thegenius

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COVID-19 has been found in wastewater in Spain from almost a year and a half ago, and no one seemed to notice. No one seems to be reporting it. And it seems pretty frickin' significant, if you ask me.

Sentinel surveillance of SARS-CoV-2 in wastewater anticipates the occurrence of COVID-19 cases
I suppose it would be significant if we all had a lot more innate immunity against it. But it seems serology antibody testing suggests anywhere between 5-15% of the majority of Americans have been exposed. It might be a little higher in really dense areas in NYC.

Who knows...maybe the Spaniards were exposed to it, developed immunity, and then lost it 6 months later. They got hit pretty hard. Maybe their testing is faulty. Or maybe a much larger of the Spanish community is now immune to it. ???

It’s hard to know what to make of this information because there was a huge rise in China in December...then it got out and March is was bad in Italy and Spain, and April was bad in the USA. I kind of doubt it was smoldering in the worldwide population for the past few years.
 
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COVID-19 has been found in wastewater in Spain from almost a year and a half ago, and no one seemed to notice. No one seems to be reporting it. And it seems pretty frickin' significant, if you ask me.

Sentinel surveillance of SARS-CoV-2 in wastewater anticipates the occurrence of COVID-19 cases
I dunno man. They found a single isolated occurrence on a single day, every other positive result demonstrated a consistent trend or recurrence. Seems more likely to be a false positive due to test failure/contamination.

Unless I missed something? The melatonin is kicking in after all...
 
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I dunno man. They found a single isolated occurrence on a single day, every other positive result demonstrated a consistent trend or recurrence. Seems more likely to be a false positive due to test failure/contamination.

Unless I missed something? The melatonin is kicking in after all...
Rarely are the comments sections worthy. They are in this case though.
the authors do not detect SARS-CoV-2 in samples from 2019 March. Rather, they do detect IP2/IP4 resembling SARS-CoV-2. Whatever virus it is it does not have the E and N1/N2 of SARS-CoV-2. Fluctuations in qRT-PCRs even in 2020 samples -different sewers- are way too high to trust the reliability of the RT-PCRs. However, their approach is amazing. I hope they use a metagenomic approach to sequence to sewers rather than doing an RT-PCR assay, which doesn't look very rigorous.
 

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I dunno man. They found a single isolated occurrence on a single day, every other positive result demonstrated a consistent trend or recurrence. Seems more likely to be a false positive due to test failure/contamination.

Unless I missed something? The melatonin is kicking in after all...
It's definitely the melatonin.
 

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Good, non-scientific article in the NYTimes on several things related to the pathophysiology behind COVID-19. One is an explanation as to why kids are less affected than adults. SARS-COV-2 apparently depletes, or can deplete, T-cells much the same way as HIV. Kids have a very active and healthy thymus and can out produce the depleting effects of the virus, while older people who do not have a thymus are screwed.

How the Coronavirus Short-Circuits the Immune System
 
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Good, non-scientific article in the NYTimes on several things related to the pathophysiology behind COVID-19. One is an explanation as to why kids are less affected than adults. SARS-COV-2 apparently depletes, or can deplete, T-cells much the same way as HIV. Kids have a very active and healthy thymus and can out produce the depleting effects of the virus, while older people who do not have a thymus are screwed.

How the Coronavirus Short-Circuits the Immune System
Oof...tracked that back to it's primary literature. I'd recommend sticking with the NYT article.
 

thegenius

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Looking at the death graphs of the US and even other countries...
why do people die the least often on Sunday?
And most often on Monday and Tuesday?

I can see the ICU doc saying..."I'm just here to hold the fort down. I'm not going to let anyone die on my shift. It's Sunday night, I ain't got no backup...I'm just going to keep people alive..."
 

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Looking at the death graphs of the US and even other countries...
why do people die the least often on Sunday?
And most often on Monday and Tuesday?

I can see the ICU doc saying..."I'm just here to hold the fort down. I'm not going to let anyone die on my shift. It's Sunday night, I ain't got no backup...I'm just going to keep people alive..."
I think it's all a reporting issue. They don't report the death until the death certificate is signed.
 

thegenius

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Hence the backlog of death certificates over the weekend all get signed on Monday and Tuesday. Makes sense
 

Birdstrike

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Looking at the death graphs of the US and even other countries...
why do people die the least often on Sunday?
And most often on Monday and Tuesday?

I can see the ICU doc saying..."I'm just here to hold the fort down. I'm not going to let anyone die on my shift. It's Sunday night, I ain't got no backup...I'm just going to keep people alive..."
Like @turkeyjerky said, it's reporting. On Worldometer, for example, the two lowest days are always Sun and Mon, corresponding to data collection the days before (Sat and Sun) which are falsely low due to health departments and such, being closed on the weekends. Similarly, Tues & Wed always are falsely high, a little bit. Therefore, the 3-day average ends up looking like this with ups and downs on a 7-day cycle.


Screen Shot 2020-06-30 at 7.16.56 PM.png




The 7-day average compensates for it, and you get a smoother trend line, like this:

Screen Shot 2020-06-30 at 7.18.33 PM.png
 
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Birdstrike

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Deaths Are No Longer Lagging COVID Case Increases, They're Not Following At All

Superimpose the national COVID cases curve with the death curves. In April there was a 7-day lag, clear as day. About 6 weeks ago, the curves separated, the deaths kept falling despite cases rising and the 7-day lag disappeared. Double check the graphs on Worldometer. They're legit. I hope the trend of decreasing deaths regardless of case counts, continues. Time will tell.


Screen Shot 2020-06-30 at 11.38.48 PM.png
 
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This virus cleared out the nursing homes in March-May and the most susceptible patients died. A high number of the remaining nursing home residents got it and and are now theoretically immune. That is probably what we are seeing now. Transmission in the under 50 year olds simply will not cause a lot of deaths.

I posted the Sweden death curve in the other forum, and had we not locked down, we might be near the end of this already as their ascent and decline were much more rapid. Admittedly our country has a much bigger geographic area so spread will always be more slow.
 

thegenius

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So someone who had an infection COVID-19 in April is showing up positive PCR in late June?

If that is the case I think that is unlikely. They might have, or likely have, positive serology Abs by now, but I doubt they still currently are shedding live active virons.
 

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So someone who had an infection COVID-19 in April is showing up positive PCR in late June?

If that is the case I think that is unlikely. They might have, or likely have, positive serology Abs by now, but I doubt they still currently are shedding live active virons.
I think turkeyjerky means that we just weren't accurately capturing all of the cases early on. Not that former cases are now showing up as positive. When this all started at our shop we weren't able to do a send out test on anyone unless they traveled to China or came in to contact with a known positive case (which was practically no one). I remember in March/April seeing a huge number of patients with viral symptoms, a negative viral panel and wasn’t able to test them for COVID-19. They were mostly all well enough to go home. Therefore the number of cases compared to deaths was inaccurately captured resulting in early curves that aren't accurate. I still question the sensitivity of the current test. We now have an in house test and are able to use it on anyone exhibiting viral symptoms. I'm seeing tons of patients in the middle of summer with viral symptoms and even viral appearing pneumonia. They have consistently tested negative on a viral panel and negative with our COVID-19 test. Seems odd to me. The only explanation that makes sense to me is that they have COVID-19 with false negative testing. Our ICU is testing the same patients repeatedly with continued negative results. Some of our intensivists liken it to folks with the influenza that only shows up on sputum when you bronch them. I suspect that by the time they are sick enough to present to the hospital, the viral load has mostly cleared out or is down in the lungs not in the oropharynx. We aren't seeing a lot of deaths, and I still think that is because the IFR is much lower than we initially thought back right when this all began.
 
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Regardless, it's generally great news. Deaths are still going down despite "spikes". We should be thankful for this for whatever reason.
Remember when NYC was blowing up, and the southern states were doing okay, but that "didn't matter"? Now only Arizona matters, and the fact that 3,000 people aren't dying every day in NY/NJ, daily deaths are down 75% nationwide, doesn't matter. Even mentioning anything that doesn't reinforce people's fear is blasphemy. It's the strangest thing.
 
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thegenius

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I think turkeyjerky means that we just weren't accurately capturing all of the cases early on. Not that former cases are now showing up as positive. When this all started at our shop we weren't able to do a send out test on anyone unless they traveled to China or came in to contact with a known positive case (which was practically no one). I remember in March/April seeing a huge number of patients with viral symptoms, a negative viral panel and wan't able to test them for COVID-19. They were mostly all well enough to go home. Therefore the number of cases compared to deaths was inaccurately captured resulting in early curves that aren't accurate. I still question the sensitivity of the current test. We now have an in house test and are able to use it on anyone exhibiting viral symptoms. I'm seeing tons of patients in the middle of summer with viral symptoms and even viral appearing pneumonia. They have consistently tested negative on a viral panel and negative with our COVID-19 test. Seems odd to me. The only explanation that makes sense to me is that they have COVID-19 with false negative testing. Our ICU is testing the same patients repeatedly with continued negative results. Some of our intensivists liken it to folks with the influenza that only shows up on sputum when you bronch them. I suspect that by the time they are sick enough to present to the hospital, the viral load has mostly cleared out or is down in the lungs not in the oropharynx. We aren't seeing a lot of deaths, and I still think that is because the IFR is much lower than we initially thought back right when this all began.
Yup, I think there are numerous reasons why the CFR (and IFR) will go down with this broad-based, penetrative viral disease. That is in opposition to, for instance, the SARS mini epidemic 2002. There it was contained...and the IFR actually WENT UP to 9% once they counted all the cases and deaths.

We, along with most other countries, fumbled around in Jan - April, couldn't effectively isolate people with it (part of it was out fault, part of it was the disease is not particularly amenable to isolation and quarantine given asymptomatic spread. Although some Asian countries were able to do so.) Once we started telling people to stay at home, don't go to work, don't be around other people, and lockdown various parts of society, the infection rate went down. No surprise there.

Now we know more about how it spreads, how to treat it, how not to treat it, we have more PPE, we have much more knowledge about it - all of this helps keep the death rate down. Younger people are getting sick, they are much more likely to survive, older people don't want to leave their homes, we are better at testing, our tests are better (although I agree the tests still suck) and overall we have more knowledge. I suspect that deaths will go up in the coming weeks / months but it will be a low hump and not look like a mountain. It will not look like the first wave when it almost went hand in hand. It is good from a world-view that deaths are going down, but now those who are dying will be young, productive, working people and not bedbound nursing home patients.

Will be interesting to see how the next 6-12 months compare here in USA vs other countries where they are not seeing nearly the degree of new infections we are.

It still is a dangerous virus. I've never admitted anyone < 50 with a dx of influenza with mild-to-moderate comorbid conditions, but we are pretty easily filling hospitals with these same people with COVID-19. My friend, who is my age, was just in the hospital w/ COVID-19 for 5 days on 4L. He lived. But it's not all about life/death. He will have to max pay his deductible, not be able to work for ~4 weeks with all that lost income, and watch his father and kids also go through this (his kids are fine).
 
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GeneralVeers

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0.06% for me. Guess there's a very high likelihood you'll have to read my comments for a while longer.
 

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0.06% for me. Guess there's a very high likelihood you'll have to read my comments for a while longer.
My chance of death comes out to 0.09%. But it jumps to 0.13% if I change my gender to female. This is a sexist, transphobic calculator. I'm literally shaking.
 

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My chance of death comes out to 0.09%. But it jumps to 0.13% if I change my gender to female. This is a sexist, transphobic calculator. I'm literally shaking.
Wait, what? Male gender is a bigger risk factor, as far as I know. The covid mortality rate with women has been lower...
 
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thegenius

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who the **** measures waist circumference when you are admitted to the hospital? LOL
who the **** asks what your waist circumference is when you are admitted to the hospital?
 

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I'm not sold on hydroxychloroquine. I don't think there should be a rush to find a treatment for a disease with a 99.8% survival rate. Given our lack of success with other respiratory viruses like Influenza, I think focus should be on a vaccine to prevent infection.

If someone is dying in the ICU from this, sure throw the kitchen sink at them.
 
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bravotwozero

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looks like decadron might be more of a game changer than anything else we've tried so far...
 
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A new Henry Ford Health System study on Hydroxychloroquine cut death rate of admitted patients in half (13% vs 26%). They attribute their positive results to a combination of giving the drug very early combined with cardiac monitoring. I'm not sure what to think of this drug.

Press release.

International Journal of Infectious Diseases.
A retrospective study with significant baseline differences and confounders. Pretty meaningless.
 

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I'm not sold on hydroxychloroquine. I don't think there should be a rush to find a treatment for a disease with a 99.8% survival rate. Given our lack of success with other respiratory viruses like Influenza, I think focus should be on a vaccine to prevent infection.

If someone is dying in the ICU from this, sure throw the kitchen sink at them.
No, provide the best evidence based care you can. In critical care, it seems the kitchen sink tends to be harmful.
 

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No, provide the best evidence based care you can. In critical care, it seems the kitchen sink tends to be harmful.
evidence based or evidence informed? If your patient is circling the drain despite your evidence based treatments, do you really need results from a randomized trial to consider alternatives at that point?
 

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We are not doing basically anything with COVID patients besides admitting them and getting rocephin and doxy/z-pack. Perhaps if they were markedly hypoxic we might start dex, but I don't think we are in much hurry to start it. The latest decadron study shows that the later they received decadron, the better they did
 

thegenius

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Meh?

Here are the conclusions from the abstract:

1. After adjustment for confounders, patients with hypertension had a two-fold increase in the relative risk of mortality as compared with patients without hypertension

2. Patients with a history of hypertension but without antihypertensive treatment (n = 140) were associated with a significantly higher risk of mortality compared with those with antihypertensive treatments

3. The mortality rates were similar between the renin–angiotensin–aldosterone system (RAAS) inhibitor (4/183) and non-RAAS inhibitors



So your risk of dying is higher if you have HTN vs not
You risk of dying is higher if you have untreated HTN vs treated HTN
Blocking RAAS (with ACE-I and ARBs) vs other anti-HTN meds don't appear to make a difference.
 

thegenius

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About 60,000 spaniards participated in a study to assess the prevalence of SARS-COV-2 antibodies in the general population. A massive n.

Results: The majority of the population is seronegative, even in hot spots.

https://www.thelancet.com/action/showPdf?pii=S0140-6736(20)31483-5

Spain Seroprevalence SARS-COV-2.jpg

My interpretation:
Without reading the paper, which I did not. Just read the abstract. Seems about right from other prevalence studies in the US and other places.


Edit:
It's also important to know that the antibody tests were run between 4/27 and 5/11, and given IgG takes a 1-2 weeks to build, this represents seroprevalence around mid-April.
 
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Meh?

Here are the conclusions from the abstract:

1. After adjustment for confounders, patients with hypertension had a two-fold increase in the relative risk of mortality as compared with patients without hypertension

2. Patients with a history of hypertension but without antihypertensive treatment (n = 140) were associated with a significantly higher risk of mortality compared with those with antihypertensive treatments

3. The mortality rates were similar between the renin–angiotensin–aldosterone system (RAAS) inhibitor (4/183) and non-RAAS inhibitors



So your risk of dying is higher if you have HTN vs not
You risk of dying is higher if you have untreated HTN vs treated HTN
Blocking RAAS (with ACE-I and ARBs) vs other anti-HTN meds don't appear to make a difference.
I'm curious if anti HTN drugs can directly reduce covid mortality. I'm hoping for more RCTs at this point.

The idea is if inflammation, hypertension and thrombosis are major factors contributing to mortality, targeting those can reduce hospital stay and decrease death rate.
 

Birdstrike

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About 60,000 spaniards participated in a study to assess the prevalence of SARS-COV-2 antibodies in the general population. A massive n.

Results: The majority of the population is seronegative, even in hot spots.

https://www.thelancet.com/action/showPdf?pii=S0140-6736(20)31483-5

View attachment 312073

My interpretation:
Without reading the paper, which I did not. Just read the abstract. Seems about right from other prevalence studies in the US and other places.


Edit:
It's also important to know that the antibody tests were run between 4/27 and 5/11, and given IgG takes a 1-2 weeks to build, this represents seroprevalence around mid-April.
Yes. I believe they found 5% with antibodies, right? But I don’t think they checked for t-cell immunity (harder to do) which in the other study I posted above was found to outnumber antibodies 2:1, I think.
 
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VA Hopeful Dr

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Yes. I believe they found 5% with antibodies, right? But I don’t think they checked for t-cell immunity (harder to do) which in the other study I posted above was found to outnumber antibodies 2:1, I think.
I thought the Germans said that those people get less severe COVID but aren't actually immune?
 

Birdstrike

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I thought the Germans said that those people get less severe COVID but aren't actually immune?
Well, yes and no. "Immunity" could be anything from exposure resulting in no infection, or exposure resulting in mild infection when you otherwise would have had severe infection or death.

"At present, determination of immunity to SARS-CoV-2 relies on the detection of SARS-CoV-2 antibody responses....Our SARS-CoV-2-specific T- cell epitopes... allowed for detection of specific T-cell responses even in donors without antibody responses, thereby providing evidence for T-cell immunity upon infection. "

"Cross-reactive SARS-CoV-2 T-cell epitopes revealed preexisting T-cell responses in 81% of unexposed individuals, and validation of similarity to common cold human coronaviruses ... "


In other words, even if only 5% have antibodies, you may have a much greater percentage without antibodies but with T-cell immunity (up to 81%). Why this is such a big deal is because people are saying, "You need 40-60% of the population immune for herd immunity. At 5%, we're a long way from that." But they're only looking at antibodies, which ignores the whole rest or our immune response.

Source- SARS-CoV-2 T-cell epitopes define heterologous and COVID-19-induced T-cell recognition
 
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thegenius

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Yes. I believe they found 5% with antibodies, right? But I don’t think they checked for t-cell immunity (harder to do) which in the other study I posted above was found to outnumber antibodies 2:1, I think.
I believe it was just a humoral immunity/prevalence study.
 
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Well, yes and no. "Immunity" could be anything from exposure resulting in no infection, or exposure resulting in mild infection when you otherwise would have had severe infection or death.

"At present, determination of immunity to SARS-CoV-2 relies on the detection of SARS-CoV-2 antibody responses....Our SARS-CoV-2-specific T- cell epitopes... allowed for detection of specific T-cell responses even in donors without antibody responses, thereby providing evidence for T-cell immunity upon infection. "

"Cross-reactive SARS-CoV-2 T-cell epitopes revealed preexisting T-cell responses in 81% of unexposed individuals, and validation of similarity to common cold human coronaviruses ... "


In other words, even if only 5% have antibodies, you may have a much greater percentage without antibodies but with T-cell immunity (up to 81%). Why this is such a big deal is because people are saying, "You need 40-60% of the population immune for herd immunity. At 5%, we're a long way from that." But they're only looking at antibodies, which ignores the whole rest or our immune response.

Source- SARS-CoV-2 T-cell epitopes define heterologous and COVID-19-induced T-cell recognition
I'm having trouble copying and pasting from the article, but several things:

1) While they found 81% had some T cell response there was no conferred immunity from that response, rather the authors noted the necessity of multiple epitopes which was only found with active infection for there to be a benefit of immunity.

2) The only thing that affected the severity of symptoms was the antibody itself rather than the intensity T cell response.

Not sure this is all that exciting, I mean it's neat that you can have a T cell response without having had the active infection but if it doesn't actually benefit you in regards to long term immunity...?
 
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Birdstrike

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I'm having trouble copying and pasting from the article, but several things:

1) While they found 81% had some T cell response there was no conferred immunity from that response, rather the authors noted the necessity of multiple epitopes which was only found with active infection for there to be a benefit of immunity.

2) The only thing that affected the severity of symptoms was the antibody itself rather than the intensity T cell response.

Not sure this is all that exciting, I mean it's neat that you can have a T cell response without having had the active infection but if it doesn't actually benefit you in regards to long term immunity...?
You always have to be careful not to make too many clinical conclusions from basic science research. I think the point of the study was to help find a way to develop a vaccine that stimulates both good antibody and T cell responses, not just one or the other. I don't know that the authors were attempting to definitively conclude anything clinical one way or the other, or that a T cell responses alone without antibodies, are a magic bullet against COVID-19. I found it interesting, though.
 
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