically protecting the elderly, has admitted failure on that last point.

    To put it another way, based on our present experience, in order to adequately protect the elderly we probably need to completely sequester them for months. In other words, you and your kids wouldn’t be allowed to visit their grandparents for the entire summer. Do you really think society would accept that? I doubt you would, let alone anyone else.

    That’s why every serious strategy calls for decreasing transmission between non-risk individuals: because it simply isn’t feasible (yet) to adequately protect the at-risk population. And it won’t be feasible for at least another few months, if at all.

    • #57
  28. Mendel Inactive
    Mendel
    @Mendel

    Hammer, The (View Comment):
    And lastly – while the moderna trials may be good news… I hesitate to put much stock in the article you cited. It has a bullet list of good and bad news, and a lot of what it talks about is just garbage.

    Agree with you here.

    We need to take all of these “good news” announcements about future therapies or vaccines with a big grain of salt. Whether they’re from a private company or an academic group, everyone is still tooting their own horn. The Moderna press release in particular has come in for a good round of criticism among quite a few respected researchers for being less than meets the eye on second glance.

    I do think there’s reason to be generally optimistic that we’ll have either a passable therapeutic or a passable vaccine by the time a potential second wave would come around this fall. I don’t base that on any specific data, just the fact that science is much better at making things than at finding things out. We can make monoclonal antibodies really well, and I think it’s only a matter of time before we find one that works well and ramp up its production.

    We’re also good at making vaccines, and given the approximately 5,280 vaccine projects currently underway, I can easily imagine one of them being just successful enough just quickly enough to keep a future wave in check just enough to keep the calls for renewed social distancing at bay.

    • #58
  29. Clifford A. Brown Member
    Clifford A. Brown
    @CliffordBrown

    MarciN (View Comment):

    Rodin: Maybe you are obscuring the data so that it doesn’t make clear the consequences of your governing philosophy?

    Definitely. I think leaders at the federal and state levels initially panicked, and rather than say they had (understandably) formed the wrong impression of who was the most vulnerable, now they are trying to justify their draconian lockdown actions after the fact.

    Pulling back the curtain would strip them of power over us.

    • #59
  30. Hammer, The Inactive
    Hammer, The
    @RyanM

    Mendel (View Comment):
    To put it another way, based on our present experience, in order to adequately protect the elderly we probably need to completely sequester them for months. In other words, you and your kids wouldn’t be allowed to visit their grandparents for the entire summer. Do you really think society would accept that? I doubt you would, let alone anyone else.

    Except we are already in that situation.  My kids are not supposed to be visiting their 66/68 year old grandparents, either.  And this is apparently the case not just for the rest of the summer, but for the foreseeable future.

    • #60
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