Sorry, I meant nursing homes. They were staffed by overworked underpaid people who continued working despite having sings of infections, providing infection vectors to vulnerable older population.
Second group who got hit hard were Somali minority. Many are unemployed and cannot read. Also, they tend to live in large families.
When our infection rates were at its peak, average age of those whop died was 82 years old. Hardly a reason to close schools then..

Good stuff!

Thing is, "Science" is the battle cry of every bit of false information surrounding this once pandemic response.

Amen. And unfortunately, there's a very large percentage of the population that believes that if the NYT, Atlantic, or CNN writes an article referencing "science" it's as good as settled truth.

Nothing could be further from reality.

There's a ton of shameful, partisan "science" out there right now. Even in the peer reviewed journals.

Yet the same fools that read a summary "science" article [typically written by some liberal arts major with zero science credentials] are the first ones to accuse others as science deniers.

And by the way, the fluffy article written by the National Review guy several threads back could serve as an Exhibit A of how this is a very much a journalistic issue that affects all. And then the internet, just like viral PCR tests, magnify these junk fragments to massively outsized proportions, thus further confusing the masses and distorting reality.

Up is down. Black is white. Slavery is freedom. War is peace.

SMH....

And by the way, I'm not suggesting that science is easy, obvious and/or clear cut. Indeed, it's usually just the opposite. And it's rarely settled. Beware anyone that claims otherwise.

This is a terrific example. One that illustrates another issue -- the education / training that needs to go into making the correct decision (especially when time to make decisions is limited).

I'd admittedly be the first guy to want to flee the burning building -- lizards don't like fire. But I suppose, with repetitive training and education (and data), I could overcome that instinct.

In the case of COVID, which was not nearly as time-sensitive from a decision standpoint, the Swedish government's (and population's) reliance on the preestablished science-based protocols (including as lack of widespread masks) is incredibly laudable. Could the protocol be improved? Sure, I think we'd all agree that the nursing homes worldwide should have better protections.

Meanwhile, the rest of the world (ex-certain Asian nations) freaked the F out. And the world largely continues to do so despite a lot of good data suggesting that this virus isn't The One.

And our non-science friends in the media and their acolytes have no interest in ending the fear mongering.

IMHO, in order for this to work we must have following igredients:

- Well researched plan that is made by cool heads during "peacetime" that has best chance of working.
- Mutual trust between government and citizens: citizens believe that plan is for their best and government believe that citizens will do their part without resorting to force.
- Government that is willing to waste an opportunity to look "decisive" and let boring scientists do their job instead.

We had that. It was thrown out for expansive emergency powers that violated citizens rights while actively making the problem worse.

“Follow the science” is the new “the check is in the mail” or “trust me.”

People dearly love to appear more intelligent than they really are. This invective speaks to them - "I'm following the science". With an air of superiority. Yet, when we ask them to explain, in detail, the science which they are following, we get all kinds or accusations from them about how we are "science deniers", or that we subscribe to wild Q-Anon conspiracy theories, or whatever - everything but an informed explanation of the "science" they are following.

Data!

I mean, did these IHME idiots at the University of Washington ever explain themselves ?

https://pbs.twimg.com/media/EYkqNH9U...g&name=900x900

Hey, but at least many lives were ruined by bad projections! We still have onerous restrictions here. 75% of the local hotels, restaurants, entertainment businesses have gone out of business after 6 months of business-killing restrictions. Kids aren't in school still. Pretty much all sports below college-level are cancelled or restricted to the point of "why bother?"

https://apnews.com/a01ddfa2e8ef839b2ee05e2cbcd63169

Somebody's got to keep the people scared, right?

That article is pathetic.

+1

Flattening the curve is great and all, but a flattened epi curve is also an elongated curve in most cases. On an extremely steep curve (no mitigating measures), more die at the beginning of the outbreak, but it's over quicker. On an extremely flattened curve (extreme mitigating measures) fewer die up front, but it persists much, much longer. There is a theoretical sweet spot between the two, but that is usually only realized in hindsight, based on several factors and timelines for effective therapeutics, vaccines, hospital capacities, population make-up/demo, etc.

Also, some people seem to think "herd immunity" is like a light switch that is turned on once an exact percentage of immune folks is reached (and/or that it is synonymous with total viral irradiation).
The fact is that the real-time R0 will continue to come down as more and more people gain immunity....and currently, we are already under the epidemic threshold.

Further, the current immunity numbers are FAR higher than being reported. Not only is the prevalence of serology tests still lacking, but they are also prone to false negatives.
On top of that, many who were infected but were asymptomatic may not show antibodies at all, but will still maintain T-cell mediated immunity.

:(

Some are only happy when others are more miserable.

They generally have the fourth letter of the alphabet after their names.

Mild cases of coronavirus disease 2019 (COVID-19) can trigger robust memory T cell responses, even in the absence of detectable virus-specific antibody responses, researchers report August 14 in the journal Cell. The authors say that memory T cell responses generated by natural exposure to or infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)--the virus that causes COVID-19--may be a significant immune component to prevent recurrent episodes of severe disease.

"We are currently facing the biggest global health emergency in decades," says senior author Marcus Buggert (@marcus_buggert) of the Karolinska Institutet. "In the absence of a protective vaccine, it is critical to determine if exposed or infected people, especially those with asymptomatic or very mild forms of the disease who likely act inadvertently as the major transmitters, develop robust adaptive immune responses against SARS-CoV-2."

To date, there is limited evidence of reinfection in humans with previously documented COVID-19. Most studies of immune protection against SARS-CoV-2 in humans have focused on the induction of neutralizing antibodies. But antibody responses tend to wane and are not detectable in all patients, especially those with less severe forms of COVID-19. Research in mice has shown that vaccine-induced memory T cell responses, which can persist for many years, protect against the related virus SARS-CoV-1, even in the absence of detectable antibodies. Until now, it was not clear how SARS-CoV-2-specific T cell responses relate to antibody responses or to the clinical course of COVID-19 in humans.

To address this gap in knowledge, Buggert and his collaborators assessed SARS-CoV-2-specific T cell and antibody responses in more than 200 individuals from Sweden across the full spectrum of exposure, infection, and disease. During the acute phase of infection, the T cell responses were associated with various clinical markers of disease severity. After recovery from COVID-19, SARS-CoV-2-specific memory T cell responses were detectable. The strongest T cell responses were present in individuals who recovered from severe COVID-19. Meanwhile, progressively lower T cell responses were observed in individuals who recovered from very mild COVID-19, and family members exposed to the virus.

In line with expectations, all 23 individuals who recovered from severe COVID-19 developed both SARS-CoV-2-specific antibody and T cell responses. But surprisingly, SARS-CoV-2-specific memory T cell responses were detected months after infection in exposed family members and in most individuals with a history of very mild COVID-19, sometimes in the absence of SARS-CoV-2-specific antibodies. Among the 28 exposed family members, only 17 (a few more than half) had detectable antibody responses, whereas nearly all (26/28) showed T cell responses. Among the 31 individuals who recovered from mild COVID-19, almost all had detectable antibody responses (27/31) and developed T cell responses (30/31).

"Our findings suggest that the reliance on antibody responses may underestimate the extent of population-level immunity against SARS-CoV-2," Buggert says. "The obvious next step is to determine whether robust memory T cell responses in the absence of detectable antibodies can protect against COVID-19 in the long-term."

https://news.ki.se/immunity-to-covid-19-is-probably-higher-than-tests-have-shown
https://twitter.com/RandPaul/status/1311331026640285706

Japan

mportance: Fatality rates related to COVID-19 in Japan have been low compared to Western Countries and have decreased despite the absence of lockdown. Serological tests monitored across the course of the second wave can provide insights into the population-level prevalence and dynamic patterns of COVID-19 infection. Objective: To assess changes in COVID-19 seroprevalence among asymptomatic employees working in Tokyo during the second wave. Design: We conducted an observational cohort study. Healthy volunteers working for a Japanese company in Tokyo were enrolled from disparate locations to determine seropositivity against COVID19 from May 26 to August 25, 2020. COVID-19 IgM and IgG antibodies were determined by a rapid COVID19 IgM/IgG test kit using fingertip blood. Across the company, tests were performed and acquired weekly. For each participant, serology tests were offered twice, separated by approximately a month, to provide self-reference of test results and to assess for seroconversion and seroreversion. Setting: Workplace setting within a large company. Participants: Healthy volunteers from 1877 employees of a large Japanese company were recruited to the study from 11 disparate locations across Tokyo. Participants having fever, cough, or shortness of breath at the time of testing were excluded. Main Outcome(s) and Measure(s): Seropositivity rate (SPR) was calculated by pooled data from each two-weeks window across the cohort. Either IgM or IgG positivity was defined as seropositive. Changes in immunological status against SARS-CoV-2 were determined by comparing results between two tests obtained from the same individual. Results: Six hundred fifteen healthy volunteers (mean + SD 40.8 + 10.0; range 19-69; 45.7 % female) received at least one test. Seroprevalence increased from 5.8 % to 46.8 % over the course of the summer. The most dramatic increase in SPR occurred in late June and early July, paralleling the rise in daily confirmed cases within Tokyo, which peaked on August 4. Out of the 350 individuals (mean + SD 42.5 + 10.0; range 19-69; 46.0 % female) who completed both offered tests, 21.4 % of those individuals who tested seronegative became seropositive and seroreversion was found in 12.2 % of initially seropositive participants. 81.1% of IgM positive cases at first testing became IgM negative in approximately one month. Conclusions and Relevance: COVID-19 infection may have spread widely across the general population of Tokyo despite the very low fatality rate. Given the temporal correlation between the rise in seropositivity and the decrease in reported COVID-19 cases that occurred without a shut-down, herd immunity may be implicated. Sequential testing for serological response against COVID-19 is useful for understanding the dynamics of COVID-19 infection at the population-level.
https://www.medrxiv.org/content/10.1101/2020.09.21.20198796v1