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Message added by Hapless Bills Fan

[This is a general message.  If you see it, please don't take it personally]

 

Now that we’re READY FOR SOME FOOTBALL, We are trying to return to a FOCUS ON FOOTBALL at Two Bills Drive

 

Because people have indicated they find this thread a useful resource, we’ve decided to leave it here but lock it.

 

I will continue to curate.  If you find updated info you’d like to include, please PM me.   If it comes from a source rated “low” for factual and “extreme” for bias, it probably won’t make it out of my PM box unless I can find a more reliable source for it (I will search)

As I have time, I will probably tighten the focus on sourced, verifiable info and prune outdated stuff, to make it easier to find.

 

GO BILLS!

 

 

 

 

Recommended Posts

Posted
2 hours ago, BillsFan4 said:

 

So to the point, if presymptomatic people can infect other people, then asymptomatic infection is by definition, something that can be defined only in hindsight.

Thus saying "don't worry about asymptomatic people" is rather useless from a public health standpoint; you can only determine if someone if someone is a- or pre-symptomatic in hindsight.  Let's just call them "people without symptoms at the time" which is lengthy but unambiguous

 

I spent a bunch of time looking for the evidence supporting what Marisa Van Kerkhove said.  I could not find it.

I say modestly, that even bereft of the tools I used to have, I am pretty good at this.  I looked for stuff from this country, from Singapore, from S. Korea, and from China.

 

Here is the best source material I could find:

Summary: https://wwwnc.cdc.gov/eid/article/26/7/20-1595_article

Article summarizes epidemiological evidence, virological evidence, and modeling. 

Key points:

-There are a number of case studies which strongly imply that virus transmission from people without symptoms at the time is occurring.

-Titer measurements of people without symptoms at the time overlap titer measurements of people with symptoms (if you have as high viral titer in your upper respiratory system as someone with symptoms, what magic would render you unable to spread virus?)
-Modeling (which of course depends upon assumptions) of different situations: "Although models are highly dependent on the assumptions built into them, these models suggest that the speed and extent of SARS-CoV-2 transmission cannot be accounted for solely by transmission from symptomatic persons"

Conclusion:

"Each of the epidemiologic, virologic, and modeling studies described has limitations. However, in the aggregate, these diverse studies suggest that SARS-CoV-2 can be transmitted by persons with presymptomatic or asymptomatic infection, which may meaningfully contribute to the propagation of the COVID-19 pandemic."

 

 

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Posted

Vaccine update.  Long overdue.  This is a punt (or shall I call it a delegation?) to long-time Pharma blogger Derek Lowe.

He put out a very good summary of the "State of the Dev" on 26 May.

https://blogs.sciencemag.org/pipeline/archives/2020/05/26/coronavirus-vaccine-update-may-26

Really good blog by a pharma Discovery guy who knows his stuff.

 

TL;DR - CanSino’s Ad5-nCoV candidate published detailed phase I results that include T-cell response and neutralizing antibodies (the gold standard) for all. 

Publication in Lancet, a reputable peer-reviewed journal.  Bad news: the Achilles Heel of an adenovirus vector is that a lot of adults have anti-adenovirus antibodies which will damp the immune response to the vector.  Here's the Lancet article: https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31208-3/fulltext

 

Lay article in Forbes on Pfizer's vaccine development effort

https://www.forbes.com/sites/nathanvardi/2020/05/20/the-man-betting-1-billion-that-pfizer-can-deliver-a-vaccine-by-this-fall/#1772a718382e

I never worked under this guy, but he sounds like a breath of fresh air.

Posted

Hydroxychloroquine for prevention of Covid-19 disease: Gold standard, double-blind study for prevention of covid-19 in exposed HCW halted for futility

https://www.nejm.org/doi/pdf/10.1056/NEJMoa2016638?articleTools=true

 

HCW were 66.4% of the study, 76.7% exposed at work

Household exposure 29.8% of the study

 

Sidebar thing that interests me: 13% of the study participants developed new covid-19 infections with no statistical difference between each group.  87.6% of them reported high-risk exposures (without eyeshield, surgical mask, or respirator).  There isn't breakdown I could find of how the exposure risks correlated to those who developed infections, but it's an obvious point of interest. 

Commentary by Derek Lowe:

https://blogs.sciencemag.org/pipeline/archives/2020/06/04/hydroxychloroquine-for-avoiding-infection

He states that a smaller group of the study participants were taking zinc (both arms), and had no difference in outcomes (for the zinc-treatment fans among us).  But, I can't find that info in a quick read through of the paper.  If anyone else can, obliged.

Posted (edited)
3 hours ago, Hapless Bills Fan said:

Hydroxychloroquine for prevention of Covid-19 disease: Gold standard, double-blind study for prevention of covid-19 in exposed HCW halted for futility

https://www.nejm.org/doi/pdf/10.1056/NEJMoa2016638?articleTools=true

 

HCW were 66.4% of the study, 76.7% exposed at work

Household exposure 29.8% of the study

 

Sidebar thing that interests me: 13% of the study participants developed new covid-19 infections with no statistical difference between each group.  87.6% of them reported high-risk exposures (without eyeshield, surgical mask, or respirator).  There isn't breakdown I could find of how the exposure risks correlated to those who developed infections, but it's an obvious point of interest. 

Commentary by Derek Lowe:

https://blogs.sciencemag.org/pipeline/archives/2020/06/04/hydroxychloroquine-for-avoiding-infection

He states that a smaller group of the study participants were taking zinc (both arms), and had no difference in outcomes (for the zinc-treatment fans among us).  But, I can't find that info in a quick read through of the paper.  If anyone else can, obliged.

Here:


The relative risk with zinc use was 1.23 (95%CI, 0.82 to 1.83)
The relative risk with vitamin C use was 1.60 (95%CI, 1.12 to 2.28).


This observational comparisons may suffer from confounding by indication, in that those who deemed themselves at highest risk of developing infection may have been more likely to additionally take either zinc or vitamin C. Regardless, there was no suggestion that zinc added to hydroxychloroquine had additional benefit. Among those randomized to hydroxychloroquine, those taking zinc had a 15.0% incidence of new Covid-19 versus 10.8% incidence of new Covid-19 without self-reported zinc use.
Zinc has received a great deal of attention as a potential adjunctive therapy to be used with hydroxychloroquine. A 2014 in vitro study by Xue et al. used human ovarian carcinoma cell culture to examine the interaction of chloroquine and ionic zinc.4 Xue found that chloroquine acts as a zinc ionophore, increasing cellular uptake of zinc in culture media and increasing the cytotoxic effect of chloroquine to cause the death of cancer cells at levels 30-fold higher than what would be achieved in plasma with our trial’s dosing.4,5 Importantly, this lab experiment was not designed to emulate zinc levels in the average human body, but in a cell culture media which started with minimal zinc. North Americans have a very low prevalence of inadequate dietary zinc intake (<15% prevalence).6 Based on this sub-group analysis, we found no evidence of supplementary zinc intake had any effect on incidence of new Covid-19 compatible illness after high-risk exposure. The exact details of zinc formulation, dose, and duration were not queried, so this is not conclusive information.

image.jpeg

 

It is on page 14 here:

 

https://www.nejm.org/doi/suppl/10.1056/NEJMoa2016638/suppl_file/nejmoa2016638_appendix.pdf

Edited by BillsFan4
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Posted

Unintentional case study on the use of masks wraps up in Springfield MO.

 

Mask use by both client and stylist

>15 minutes of close contact with a known symptomatic infected person

42 tested people: 0 positives (Everyone was offered testing, many declined - unfortunate)

Everyone (146 people 140 clients 6 stylists): > 2 weeks quarantine with 2x/day health checks by DPH - 0 symptoms

 

No one wanted it to happen, and it wouldn't have been ethical to set up a study like this, but the results are very encouraging. 

 

https://www.springfieldmo.gov/CivicAlerts.aspx?AID=6941

The health department is currently gathering further information about the type of masks worn, how they were used, etc

 

 

  • Like (+1) 1
Posted

https://www.medrxiv.org/content/10.1101/2020.04.02.20051417v2.full.pdf

From Hapless’s boy, Trevor Bedford (and many other authors). This paper is from a while back.

 

Cryptic transmission of SARS-CoV-2 in Washington State

Quote

Genome sequencing of SARS-CoV-2 strains allows for the reconstruction of transmission history connecting these infections. Here, we analyze 346 SARS-CoV-2 genomes from samples collected between 20 February and 15 March 2020 from infected patients in Washington State, USA. We found that the large majority of SARS-CoV-2 infections sampled during this time frame appeared to have derived from a single introduction event into the state in late January or early February 2020 and subsequent local spread, indicating cryptic spread of COVID-19 before active community surveillance was implemented. We estimate a common ancestor of this outbreak clade as occurring between 18 January and 9 February 2020. From genomic data, we estimate an exponential doubling between 2.4 and 5.1 days. These results highlight the need for large-scale community surveillance for SARS-CoV-2 and the power of pathogen genomics to inform epidemiological understanding.

 

Quote

Here we report on the putative history of community transmission in Washington State as revealed by genomic epidemiology. We conclude that SARS-CoV-2 was circulating cryptically, ie undetected by the surveillance apparatus, in Washington State since January 2020...

 

Quote

We analyzed the sequences of 346 SARS-CoV-2 viruses from the Washington State outbreak collected between 20 February and 15 March 2020. The large majority (293, 85%) of these viruses fall into a closely related clade, and all share the mutations possessed by WA1 and the additional mutations C17747T and A17858G.

 

 

 

 

Quote

We sought to test these two hypotheses: (a) SARS-CoV-2 was introduced into Washington State on 15 January 2020 with the arrival of WA1; subsequent cryptic transmission led to a community outbreak first detected on 28 February 2020 and (b) SARS-CoV-2 was imported on 15 January 2020 but this infection did not transmit onwards; a second, initially undetected importation event of a genetically identical or highly similar virus occurred, followed by cryptic transmission that led to a community outbreak.

 

 

Quote

In addition to the 293 viruses sampled from Washington State falling into the WA1 outbreak clade, we observe that seven viruses sampled from the Grand Princess cruise ship in late February and early Mar 2020 all group into the same outbreak clade (Fig. 1A). The genetic relationship among these viruses is consistent with a single introduction onto the Grand Princess cruise ship of the basal outbreak variant, possessing C17747T and A17858G, and subsequent transmission and evolution on the ship.

 

 

 

 

Quote

In January and February, 2020, screening for SARS-CoV-2 in the United States was directed at travelers with fever, cough and shortness of breath, with the geographic areas increasing as new outbreaks were identified, but also specifying travel to China up until 24 February 2020 (18, 19) . Our analysis suggests that a single clade of SARS-CoV-2 had likely been circulating in the Seattle area for 4–6 weeks by the time the virus was first detected in a non-traveler on 28 Feb 2020. By then, variants within this clade constituted the majority of confirmed infections in the region (293 of 346;85%). 

 

Quote

Several factors could have contributed to the delayed detection of presumptive community spread, including limited testing among non-travelers or the presence of asymptomatic or mild illnesses. Genetic evidence suggests that this cluster may descend from an initial introduction in mid-January with the WA1 travel case, but other origin scenarios are also possible.

 

Quote

Our results highlight the critical need for widespread surveillance for community transmission of SARS-CoV-2 throughout the United States and the rest of the world even after the current pandemic is brought under control. The broad spectrum of disease severity (20) makes surveillance challenging (21). The combination of traditional public health surveillance and genomic epidemiology can provide actionable insights....

....We see the combination of community surveillance, genomic analysis and public real-time sharing of results as empowering new systems for infectious disease surveillance.

 

 

Posted

 

 

One of the first things I've seen with promise for late-stage Covid patients. Pretty good-sized study here too, and a widely available drug (at least it was before this study!).

 

My medical friends who treat this, as well as the stuff I've read, have termed the ventilator as the Hail Mary moment for Covid. Not many good outcomes if you have to go on one. 

 

 

On 6/16/2020 at 9:43 AM, Buddo said:

 

It's also saying that it reduced death in instances where people needed oxygen only, i.e. 'unventilated' by a fifth. It appears it doen't make any difference to people who don't need any oxygen treatment of any sort.

 

If it had been used from the start of the pandemic in the UK, it's estimated that 5,000 lives might have been saved. No idea what that might have meant for other countries, but at least it holds out some more hope for people affected in the future, throughout the world.

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Posted
12 hours ago, Nelius said:

This thread is crazy. It's a "novel" coronavirus for a reason, as you can tell by the breadth of responses here. There's still a tremendous amount of questions which is why there will be no normal any time soon. At best I'm hoping for some kind of truncated season in a bubble, and I'm convinced that there's no way any of us will be attending a major sporting event live for at least the rest of 2020.

 

 

Genuinely curious if there's any truth to the immunity part? I've heard otherwise but have been taking a bit of a media break lately so may have missed an update. Awesome if true, but if not, then this is exactly the kind of serious confusion that I'm talking about.

 

This was asked in TSW by @Nelius, and because I am trying to keep a bunch of threads from becoming "covid-19 discussion threads", I'll answer here.  It would be nice if a true immunologist would "out" themselves and step up.  I'm not an immunologist, I've just worked on vaccines and gone to the project meetings.

 

Briefly put, when people are infected their early immune response is non-specific.  It includes various white blood cells and soluble factors (cytokines and complement factors).  After 1-3 weeks, they develop adaptive immunity, which ideally confers long term immunity.  Adaptive immunity includes B-cells, T-cells, and antibodies (first IgM, then IgGs).

Wiki about it

 

What we know about people who have recovered from covid-19: those who have been tested (serology or blood testing) [Edit: at least 3 weeks post symptoms] have antibodies against the virus.  Most antibody tests are just +/-. The testing that has measured the quantity of antibodies in people who have been infected, indicate that the level of antibodies people have vary widely.  That's not uncommon.  The quantity of antibodies a person has in their blood after they recover from a disease doesn't really indicate how effective their immunity is; what's more relevant is how rapidly the person's immune system can "dial it up" in response to a new challenge with that organism (not ethical to assess in humans) and whether a long-term B cell and T cell response has been induced (see below).

 

What we don't know about people who have recovered from covid-19 and have antibodies: 1) whether they all have neutralizing antibodies (antibodies that can prevent the virus from entering and infecting cells) 2) whether they have a T cell and B cell response (important to efficient lasting immunity).  The reason we don't know this is testing for T cells and for neutralizing antibodies, antibodies able to keep the virus from infecting cells) is more complicated and needs to be performed with live virus in a high-level biocontainment facility, so it's not widely done.  3) how long their immune response will persist and be effective.    Adaptive immunity to some diseases is lifelong - measles is an example.  What was found with SARS and MERS is that the antibodies persisted 6 months - 2 years.  That's the current guess with covid-19: that people previously infected will be immune, but that the immunity will only ~2 years.  In part this is because of....

 

....viral mutation rate.  The "money" part of measles virus, the part the virus needs to infect cells, effectively doesn't mutate.  A vaccine developed decades ago is still good. Influenza virus, on the other hand, has the ability to infect with dozens of strains that look "different enough" to the immune system that every few years our immune system is effectively a "blank slate".  Virologists are studying the mutation rate of covid-19 intensely and so far it looks to mutate way more than measles, but for the "money" part, the part needed to infect cells, more slowly than influenza.

 

What we can do is infect or vaccinate non-human primates, like rhesus monkeys, then expose them again and see if they get sick.  The studies that have been done so far say they are protected and don't get sick.  Because the virus hasn't been around that long, we can't say yet how long the protection will last.

 

So, bottom line: we think having anti-covid-19 antibodies means you're immune to covid-19, but we don't KNOW that for a fact, nor do we know how long it will last.

 

A note about vaccines: vaccines never "essentially give someone the virus".  There's a hundred-year-old process that did that for smallpox, called "variolation".  The first vaccines, for smallpox, used a related virus and gave people the related virus, cowpox.  We don't do that any more.    What modern vaccines do is:

1) inject a different, related virus that will produce an immune response to the target disease.  Smallpox vaccine was an example - it used cowpox.  BCG for tuberculosis is another example.

2) Use an inactivated virus combined with chemicals (adjuvants) that arouse a better immune response.  The virus is dead, it can not make you sick.  This has probably been the most common strategy, and once proper manufacturing controls and release tests were instituted to ensure that the virus is really, truly dead, it's safe.

3) Inject a live, but attenuated virus that is selected, treated, or mutated to make it too wimpy to cause the disease.  Oral polio vaccine is an example.  It's an effective vaccine but it can (very rarely) back mutate in the intestinal tract and cause polio in a non-immune person.  It's no longer given in the US for that reason.

4) Conjugate vaccines - we take part of the viral coat protein and combine it with a carrier protein that arouses the immune system, manufacture and purify it, then combine it with adjuvants.  Pneumoccal pneumonia,  meningitis, and modern whooping cough vaccines are examples of this.  These are very safe vaccines, but don't necessarily produce as lasting an immune response.

5) Viral coat protein without the viral genetic material.  HPV vaccine is an example of this.  Because the virus genetic material isn't there, it can not replicate and make you sick.  (This works best for viruses with a self-assembling protein shell rather than a bunch of proteins embedded in lipid.)

6) DNA and RNA vaccines - we combine genetic material that our bodies can translate to make part of the viral coat protein.  It will either be packaged inside the coat protein of another virus (adenovirus is common) or with some other carrier material.  It's an exciting approach because it can be fast - all you need is the genetic sequence of the virus coat protein to throw it into your platform system and start manufacture.  But experience is limited.  So far only one vaccine has been approved using this approach (equine encephalitis).

 

Approaches being attempted for covid-19 include 4 and 6; someone may be trying for 3).  Most of the focus is on 6 - the Moderna, Can-sino and Pfizer vaccines for example, are all variations of this using different carriers and perhaps different pieces of the spike protein.

 

Hope this helps.

  • Thank you (+1) 3
Posted

Are we past the peak?

 

This is a set of tools from JHU web site showing  a 3 day average of new confirmed cases

https://coronavirus.jhu.edu/data/new-cases-50-states

Pick your state

 

My interpretation is that except in a few states, we are not "past peak". 

NYC had so many cases that it dominated the data for the country as a whole for a long time, but if we compare the NYS graph to the US graph here on the same site:

https://coronavirus.jhu.edu/data/new-cases

That's no longer true.

 

Note that these are total daily cases, not per capita daily cases.  Would love a source for the latter

Another source, again total daily cases per state.  I can't find an explanation for how they color-code, but this site allows one to access county by county data

https://www.endcoronavirus.org/states?fbclid=IwAR04j_L3gO5IZcm2Ev35j02QKBOKrJZNUG6hv-h_GZ3YaEfRsUSM9RPV4Xw

 

 

Posted

so much for antibodies presenting a second infection of covis-19....I dont know how,  if this is widespread or just an anomaly but the implications are  Resurgence is a possibility months later even with antibodies. Just a part of the article quoted.

https://www.msn.com/en-us/health/hea...enf?li=BBnb7Kz

 

Quote

 

Dallas Woman Tests Positive for Coronavirus Again After 4 Months: 'I Was Floored'

 

 

Dallas Woman Tests Positive for Coronavirus Again After 4 Months: 'I Was Floored'

 





A woman in Dallas is fighting her second battle against Covid-19.  Doctors are unsure why the virus sometimes reappears — or if it is contagious the second time aroundMeredith McKee first tested positive for the potentially deadly virus in February, diagnosed after feeling "clear and obvious" symptoms, she told NBC 5.

"I had a dry cough like you would not believe. It would not stop,” McKee recalled, explaining that she managed to fight off the first bout of the virus from home.
She even donated some of her plasma after testing positive for antibodies.
"I felt great finally [doing] something good coming out of the hell that I’ve been through because I'm going to help up to eight people with this plasma,” she said.
However, last week, McKee shared a tearful photo of herself from a hospital bed at Texas Health Presbyterian in Dallas. After admitting herself with high blood pressure and a headache on Friday, she found out she was one again positive for COVID-19 four months after her initial diagnosis.
"I was floored when it was positive," McKee said.

 

 

 

Some other cases:

https://www.newsweek.com/italian-woman-tests-positive-covid-19-after-60-days-quarantine-swabbing-1500202

https://www.washingtonpost.com/health/2020/06/11/coronavirus-chronic/?arc404=true

 

Just now, Hapless Bills Fan said:

 

So the big unanswered question here is: are these people being reinfected?

Or is the virus simply persisting in a reservoir somewhere in their body and resurging in response to something? (known to happen with other viruses)

 

Or, has their immune system been thrown out of whack, and now they're dealing with the aftereffects of an over-reactive immune system?

 

We don't have answers at this point.

 

It's a valid point that these folks have antibodies and the antibodies clearly aren't kicking virus butt.  The immune response is more than just antibodies, obviously (see post above) so another question is, is there a problem with their T cell or B cell or innate immune response?

 

It's clear this is something real that is affecting some people.  So far it seems a relatively small number.

 

It may fall into the category of "when you have somewhere between 8 million and 160 million people worldwide infected with a novel virus, you're gonna see some weird ***** go down" (to use a technical term)

Posted

PSA:  Help!  My mask is making my glasses fog up!

 

#1 solution: mask with a flexible wire along the top that will allow it to be fit against your nose/cheeks.  Can add a pipe cleaner, coffee bag wire, or pipe cleaner - stitch at each end and in middle on outside of mask  (or hot glue - won't hold as well).

#2 solution: double-sided Fashion tape.  Designed to hold against sweat and body oils

#3 solution: treat glasses with baby shampoo or soap solution and allow to dry

 

https://www.nytimes.com/article/glasses-fog-wearing-mask-coronavirus.html

Posted

Is it more testing?  Probably not.

Covid-19 in US vs EU, 7 day rolling average of new cases March-June

image.thumb.png.69fbffef05841e4c0826bdaf76f6a311.png

 

The population of the EU is estimated at 445 million people as of Feb 2020

The member EU states have performed approximately 53,000 covid-19 tests per 1M population (obtained by summing individual EU member data on Worldometer)

 

The population of the USA is estimated at 330 million people as of Dec 2019

The US has performed approximately 83,000 covid-19 tests per 1M population

 

However, testing differences are probably not the explanation here.  The US has a positive test rate of ~8.4% (~7,000 cases/1M population, ~83,000 tests/1M population).  The EU has an estimated positive test rate of ~5% (again, summing individual EU member data (2,770 cases/1M population, 53,000 tests/1M population).  Both regions preferentially tested sick people during the height of the initial epidemic and are now testing more broadly.

 

For a graphical representation, in case the math behind that seems obscure let's look at 6 individual EU countries - the most populous and 2 with the highest rates of per capita testing.  Says to me their cases are declining (including in 4 countries with similar or higher per capita testing than USA)

 

4 most populous countries in EU:

Germany 60,000 tests/1M

image.thumb.png.21d6d74b9e92c825ad78a7098ed482ab.png

France 21,000 tests/1M

image.thumb.png.4fd0e795363f81460471776fb5b2dd21.png

Italy 81,700 tests/1M

image.thumb.png.bcfbbe0aa7b2d5c4c98a7686bae19205.png

Spain 103,000 tests/ 1M

image.thumb.png.bc6e6ce7ae21cb8ddf01814b6f2b9c70.png

 

two bonus countries with high test rates

Belgium 94,800 cases/1M

image.thumb.png.8377fc97d51b503e29b0dcda65132b5c.png

 

Portugal 102,700 cases/1M

image.thumb.png.6a5d33856cc70094a8572c803607eb6b.png

 

My conclusion: EU (which is also re-opening) has done a far better job of kicking covid-19 butt than US, which appears stuck on "covid plateau" and may be increasing.

 

  • Like (+1) 1
Posted

Hi @Hapless Bills Fan. I have a question if that's ok. Has there been a lower rate of cases vs deaths? I feel like I keep reading that test cases coming in positive recently have had a large percentage of asymptomatic subjects. Thanks!

 

EDIT: Great question, ndirish1978 and I'm not sure of the answer.  

In the US and globally, we're running about 5.1% CFR (case fatality rate), with of course a bunch of patients still hospitalized and outcomes uncertain.

At one point I think we were running 8% CFR in the US, which was 10-13% in NYC and 3% everywhere else.

https://coronavirus.jhu.edu/map.html

 

It really can't be otherwise - early in the epidemic, you had to have flown back from Wuhan where you swore you licked a pneumonia patient to get a test.  In NYC people who had clearly covid-19 relevant symptoms but weren't critically ill were given a sheet of instructions, no test, and sent home.  Only very sick people got admitted to hospital and only hospital admits got tests.

We have more hospital capacity now, so we can start hospitalizing and treating people before they're desperately ill, and we have more testing capacity so we can test people who have just been exposed.

 

I don't think that's all of it though  - I think we have better treatment protocols, and a better handle on which existing medications are truly helpful, so people who are seriously ill have better outcomes as long as we maintain hospital capacity

Opinion: I think the infected, asymptomatic younger people were always there, we just didn't have the testing capacity to know they were there before.

 

Posted

Taken from the dataisbeautiful sub on reddit.I believe it shows 2 regions decreasing in cases and 2 regions increasing (using key on the left).  Accurate as of June 22nd.  Reading graphs isn't a strong point of mine.

nvkxjqhzgo651.png

 

[Edit: read it perfectly as far as I can tell.  Point is showing that the overall US cases shape can obscure the actual pattern in different regions of the country, some falling, some rising - quickly.  -Hap]

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Posted
On 6/23/2020 at 4:17 PM, The Dean said:

 

 

Why? The LA Times is a respectable newspaper that follows the basic tenants of journalism. You will note, unlike purposefully biased news outlets, they report events irrespective of the political implications, as does the NY Times and the Washington Post. All of these papers have reported (and even broken) stories damaging to both liberal/Democrat and conservative/Republican politicians. Look to see if your "alternative to mainstream" news sources have that same integrity. If they are committed to reporting only stories that support their bias, then you know you have a source that isn't to be trusted.

They may report them equally but the bias is still there...here is an interesting site that reveals political leaning of news sources, it also has a link to Allsides which rates the bias of about 600 media outlets. 

https://guides.lib.umich.edu/c.php?g=637508&p=4462444

Edit: leaving this here because of very useful link to media bias ratings from NG, but in general, if we want to discuss media bias, elsewhere please.

I started this thread upon request of several folks to have a covid-19 thread that was just links and info.  Discussion -> discussion thread please!]

 

And also links from The Dean:

On 6/24/2020 at 10:39 AM, The Dean said:

In general the straight forward bias rating sites have the major networks, NY Times, Wash Post as "slightly left". Those that also rank reliability place them in the "high reliability" sector as well. Some outlets like Brietbart (for example) are found to lean heavily to one side and have low reliability. In general, the further to the left or right one outlet strays, the less reliable they are.

 

Here's a site that ranks both bias and reliability

https://www.adfontesmedia.com/interactive-media-bias-chart/

 

Of course, the devil is in the details (methodology, bias of the data interpreters, etc). The good thing is, for the most part these relatively unbiased rankings are in general agreement on the lean of the bias. Shooting for sources with high reliability and a minimum of bias is probably your best bet if you are looking to be well informed.

 

Now I don't want to get too technical here, but the study of news bias was my main concentration of study for my Masters degree and all my PhD work. That was years ago, of course, and some things have changed. But I'm pretty sure the major bias in most new gathering/reporting organizations that still cling to traditional journalistic values, is that of getting the work done quickly, while still getting the story accurate.

 

 

 

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