Coronavirus: How dangerous a threat?

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Well, sort of, I'm asking if there is any data out there about how effective just scrubbing under running water is.

My assumption is that her problem is an allergy to the soap here at work. They buy it in five gallon buckets on a pallet, and I'm sure its the least expensive stuff they can find so its probably barely OK for human use.

I too am concerned about what is coming this winter!
Someone I know (one of the managers of a local grocery store) told me that it's the friction of rubbing the hands together that helps to get the virus off your hands. She did start nursing school, and that's one of the few things that has stayed with her. She switched her major because part way through she realized nursing wasn't for her. Having soap is still better, but the friction does help.
 
States the error rate for false positives from the PCR test is over 50%
It depends on how you define false positive. If you mean the % of negative people who test positive, it's very low, probably less than 1% or even 0.!% in a lab that knows what it's doing. But if you mean the % of people who test positive, it can be as high as 50%.

If the population being tested has a very low rate of true positives, say 1%, and 1% of negative people test positive, then half the people who test positive are false positives. That's why false positives are such a problem in bubbles, leading to testing twice to increase certainty. The lower the incidence of true positives, the greater the false positive rate in the second sense.
 
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It depends on how you define false positive. If you mean the % of negative people who test positive, it's very low, probably less than 1% or even 0.!% in a lab that knows what it's doing. But if you mean the % of people who test positive, it can be as high as 50%.

If the population being tested has a very low rate of true positives, say 1%, and 1% of negative people test positive, then half the people who test positive are false positives. That's why false positives are such a problem in bubbles, leading to testing twice to increase certainty. The lower the incidence of true positives, the greater the false positive rate in the second sense.
I've never hear it defined the second way.
 
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Question for everybody, but especially dj et al who work in this field: does vigorously rubbing your hands under running water remove most virus? I'm asking because a colleague's hand are absolutely raw from the soap here at work and whatever hand sanitizer she is using between washes (my hands get dry, but hers look angry!). I encouraged her to use lotion, try other hand sanitizers, and maybe bring her own soap to work, but if rubbing her hands under running water could reduce the number of times that she has to fully wash her hands that might help as well. ??
Never mind. She just told the boss (main boss not team boss) that if she can't work from home, she is going to resign.
 
To me it seemed like a struggle to repackage the arguments given to him by Atlas. He also mentioned excess mortality figures last night. Where else have we heard that rationale recently? Atlas is the one who has the sway on the task force.

Good information coming from hearings in DC. Redfield of the CDC saying that vaccines will not be widespread until next summer. That shouldn't be news to people here, but worth repeating.

Peak Florida. I just don't think people who live in Europe realize how nuts people are here. And how easily a some people slip from being anti- lockdown to anti-mask to anti-test.

View: https://twitter.com/KFoleyFL/status/1306254415754559488
 
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To me it seemed like a struggle to repackage the arguments given to him by Atlas. He also mentioned excess mortality figures last night. Where else have we heard that rationale recently? Atlas is the one who has the sway on the task force.

Good information coming from hearings in DC. Redfield of the CDC saying that vaccines will not be widespread until next summer. That shouldn't be news to people here, but worth repeating.

Peak Florida. I just don't think people who live in Europe realize how nuts people are here. And how easily a some people slip from being anti- lockdown to anti-mask to anti-test.

View: https://twitter.com/KFoleyFL/status/1306254415754559488
Now with the Big Ten committing to a season every jerk with a kid wanting to play football will throw the 1st Amendment argument forward to allow unchecked activities. Not blaming the Big Ten; it seems anything that allows spoiled Americans to reclaim their niche identities is the only thing they'll fight over. Nothing reasonable and forward planning is considered possible; in fact the buzzwords of "manifesto" and "socialism" are almost immediately attached.
It's way past embarrassing to witness.
 
Interesting that the Big Ten re-opening hinges on rapid antigen tests performed daily. So many examples of what this kind of tech can accomplish to restore normalcy in small privileged samples and so little momentum to make this widespread for the rest of us. I still maintain that starting and finishing a football season are vastly different probabilities. I am curious about the part below. With the 5% player kill switch, I can understand why they would opt for the less sensitive antigen test. But the 7.5% is going to cause problems unless there is some fine print. "Population" leaves them an out to cherrypick TBH. Wisconsin is around 14% right now. Iowa and Nebraska are over too and Minnesota is trending in the wrong direction. Iowa hasn't been under 7.5% since July.

ETA. On a separate football note, it looks like there is resolution on the Jamain Stephens story and it looks like the death was caused by a clot due to COVID-19. He was on campus working out, but did not catch it with the team.
View: https://twitter.com/ByPatForde/status/1306223732822880257
 
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A little hope on the treatment side for Covid. Eli Lilly is one of two companies working on an antibody treatment. They released preliminary results of their trial of people with mild/moderate symptoms (not yet hospitalized). There appears to be a little good news in this. Here's the link to an article about it.

 
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The allure of easy answers to complex problems allow people to think that they personally will get a vaccine soon after one is approved. Responsible people should disabuse that notion. The logistics of immunizing 300m+ people is not something that will sort itself out quickly. And that assumes that there is no issue with supply, which is a big assumption. And the kicker is that it is likely the vaccine approved will require 2 doses, complicating things further. By the end of October, it is debatable whether there will be enough infection within the two arms to declare whether the vaccine works or not. Anyone that suggests that vaccinations will happen in October is blowing smoke up your orifice IMO.
 
SARS 1.0 disappeared before the vaccine was ready to be tested. You are misrepresenting what happened there. The vaccine did not fail by any definition and animal models suggest that it would be successful in humans. Speculating that the vaccine will be unsafe given that tens of thousands that have taken them is a bit overdramatic. They would not be in Phase III if they didn't pass safety benchmarks.
I'm not misrepresenting anything: Chien - Te Tseng et al tested a vaccine against SARS-CoV-1 back in 2012. The animal models showed a robust antibody response but on challenge all the animals suffered a hyper-immune response including serious pulmonary inflammation:


Oxford's ChadOxl vaccine for COVID-19 tested the vaccine which failed to prevent infections in the animal models:


And Moderna's vaccine is deploying an experimental RNA technology. RNA tech has never been approved for any product.

Do you have any links on the results of the successful animal models you pointed out? (I'm assuming that included a challenge phase as well?).
 
ETA. On a separate football note, it looks like there is resolution on the Jamain Stephens story and it looks like the death was caused by a clot due to COVID-19. He was on campus working out, but did not catch it with the team.
They're reporting a heart blood clot(s) - coronary thrombosis. High BMIs are a major risk factor for thrombotic disease. Stephens was a big guy with a BMI of ~44.


WACO, Texas (KWTX) - California University of Pennsylvania initially announced Tuesday the death of football player Jamain Stephens was due to COVID-19 complications, but backtracked on that statement, saying there’s been no confirmed cause of death.

LCR Health Chief Medical Officer Dr. Rand McClain says if it was, in fact, due to the coronavirus, Stephens' 6′3″, 355-pound stature could’ve contributed to those complications.

“It’s not unusual for a gentleman, who gets this disease in that state and has that body mass, that he would suffer complications,” Dr. McClain said. “Despite his youth, he had a bigger strike against him, which would be the obesity factor.”
Stephens was just 20 years old, which is in an age range that is responsible for 0.0018% of all COVID-19 deaths in the United States according to the CDC.

Dr. McClain also says even if an overweight or obese athlete is in seemingly good physical shape, they could still be considered at higher risk to deal with COVID-19 issues.

“Take a bodybuilder, for example, if he’s got no body fat, how can you call him obese,” Dr. McClain said. “That’s not what were talking about here. It’s not necessarily fat. It’s a calculation. It’s important to note that obesity as defined by calculation. Fat or not, but just being heavy for your height is a big risk factor for COVID.”

If a person’s Body Mass Index (BMI) is 30.0 or higher, it falls within the obese range. A BMI number ranging from 25.0 to 29.9 is overweight, while 18.5-24.9 is normal.

“That message I think needs to get across to everyone out there. Big guys and gals, whether their bodies have more fat or not, need to be more careful because they’re at higher risk,” McClain said.
 
I'm not misrepresenting anything: Chien - Te Tseng et al tested a vaccine against SARS-CoV-1 back in 2012. The animal models showed a robust antibody response but on challenge all the animals suffered a hyper-immune response including serious pulmonary inflammation:

Oxford's ChadOxl vaccine for COVID-19 tested the vaccine which failed to prevent infections in the animal models:

And Moderna's vaccine is deploying an experimental RNA technology. RNA tech has never been approved for any product.
Here is the most recent paper on the subject. One of the authors, Hotez, is on TV regularly and has talked about SARS vaccine development.
In this work, the RBD219-N1 formulated with Alhydrogel® resulted in significantly increased antigen-specific IgG titers and neutralizing antibody responses when compared to other RBD constructs. After challenge with SARS-CoV, 100% of mice immunized with RBD219-N1 survived, while only 89% of mice immunized with other RBD constructs and less than 70% of the mice immunized with SARS-CoV spike protein survived and none survived in the control group.
It is worth reading the introduction as they have a discussion of why the other vaccine may have failed. If your argument is that some vaccines failed for SARS in preclinical models, that is correct. But claiming that the vaccine process failed is incorrect IMO. A vaccine with a reasonable high probability of success was developed and ready to be tested in humans, but the will to test it in humans was lost due to SARS being effectively eradicated. Hard to get grant money or Pharma support for something like this nowadays. The beneficial part of that research was finding out what vaccine platforms did not work. The COVID-19 vaccines benefitted from that process and are not using the type of vaccine platform that failed for SARS.

I think that article is missing the point. The vaccine prevented disease in the monkeys. I mentioned this before, but it might not be possible to prevent infection in the upper airways, but if a vaccine can prevent infection of the lungs, that will be very beneficial. There is a reason why they moved it to phase III. And AFAIK, all the phase III trials ongoing are not swabbing the enrollees on a regular basis to test for subclinical infection. They are only monitoring clinical symptoms and testing people with more serious cases. So, the clinical trial efficacy readouts will be whether the vaccine prevents disease, not infection. There has been some debate as to whether the ultimate goal should be a vaccine that can prevent infection (and transmission), but that is not something that will be knowable in the near future with the ones that are about to yield data.

I've also mentioned this before, but COVID-19 has provided a good opportunity to test new vaccine tech on a level that would not have been doable before due to the influx of $$$$. Some of these will not work, but we might see the development of new delivery types that improve on past vaccines. But the new ones do merit extra scrutiny.
Agree with this. The benefit to a live vaccine is that it will induce cytotoxic T cells as well as antibody and the phase I results from the Oxford group are consistent with that theory. In general, there is more of a threat to adverse reactions with a live vaccine, but these vectors have been widely tested in people as a vaccine vector for diseases like Malaria, Ebola, etc. One of the reasons that groups were so quick to get vaccines into humans was because the technological framework to make them was well established. The Moderna RNA vaccine had the worst adverse reactions in the early trials despite it being a 'safer' subunit vaccine, so I would be more hesitant about that one. The technology has never led to FDA approval, so it is bit more of a wild card.
They're reporting a heart blood clot(s) - coronary thrombosis. High BMIs are a major risk factor for thrombotic disease. Stephens was a big guy with a BMI of ~44.
Good thing that BMI is generally low in.. <checks notes>.. football players?!?! That really is an MO of COVID-19. It is very good at tipping vulnerable people over the edge. Doubtful he dies of a clot without the infection, but that is all speculation.
 
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Dorms... who could've guessed? From what I gather the greek houses have also been a problem. Another hard to foresee development. Rampant partying in the frat houses.

View: https://twitter.com/thedailybeast/status/1306376912248471552


That is on the heels of 29 players and staff testing positive on the football team between 9/1 and 9/15. I believe that is well north of the Big 10's 5% threshold. How are they supposed to be playing in 5 weeks? Wisconsin is going to be one of the next big hotspots. They have largely avoided the first two surges, but bringing all the students back is going to hurt.
 
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The allure of easy answers to complex problems allow people to think that they personally will get a vaccine soon after one is approved. Responsible people should disabuse that notion. The logistics of immunizing 300m+ people is not something that will sort itself out quickly. And that assumes that there is no issue with supply, which is a big assumption. And the kicker is that it is likely the vaccine approved will require 2 doses, complicating things further. By the end of October, it is debatable whether there will be enough infection within the two arms to declare whether the vaccine works or not. Anyone that suggests that vaccinations will happen in October is blowing smoke up your orifice IMO.
I can't see how any of the companies will have much data by October when most of the volunteers haven't had 2 doses of the vaccine yet. Until the majority of the people in the trail have two doses and have had some time after the second does I can't see how they will have much information. Just assuming most of the trail participants currently enrolled have gotten a second dose by the end of September I can't see how they get any usable data until mid to late November.
 
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We don't know what the vaccine companies are targeting for infection events because they have not been transparent about their methodologies. Until today when that changed. Seems like they need about 150-60 to get clinical disease. Depends on who is enrolled, but even with 30k people, that might take awhile. Also interesting that they are both expecting 60% efficacy.

View: https://mobile.twitter.com/virginiahughes/status/1306763103913246720
 
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We don't know what the vaccine companies are targeting for infection events because they have not been transparent about their methodologies. Until today when that changed. Seems like they need about 150-60 to get clinical disease. Depends on who is enrolled, but even with 30k people, that might take awhile. Also interesting that they are both expecting 60% efficacy.

View: https://mobile.twitter.com/virginiahughes/status/1306763103913246720

That explains why they are specifically wanting people who are part of the essential workforce and won't enroll anyone who isn't out working.

Just saw something that said Moderna is saying that November is the earliest they will have any usable data on their vaccine.
 
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