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Formerly DT: COVID-19 - Featuring Lots of Politics, now CR because political talk not going away


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Two weeks is the earliest we'd expect any impact whatsoever.  There won't be a noticable trend until next week at some point.  Basically now is when the data collection starts not when it is complete.

This is spiking the football on the way into the endzone.

Edited by JBJ
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6 hours ago, Vic Mackey said:

Hell no it isn't. I have not worn a mask one single instance and had zero problems. In fact, I see the percentage of people wearing masks slowly starting to dwindle as the days go by. The hype is wearing off for many.

You’re part of the problem. No surprise there though

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26 minutes ago, Js1 said:

Someone here in ATL posted a lot of restaurants remained closed. Don’t think people rushed out to fill up public spaces and stores. 

Yes a friend in Atlanta told me that, like Austin, many restaurants remained closed even though they're allowed to reopen.  

 

 

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29 minutes ago, utee94 said:

Yes a friend in Atlanta told me that, like Austin, many restaurants remained closed even though they're allowed to reopen.  

 

 

Staffing is a challenge.  So is supply chain.

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21 minutes ago, Iceman said:

If 400 pounds sitting on his face doesn’t kill him, CV-19 aint gotta chance. 

Except that masks aren't really for the person wearing them.

...and, as you mention, he's in close proximity to some folks with a few underlying health issues.

Edited by aggie08
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1 hour ago, JBJ said:

Two weeks is the earliest we'd expect any impact whatsoever.  There won't be a noticable trend until next week at some point.  Basically now is when the data collection starts not when it is complete.

This is spiking the football on the way into the endzone.

Right.  Figure 5 days to onset of symptoms, with range of 3-14 and recall the shape the case growth takes. It is good that we are not seeing a spike after two weeks, but give it another 2-4 to really draw some conclusions. 

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10 hours ago, Incredulity said:

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So if your gf/bf/wife/husband spent 2 hours plus with a contagious person in a car/enclosed space for whatever the fuck reason, you're saying your response would be, "Honey, don't forget to kiss the kids goodnight and hug them extra hard before bed since we'll be road tripping all day to go see grandma and grandpa, don't worry about the masks, we don't need them!! Can't wait!"

Right? 

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6 minutes ago, achooloco said:

So if your gf/bf/wife/husband spent 2 hours plus with a contagious person in a car/enclosed space for whatever the fuck reason, you're saying your response would be, "Honey, don't forget to kiss the kids goodnight and hug them extra hard before bed since we'll be road tripping all day to go see grandma and grandpa, don't worry about the masks, we don't need them!! Can't wait!"

Right? 

If I had a "GF/BF/WIFE/HUSBAND" I am sure mood swings and wardrobe changes would be a bigger concern.

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2 hours ago, Onboard 2.0 said:

I think 2 weeks is just where you'll either see it's working or another spike will occur.  

Based on the initial outbreak, I think more like 3-4 weeks. A case spike in rural southern states could be hard to detect. You need enough cases that are severe enough to warrant testing and enough tests to identify them. So in Georgia that essentially means a major spreading event in one major metro or three small ones.  You could have 50% of the population get covid-19 outside of those areas and probably wouldn't test more than 20K people due to a combination ignorance, poverty, lack of care, access, etc.

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Without getting all the way into this thread, it’s crazy to me how different places like Texas, Arizona, and Florida are handling this situation compared to California (NY, and especially NYC is just a different animal because of how the city is set up). Out here in Arizona, starting on Monday literally everything will be open with limited capacity. Someone is going to be loud wrong about this situation, and we can only hope it’s Cali for being overly concerned. I’d love to say that i think they are, but who the fuck knows. 

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2 minutes ago, youdunnf'dup said:

Without getting all the way into this thread, it’s crazy to me how different places like Texas, Arizona, and Florida are handling this situation compared to California (NY, and especially NYC is just a different animal because of how the city is set up). Out here in Arizona, starting on Monday literally everything will be open with limited capacity. Someone is going to be loud wrong about this situation, and we can only hope it’s Cali for being overly concerned. I’d love to say that i think they are, but who the fuck knows. 

Warm weather and lack of public transportation have to be part of it, outside of Atlanta. 

Hopefully this virus acts like others in that respect and things calm down over the summer before the fall wave. 

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As for Illinois, the Public Health Director said 90% of deaths have an underlying condition. 

More evidence we dont all have the same risk profile and we need to open up intelligently. 

Spend our resources protecting those at risk and lets be smart and start the comeback. 

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1 hour ago, Anastasis said:

Right.  Figure 5 days to onset of symptoms, with range of 3-14 and recall the shape the case growth takes. It is good that we are not seeing a spike after two weeks, but give it another 2-4 to really draw some conclusions. 

I've circled the first week of June since things started opening back up.  If we get through that week with no meaningful growth then a really good sign.  Of course then the speculation will turn to what happens if things open up completely and/or the extent  the impact warmer weather has on the spread. 

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Continuing the charts I've posted sporadically from @lymanstoneky on twitter.

Number of tests increasing and rate of positive tests decreasing:

Spoiler

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Deaths in US considering CT, NJ, and NY:

Spoiler

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Predicting the % of people who have actually contracted COVID based on the reported deaths. We're extraordinarily far from heard immunity if these are even close to accurate.

Spoiler

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Finally, Hong Kong's tracking of other infectious diseases, including pink eye, GI, and flu-like illnesses compared to past 10 years:

Spoiler

EX-bfOeVAAAQF0D?format=png&name=900x900

 

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44 minutes ago, bullzak said:

As for Illinois, the Public Health Director said 90% of deaths have an underlying condition. 

More evidence we dont all have the same risk profile and we need to open up intelligently. 

Spend our resources protecting those at risk and lets be smart and start the comeback. 

Right, but what is that really telling us? Most of our population has underlying issues, so we really aren't able to narrow down where to spend our resources based on that. What we really need is more specifics on type and severity of the underlying conditions and their interaction with Covid-19. 

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1 hour ago, Casual Encounter said:

I mean, people brag about not wearing condoms while having sex with sluts.

I love sluts. I mean, I don’t really want to put my dick in them, but I like to look at them. If they’re lucky, I’ll jerk off to them, cum on the floor then let them lick it up. 

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3 hours ago, South Austin said:

The Georgia story is all over the headlines this morning, and rightly so.  If an aggressive reopening with proper safety requirements don't result in a significant spike, that's great news for all of us. 

But I'm cautious about the numbers, so here are my questions:  Is two weeks out a good measure of success?  In other words, there's going to be a gradual delay of the masses venturing out after retail, restaurants, workplaces, etc. open up, and with additional delays of transmission, symptoms, testing, and outcomes, do we really have an accurate picture of how Georgia's aggressive opening will pan out?  Will another two weeks give us a better picture?  I ask this as someone who is anxious--no, desperate--to break free from this fucking holding pattern. 

I'll hang up and listen. 

I live in Atlanta and while there are more people out, the restaurants that are open are pretty much empty. Still a lot of masks in the grocery store.  Still people are being cautious.  Not much different than two weeks ago in the city. 

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1 minute ago, EuroHorn said:

I live in Atlanta and while there are more people out, the restaurants that are open are pretty much empty. Still a lot of masks in the grocery store.  Still people are being cautious 

Good, insomuch as things are open but people are being cautious so the spread might stay manageable over time. Sucks for people that wait tables and serve drinks for a living though. Can we count on the majority of the country self regulating?

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12 minutes ago, Pato del Muerto said:

Skipping about 4 pages/24 hours of posts here. 
 

has this been posted/discussed?

https://www.nytimes.com/2020/05/13/health/coronavirus-children-kawasaki-pmis.html

I don't think so, was reading about it on CNN and of course---has me freaked the fuck out.  Great time to be yelling at people who caution us to open schools more carefully and to perhaps wait for more data.  

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16 minutes ago, EuroHorn said:

I live in Atlanta and while there are more people out, the restaurants that are open are pretty much empty. Still a lot of masks in the grocery store.  Still people are being cautious.  Not much different than two weeks ago in the city. 

Username does not check out.

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6 minutes ago, Lobo said:

I don't think so, was reading about it on CNN and of course---has me freaked the fuck out.  Great time to be yelling at people who caution us to open schools more carefully and to perhaps wait for more data.  

Yeah, I've been following. Fortunately, it appears to be a very rare reaction (1/1000 or .1%), but definitely something I'm concerned about as a parent of child in the same age group. 

Here is another good article on it (Covid-19 Linked to 30 Fold Increase in Rare Childhood Inflammatory Disease) :

Quote

 

Evidence is stacking up to support a link between COVID-19 and a rare, mysterious inflammatory disease in children, which can be life-threatening.

Though reports of the new disease have trickled in from several countries, many of them have been anecdotal to this point. Now, doctors in an area of Italy hardest hit by the COVID-19 pandemic have published detailed data on a cluster of 10 children who experienced an unusual inflammatory disease amid the outbreak, lending solid support for the link. Their report appeared Wednesday in The Lancet.

The doctors describe the condition they saw as “Kawasaki-like,” referring to a rare disease in children that causes inflammation of blood vessels. Kawasaki disease—identified in Japan in 1967 by Tomisaku Kawasaki—is typically marked by sustained fever, rash, swelling of hands and feet, and swollen lymph nodes in the neck. In the worst cases, it can lead to heart problems and aneurysms.

Despite being identified decades ago, Kawasaki’s cause still remains unclear. Researchers have widely hypothesized that infectious agents—like viruses—trigger berserk immune responses in certain children with genetic predispositions. But no single germy culprit or genetic factors have been firmly nailed down. As such, it’s still unclear who will end up afflicted by the condition. Researchers have only determined that Kawasaki primarily strikes children younger than five, often boys, and often people of Asian and Pacific Island descent.

Since the pandemic began, there have been scattered reports of an uptick in cases of a disease similar to Kawasaki in children. The cases seem linked to outbreaks of COVID-19. However, they don’t always fit the “classic” definitions of Kawasaki.

In the new Lancet study, the Italian doctors offer a clear connection between infection with SARS-CoV-2 and the Kawasaki-like disease. They also lay out in detail how the cases they saw differ from the classic forms of the disease, laying the groundwork for a COVID-19-specific form of the disease.

Surprising spike

To do that, the doctors reviewed medical records of children who were diagnosed with Kawasaki disease between January 1, 2015 and April 20, 2020 at a hospital in Bergamo, Italy. At the time of the study, the city of Bergamo had the highest rate of COVID-19 infections and deaths in Italy, which was ravaged by the pandemic.

The doctors identified only 29 cases in that time frame, 19 of which were diagnosed between January 1, 2015 and Feb 17, 2020. The other 10 were identified between March 17 and April 14, 2020, as the COVID-19 outbreak raged. That spike during the outbreak represents a thirtyfold increase in incidence of the inflammatory condition.

The doctors suspected that all 10 of the Kawasaki cases during the outbreak had been infected with the new coronavirus, SARS-CoV-2, which causes COVID-19. But only eight of the children tested positive for SARS-CoV-2 antibodies, which are Y-shaped proteins made by the immune system to fight off the virus. The presence of the antibodies means that the children had been infected. The doctors suspect that the other two children were false negatives. One, for instance, had received a treatment of immunoglobulin, which may have interfered with the antibody test.

They also noted that previous studies done in 2005 and 2014 had also linked coronaviruses—in these cases, ones that cause seasonal colds—to Kawasaki disease. Though other studies failed to find such a link, the authors argued that, together, “this suggests that the coronavirus family might represent one of the triggers of Kawasaki disease, SARS-CoV-2 being a particularly virulent strain able to elicit a powerful immune response in the host.”

The presence of the virus in nearly all of the cases during the outbreak and the fact that the spike in inflammatory cases “has a clear starting point after the first case of COVID-19 was diagnosed in our area,” convinced the doctors.

“All these results and considerations support the hypothesis that the immune response to SARS-CoV-2 is responsible for a Kawasaki-like disease in susceptible patients,” they concluded.

Mounting mysteries

But the doctors noted that the inflammatory disease was slightly different from the cases seen in the past. The children afflicted during the outbreak tended to be older, with an average age of 7.5, compared with the 19 pre-COVID cases, which had an average age of 3.

The outbreak cases also had more severe diseases. Six of the 10 had heart complications, compared with just two of the 19 cases from the pre-COVID era. Two outbreak cases had signs of toxic shock, which was not seen in any of the earlier cases. Finally, eight of the outbreak cases needed additional steroid treatments to recover, which was only needed in three of the pre-COVID cases.

Ultimately, the doctors were careful to call the cases seen during the outbreak a “Kawasaki-like” disease.

In an accompanying editorial, Russell Viner, president of the Royal College of Paediatrics, and Elizabeth Whittaker, a pediatric infectious diseases expert at Imperial College London, tried to tease this apart. They write: “These differences raise the question as to whether this cluster is Kawasaki disease with SARS-CoV-2 as the triggering agent, or represents an emerging Kawasaki-like disease characterised by multisystem inflammation.”

Like the Italian doctors, they highlight that—however frightening—this inflammatory disease is still rare, likely affecting no more than one in 1,000 children infected with SARS-CoV-2. Parents and doctors should be aware of it but also keep in mind that children are minimally affected by COVID-19 overall.

But, Viner and Whittaker note, that insight into what’s going on with immune responses in this rare condition could help explain other mysteries of the illness.

 

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13 minutes ago, Lobo said:

I don't think so, was reading about it on CNN and of course---has me freaked the fuck out.  Great time to be yelling at people who caution us to open schools more carefully and to perhaps wait for more data.  

Was at the pediatrician with our newborn this week and asked about this.  Pediatrician basically said it is super low probability and we (the medical community) know how to deal with it but to be extra careful with the newborn

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2 hours ago, Texas Jeff said:

Crazy idea ... maybe there is a reasonably moderate path to walk so long as cases start to drop and keep dropping.  Somewhere between mask-free rave mode and staying in your bathroom covered in hand sanitizer.

Right now, cases in Texas are not dropping (which is bad) but the number of positive test results is low (around 5%, which is good).  rt.live has our R number at 0.84 (good, less than 1, a path to no disease) but epiforcasts.io has it at 1.2 (moderately bad, a path to a big problem). The truth is probably in the middle somewhere.  We have a problem and it it is likely slowly growing.  Some projections show it slowing down in the future but right now the numbers are still going in the wrong direction.  We are on a slowly rising plateau looking at two futures, one where cases slowly drop and one where they rise until they are out of control.

You, my fellow Texan, can help make the problem go away.  Spread out, wear a mask when appropriate, and wash your hands.  You don't have to, but if you do it will help.  Stay home if you feel sick and especially if you know you have come in contact with someone who has it.  Not forever, but for a little while.  Ask your neighbor how they are doing.  They might be sad, lonely or just need someone to run to the store. A five minute chat across a front yard might cheer them up.

Every little thing you do reduces the chance that one person will infect another person, which reduces the size of the problem.  It keeps that R number just a little bit lower which makes the problem go away faster.  Doctors and nurses have less emergency work to do in a less risky environment and can work more on the other problems we have.  You'll never know if you saved the life of a kid or a grandma, but maybe you did.

I see a risk in our polarized society that we will start choosing extreme paths on one side or the other, regardless of the data, based on which leaders we like.  And that we will be too critical of each other for being on the other side.  I would instead ask you to do what you are willing to do and watch those case numbers.  If they are not dropping, consider doing more until they are.

Here’s the deal, outbreaks ARE GOING TO HAPPEN.  They are unavoidable. It requires a basic understanding of human behavior and science to come to this conclusion. The virus is not going to magically go away.

The hard questions we are dealing with now:

1. How do we best minimize the intensity of outbreaks without going into a full lockdown?  We wear masks, we physically distance, we wash hands, we keep the population informed with accurate information, we stay vigilant, we test and trace quickly to isolate outbreaks when they happen so grandma doesn’t die. 
 

2. Are we as a society prepared to work together to do this? 
 

3. Do we have all the resources available to quickly test and trace when outbreaks occur? 
 

4. If we choose not to take these precautionary measures, what will be the consequences?  
 

I fear we’re going to find out the answer to #4 the hard way. 

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https://blogs.sciencemag.org/pipeline/archives/2020/05/15/good-news-on-the-human-immune-response-to-the-coronavirus

Good News on the Human Immune Response to the Coronavirus

By Derek Lowe 15 May, 2020

One of the big (and so far unanswered) questions about the coronavirus epidemic is what kind of immunity people have after becoming infected. This is important for the idea of “re-infection” (is it even possible?) and of course for vaccine development. We’re getting more and more information in this area, though, and this new paper is a good example. A team from the La Jolla Institute for Immunology, UNC, UCSD, and Mt. Sinai (NY) reports details about the T cells of people who have recovered from the virus. To get into this, a quick explainer seems appropriate, so the next bit will be on the background of T cells and adaptive immunity – then we’ll get into these latest results.

So everyone’s heard of the broad category of white blood cells. One group of those are the lymphocytes (literally “lymph cells”, where they’re most easily found), and the lymphocytes include T cells, B cells, and NK cells. You’re looking at three big branches of the immune system right there. The NK (“natural killer”) cells are part of the innate immunity, the nonspecific kind, and they’re in the cell-mediated cytotoxic wing of that. The other side of the immune system is adaptive immunity. The B cells feature in my antibody background posts, because as part of the adaptive system they’re the ones that produce more of some specific antibody once one of the zillions of them present in the body turns out to fit onto a new antigen. The T cells are in the adaptive side as well, but they’re in the cell-mediated part of that army.

T cells come from the thymus (thus the “T”), so if you’ve been wondering what your thymus has done for you lately, that’s one good answer. They all have a particular surface protein, the T cell receptor. Similar to the way that the immune system generates a huge number of antibodies by shuffling and mixing protein expression, there are a huge number of different T cell receptors waiting to recognize what antigens may come along. The precursors of T cells come from the bone marrow and migrate to the thymus, where they branch out into different lines (and that branching out continues even once they leave the thymus and begin circulating in the lymph and in the blood.

The most direct of those are the cytotoxic T cells, also known as CD8+ T cells and by several other names. CD8 is another particular cell-surface protein that distinguishes this type. These cells aren’t going after viral particles; they’re going after the body’s own virus-infected cells and killing them off before they can break open and spread more viral particles. They’ll kill off bacterial cells in the same way. These are also the ones that the CAR-T therapies are trying to mobilize so that they’ll recognize cancer cells and do the same thing to them. How do they accomplish the deed? They’re thorough; there are several deadly mechanisms that kick in. One general one is to secrete cytokines, especially TNF-alpha and interferon-gamma, that alert other cellular systems to the fact that they’ve detected targets to attack. (The monoclonal antibody drugs for arthritis are actually aimed to shut down that TNF-alpha pathway, because in RA the T cells are – very inappropriately – attacking the body’s own joint tissue). A second CD8+ action is to release “cytotoxic granules”. These are payloads of destruction aimed at the target cell once the T cell is closely connected to it (the “immune synapse”). You need that proximity because cytotoxic granules are bad news – they contain proteins that open up pores in the target cell, and blunderbuss serine protease enzymes that slide in through them, whereupon they start vigorously cleaving intracellular proteins and causing general chaos (and eventually cell death). And the third killing mode is via another cell-surface protein the CD8+ cells have called FasL – it binds to a common protein on the target cells called Fas, and that sets off a signaling cascade inside the target cells that also leads to cell death. (Interestingly, the CD8+ cells use this system after an infection has subsided to kill each other off and get their levels back down to normal!)

And then there’s another crowd, the CD4+ T cells, also known as T-helper cells and by other names. They work with another class of immune cells, the antigen-presenting cells, which go around taking in all sorts of foreign proteins and presenting them on their cell surfaces. A CD4+ cell, when it encounters one of those, goes through a two-stage activation process kicks in (the second stage is sort of a verification check to make sure that it’s really a foreign antigen and not something already present in the body). If that’s successful, they start to proliferate. And you’re going to hate me for saying this, but that’s where things get complicated. Immunology! The helper T cells have a list of immune functions as long as your leg, interacting with many other cell types. Among other things, they help set off proliferation of the CD8+ cells just detailed, they activate B cells to start producing specific antibodies, and they’re involved with secretion of more cytokine signaling molecules than I can even stand to list here. These are in fact the cells targeted by HIV, and it’s the loss of such crucial players in the immune response that makes that disease so devastating.

OK, there’s some background for this new paper. What it’s looking at in detail are the virus-specific CD8+ and CD4+ cells that have been raised up in response to the infection in recovering patients. As you’ve seen, both of these subtypes are adaptive; they’re recognizing particular antigens and responding to those – so how robust was this response, and what coronavirus antigens set things off? You can see how important these details are – depending on what happens, you could have an infection that doesn’t set off enough of a response to leave behind B and T cells that will remember what happened, leaving people vulnerable to re-infection. Or you could set off too huge a response – all those cytokines in the “cytokine storm” that you hear about? CD4+ cells are right in the middle of that, and I’ve already mentioned the TNF-alpha problems that are a sign of misaligned CD8+ response. The current coronavirus is pretty good at evading the innate immune system, unfortunately, so the adaptive immune system is under more pressure to deliver. And one reason (among many) that the disease is more severe in elderly patients is that the number of those antigen-presenting cells decline with age, so one of the key early steps of that response gets muted. That can lead to a too-late too-heavy T cell response when things finally do get going, which is your cytokine storm, etc. In between the extremes is what you want: a robust response that clears the virus, remembers what happened for later, and doesn’t go on to attack the body’s own tissues in the process.

Comparing infected patients with those who have not been exposed to the coronavirus, this team went through the list of 25 viral proteins that it produces. In the CD4+ cells, the Spike protein, the M protein, and the N protein stood out: 100% of the exposed patients had CD4+ cells that responded to all three of these. There were also significant CD4+ responses to other viral proteins: nsp3, nsp4, ORF3s, ORF7a, nsp12 and ORF8. The conclusion is that a vaccine that uses Spike protein epitopes should be sufficient for a good immune response, but that there are other possibilities as well – specifically, adding in M and N protein epitopes might do an even more thorough job of making a vaccine mimic a real coronavirus infection to train the immune system.

As for the CD8+ cells, the situation looked a bit different. The M protein and the Spike protein were both strong, with the N protein and two others (nsp6 and ORF3a) behind it. Those last three, though, were still about 50% of the response, when put together, so there was no one single dominant protein response. So if you’re looking for a good CD8+ response, adding in epitopes from one or more of those other proteins to the Spike epitope looks like a good plan – otherwise the response might be a bit narrow.

And here’s something to think about: 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. And vaccine developers will want to think about adding in some of the other antigens mentioned in this paper, in addition to the Spike antigens that have been the focus thus far. It seems fair to say, though, that the first wave of vaccines will likely be Spike-o-centric, and later vaccines might have these other antigens included in the mix. But it also seems that Spike-protein-targeted vaccines should be pretty effective, so that’s good. The other good news is that this team looked for the signs of an antibody-dependent-enhancement response, which would be bad news, and did not find evidence of it in the recovering patients (I didn’t go into these details, but wanted to mention that finding, which is quite reassuring).

Onward from here, then – there will be more studies like this coming, but this is a good, solid look into the human immunology of this outbreak. And so far, so good.

 

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3 hours ago, Brew said:

Most people with a brain are going to be ultra cautious for right now, so the two week measurement doesn’t prove anything. As that caution starts to subside or some states allow large gatherings again, it will be interesting to see what happens.

Yep, here in Austin, plenty of business are still curbside, plenty of people are still wearing masks and still doing curbside/online, so hopefully we keep our little curve fairly flat.

I don't like that cases seem to be trending up in Texas, although it was to be expected, since we didn't follow the CDC guidelines, but we are also testing more as well. 

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41 minutes ago, Pato del Muerto said:

Good, insomuch as things are open but people are being cautious so the spread might stay manageable over time. Sucks for people that wait tables and serve drinks for a living though.

There's no stimulus checks on the horizon, at least not before late June or into July at a minimum, or anything like that, so it's going to be rough for a lot of those folks and businesses.   Hopefully we can get this right as far as hygiene and keeping the numbers down, and still keep those businesses open and those folks still pulling in paychecks/tips.

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I've circled the first week of June since things started opening back up.  If we get through that week with no meaningful growth then a really good sign.  Of course then the speculation will turn to what happens if things open up completely and/or the extent  the impact warmer weather has on the spread. 

Immunity could be a huge factor this winter to reduce the thread immensely
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19 minutes ago, atomheartbevo said:

I don't like that cases seem to be trending up in Texas, although it was to be expected, since we didn't follow the CDC guidelines, but we are also testing more as well. 

Confirmed cases are trending but so far I haven't seen any data that leads me to believe it isn't a result of increased testing.   For a long time you had to be pretty sick to get tested as evidenced by 28% of confirmed cases needing hospitalization per April 10th Dallas data.  From that same report through  5/12 , the hospitalization rate was 7% for that 1 month period bringing the aggregate blended rate down to 18%.   That's pretty damn compelling evidence we're just catching a lot more cases than we were previously.   

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57 minutes ago, atomheartbevo said:

Yep, here in Austin, plenty of business are still curbside, plenty of people are still wearing masks and still doing curbside/online, so hopefully we keep our little curve fairly flat.

I don't like that cases seem to be trending up in Texas, although it was to be expected, since we didn't follow the CDC guidelines, but we are also testing more as well. 

In TN post opening and FL now post opening, the people that aren’t being cautious before are the same ones not being cautious now. The grocery stores down here are one way with some being mask required and some preferred and it’s few and far between the people that are going backwards with no masks to prove a point.

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For your livestock update, packer runs for cattle and hogs were better, with bigger Saturday runs expected, more improvement should come next week. Pork values have plateaued but have seen good support with restocking and the catch up of skilled labor in fabricating. Beef values are about 10% below the peak, with a plateau likely coming soon in the 380 to 410 range. 

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1 hour ago, Hugo Stiglitz said:

Here’s the deal, outbreaks ARE GOING TO HAPPEN.  They are unavoidable. It requires a basic understanding of human behavior and science to come to this conclusion. The virus is not going to magically go away.

The hard questions we are dealing with now:

1. How do we best minimize the intensity of outbreaks without going into a full lockdown?  We wear masks, we physically distance, we wash hands, we keep the population informed with accurate information, we stay vigilant, we test and trace quickly to isolate outbreaks when they happen so grandma doesn’t die. 
 

2. Are we as a society prepared to work together to do this? 
 

3. Do we have all the resources available to quickly test and trace when outbreaks occur? 
 

4. If we choose not to take these precautionary measures, what will be the consequences?  
 

I fear we’re going to find out the answer to #4 the hard way. 

1. I think most informed observers agree.

2. I trust that we'll physically distance, but hand washing will be questionable (is hand sanitizer even widely available yet?), and people are going to congregate indoors where social distancing won't help... high quality accurate information that everyone will see is not happening unless google spear heads it. I don't think nearly enough people would install a contact tracing app, even if it was made by google and apple, so it will have to be done manually.  

3. Has there been any successful example of contact tracing and isolation in the US so far? Surely some small town has stopped the spread and we have proof that we can do it?

 

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30 minutes ago, Skipper said:

Confirmed cases are trending but so far I haven't seen any data that leads me to believe it isn't a result of increased testing.   For a long time you had to be pretty sick to get tested as evidenced by 28% of confirmed cases needing hospitalization per April 10th Dallas data.  From that same report through  5/12 , the hospitalization rate was 7% for that 1 month period bringing the aggregate blended rate down to 18%.   That's pretty damn compelling evidence we're just catching a lot more cases than we were previously.   

Really appreciate that you're paying attention and sharing your findings. Keep 'em coming. Can you do Austin too? ha

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38 minutes ago, MNLonghornFUKM said:

Immunity could be a huge factor this winter to reduce the thread immensely

Immunity to that particularly strain.  Couldn't we have a flue/cold situation where you have to get flu shots every year (and it's not a guarantee), and whether you get a cold or not is luck of the draw?

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  • hayden_horn changed the title to Formerly DT: COVID-19 - Featuring Lots of Politics, now CR because political talk not going away


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