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Hapless Bills Fan

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About Hapless Bills Fan

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    It's like trying to maintain a Pee-free Zone in a Swimming Pool

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  1. One thing that's interesting is the references to inoculation and to vaccines. I hadn't remembered this but they did, indeed, develop a vaccine during the influenza epidemic. Unfortunately for vaccine effectiveness, a bacteria had been isolated from influenza patients, and was believed at the time to be the cause of the 'flu Since it wasn't eliciting an immune response to the actual cause (influenza virus)....it didn't work 😥
  2. I think this belongs here, but please respect the request to discuss in the discussion thread NY State DOH report on covid-19 deaths in nursing homes. It is exculpatory and concludes that the 6,500 covid-19 positive patients sent to nursing homes in NYS were not the driver of infection, but rather community-acquired infection of up to 1 in 4 staff members Actual report: https://health.ny.gov/press/releases/2020/docs/nh_factors_report.pdf Article about it: https://www.news10.com/news/ny-capitol-news/new-report-out-from-nys-doh-on-coronavirus-in-nursing-homes/
  3. Sure. Well at least, I'll take a crack at it. An immunologist I ain't and I keep hoping we have one here who will "out" him or her self, but I've got a couple threads by actual immunologists and stuff. Upthread I posted a link to a decent overview of immune response with a little picture and all Unroll of Twitter thread referenced in that article Here's a link to another Twitter thread with a bunch of sketches about immune response that ID the key players Unroll of the same thread: https://threadreaderapp.com/thread/1278357445023109121.html Here's a link to the article referenced by Lowe My TL;DR best guess response: we measure antibodies to look for immunity because they're easy to measure. But they're only part of the adaptive immune response, and (quite probably) for covid-19, not the most important part. Adaptive mucosal immune response and T-cell response may play a larger role and be more important for covid-19 infection as T-cells eliminate virus-infected cells. Makes sense right - the virus has to get through the mucosal layer to bind to ACE2 and get into the cells it infects in the lungs (or gut, or whereever), and then once it subverts the cell to become a little virus factory, its goal is to bud and burst and release a bunch of virus to repeat the cycle. If your immune system is doing a great job of nipping that process in the bud (ha! see what I did there?), you never have enough virus rolling around in your bloodstream to get your B-cells all worked up about making lotsa antibodies. Doesn't mean they can't, but why bother? Your immune system is just like anything else, doesn't want to work any harder than it must. So you make antibodies while you're fighting the infection, then you quit, and within a few weeks the ones you made get cleared. Often, the presence of antibodies and their persistence are correlated to other forms of adaptive immune response such as T-cell response and memory B-cell response (B-cells make antibodies; memory B-cells hang out for decades and hand out instructions "how to make THESE antibodies"). Here's a paper in Cell which actually looked at T-cell response and antibodies in covid+ patients. But they're not always correlated, or another way to put it would be just because you aren't still putting out antibodies, doesn't mean you don't have the fly swatter (rest of adaptive immune response) ready to hand. For example, a study found that while 90% of people with a positive RT-PCR test had antibodies a few weeks later, 40% of asymptomatically infected people went negative (for antibodies) during their convalescence. That probably doesn't mean that their immune systems are ill-equipped to deal with a repeat challenge of covid-19 viral infection - to the contrary, their immune systems Did There Job the first time like a fly swatter and swatted that virus like a buuuugggg so why wouldn't they keep up the good work? The fly-swatter just didn't involve heavy IgG response so no reason to keep making 'em. For an effective, lasting immune response to be elicited by a vaccine, we need to elicit the entire spectrum of adaptive immunity, not just antibody response.
  4. All I can think is that the man really, really, REALLY hates Christmas music
  5. Good question. It has to do with how the test works. The solution to be tested, containing (or not containing) the extracted viral RNA is heated to denature it, then cooled so that 2 sets of primers to RNA unique to the virus can bind -“anneal”. The annealing temperature is chosen so that the primers can bind only where they have a complete or nearly complete match to the viral RNA sequence. Otherwise they fall off. The enzyme that amplifies the RNA then goes to work. The cycle is repeated a number of times - 45x in the CDC test. But if the extracted viral RNA is not there, the primers have nothing to bind to, the enzyme can’t go to work, and the amplification won’t take place. So unless the technician really f’s it up (and a lot of this is done robotically) it’s very hard to get a false positive. (And there are negative controls in each plate, so the most usual ways to f’ up has the negative controls fail and you know something is wrong). On the other hand, as something WEO said implied, there are lots of ways to get a false negative. The sample collection swab can not go deep enough to hit the right place and collect enough virus, or if it’s a saliva sample the stabilizing solution doesn’t do its thing. The sample can be stored improperly or for too long a time. But most probable, the concentration of virus may be below the limit of detection at the sampled location - maybe it’s hanging out in the lungs, or the GI tract instead of the nasopharynx, or maybe the patient’s immune system is beating it down with a club. I was thinking what a good analogy would be, and I came up with growing plants in sterilized soil in a greenhouse. It’s easy to get a “false negative” where the seeds don’t grow even though you planted them. Maybe the seeds were too old to germinate well, or were planted too deep, or not deep enough. Maybe the soil tray wasn’t treated properly - allowed to dry out. But it’s not easy to get a false positive in a sterilized growing tray in a greenhouse - no seeds => no plants
  6. @Gugny just posted this in the Shoutbox Looks very interesting - not a re-design of the helmet/mask but a visor and a channeled extension down around the mouth. From your mouth to the NFL’s ears I guess?
  7. I just posted a Science News article on this study in the OTW “Facts” thread. Those results show that the probability of a “negative” declines from 67% in the first 4 days, to 38% 5 days post infection (first day of symptoms for many) to 20% at 8 days post infection. But it’s still 20%. Reduced, yes. Eliminated, no. I didn’t see data on how a totally asymptomatic infection influences these, beyond the scope I expect.
  8. I don’t know what will happen. I want, with all my heart, for there to be football. In SW MO, the delay time for test results is running 5-7 days. Contact tracing and even a “box in” strategy is impossible in those circumstances. Across S. Mo, hospital bed capacity is quite limited. Let the virus get into a bunch of care homes and it won’t be pretty, and how can it be kept out if it’s widespread in the community and the aides can’t get tested promptly and repeatedly? I want, with all my heart, for there to be football. But the thought of healthy football players being tested every day or every 3-4 days and getting prompt turn around while testing capacity is so limited that parts of the country can’t box in, contact trace, or test nursing home workers and residents - Epidemiology 101 for this - well, as a guy who worked for me used to say “That Ain’t Right”.
  9. Power, no. But historically, when the Federal Government has issued public health guidance, it has been hugely influential - polio vaccination campaigns, for example. The states that are currently doing best at containing the virus (NYS, knock on wood) are actually following the federal CDC guidance for reopening. The problem we’re seeing today is not lack of states “listening to Trump”, it’s a persistent mixed message from the Federal Government - on the one hand, CDC guidelines about not reopening until certain benchmarks for testing, contact tracing, declining tests, and hospital capacity are met - and “dialing it back” if things start to go in the wrong direction. On the other hand, Trump tweets of support for “very good people who just want their lives back” protesting lockdowns and pushing for reopening, “99% harmless” (CDC data: hospitalization rate is at least 6% overall, not counting people who may have died without being tested who had COVID-like symptoms but negative RT-PCR test) Like dogs, kids, or anyone really, when there’s a mixed message, people are gonna choose what they want to hear
  10. JHU study on RT-PCR false negative rate. Data have been made publicly available and will be added to as additional data are collected. Key findings: 1) false negative rate lowest 8 days post infection (3 days after symptom onset), but still 20% 2) at symptom onset (average 5 days post infection) false negative rate 38% 3) in the first 4 days post infection, 67% negative rate (in people who eventually develop symptom and test positive) Key quote: "We are using these tests to rule out COVID-19, and basing decisions about what steps we take to prevent onward transmission, such as selection of personal protective equipment for health care workers," says Kucirka. "As we develop strategies to reopen services, businesses and other venues that rely on testing and contact tracing, it is important to understand the limitations of these tests."
  11. This happens to us all the time - USPS shows a package was delivered to the Kid, who doesn't have it. So far always shows up the next day.
  12. That's A Winner! My contribution: "My parole officer's calling"
  13. The first step in the standard RT-PCR test is RNA extraction from the intact virus particles. The RNA is not bopping around the saliva solution on its own; it’s wrapped up in a lipoprotein coat. So the salivary enzymes really should not be a factor. I believe there are also RNAses in the nasopharynx as well - there are RNAses pretty much everywhere else in mucus and in serum. I know for DNA sampling from saliva or cheek swabs, there’s usually a nuclease cocktail added to stabilize it. I also know RNA purification from saliva samples has been done successfully by a number of research groups (but again, we’re not going after salivary RNA here but RNA packed up in a virus) It’s appropriate to have concerns about lower sensitivity and sample degradation but if reputable groups have worked out the protocol and shown that it’s as sensitive (using their techniques) at some point one needs to adapt.
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