You’re implying that regardless if you lock down or not, the result is the same. That is definitely not true, so I disagree.
COVID-19 Pandemic: Transmissions, Deaths, Treatments, Vaccines, Interventions and More...
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You’re implying that regardless if you lock down or not, the result is the same. That is definitely not true, so I disagree.
That is not even close to what I was implying. Nice try though.
Although your suggestion does have some merit as long as you do not overrun hospitals and vulnerable are protected. Always remember the concept was called "flatten the curve" not change the area under the curve. Nonetheless that is a topic for a different day.
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Hey big people or families/friends of the large.. WebMD has a decent article on CoVid risks to the obese.. BMI over 30 (that's 40% of Americans)
This morning I worked at RWJ in Brunswick. I was talking with one of the maintenance workers and he was telling me the hospital is just about running normal. He said there are about 7 Covid patients in there now. Hopefully down to zero soon.
Anyone notice how Sweden has been doing?
This is a bit like looking at the 1962 standings and saying, “hey, the Mets finished the season too!”
Look at Sweden’s peers — not just the stuff others here have pointed out about deaths per capita — but also look at the climb of the Y axis relative to the progression along the x axis.
You’ll see that Sweden had the least desirable outcome. The only reason we should envy them is that they appear to be realizing something that resembles a finish line, while we apparently signed up for an extended season.
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well.. it could be some lone ranger doing it thinking people only look at the bottom line number.. arrogance.. or, more likely imho, a dumb and/or lazy person entring the numbers thinking they only care about the number infected... or a bunch of those people spread out collecting the numbers or reporting the numbers or collecting the numbers
FL for sure looks like they are willing to test it out.
I'm still skeptical but it would certainly be great news if true.
remember how people here and all over social media melted down when the women who worked for the Florida reporting system was canned. Now they just shrug their shoulders here and say its just a mistake
Maybe but my guess is it's just a reporting issue. Check John Hopkins and in certain states you'll see days around 100%, then the next day the number of tests go through the roof. Much like a state like AZ will have days with zero deaths, then the next day 100 deaths. Then 40 deaths the next day.
There are other odd data reporting quirks that you see out there. So this being another makes more sense to me then some sort of conspiracy theory that is founded upon a potential arrogant lone ranger posting #'s that would raise red flags on first look.
Uh, she was fired and now we see this. So maybe firing her was not a great idea?
Just wanted to point out the obvious flaw in your argument.
If you flatten the curve enough, it could get you to a time where you can change the area under the curve.
Flattening the case curve has already gotten us to a point where we are able, thanks to therapies, to lessen the area under the death curve.
Article partly about Sweden and how the people went into more stringent behavior and social distancing than the government required.
https://www.statnews.com/2020/07/15/covid19-accidental-sweden-fall-could-be-catastrophic/
https://www.statnews.com/2020/07/15/covid19-accidental-sweden-fall-could-be-catastrophic/
Masks help to mitigate the risk. Is that still a question? The experts say that it is the combination of reopening, lack of enforcement, spread in multi family dwellings and increased testing.
i wouldnt know..who are the experts, because no one is talking about California, they are talking about 3 other states
World meter second time USA over 70,000 new cases instead of in the 60’s. Death close to 1,000 a day two days in a row. It’s all growing.
Good article and why rates are dropping there (not because it’s magically going away due to a low herd immunity threshold)
California reclosing businesses was not a big story?
Let’s talk about it then. Normalized by population California isn’t even in the top ten for number of cases 7 day average. Therefore that tells me that their mitigation strategies are working better then other states. Those states are in order; Florida, Arizona, Louisiana, South Carolina, Alabama, Georgia, Texas, Tennessee, Nevada, Mississippi and Arkansas. California’s hospitalization rate is also not nearly as much as some of these other states.
I googled California - covid and found numerous articles.
Because, right or wrong, they are more aggressive in limiting the spread of Covid.
Who do you believe? An article written by
Paul W Franks
Professor of Genetic Epidemiology, Lund University
Joacim Rocklöv
Professor of Epidemiology, Umeå University
https://theconversation.com/coronav...t-after-20-of-a-population-is-infected-141584
or
Sharon Begley
Sharon covers science and discovery.
Andrew Joseph
General Assignment Reporter
https://www.statnews.com/2020/07/15/covid19-accidental-sweden-fall-could-be-catastrophic/
Up there with Florida and Texas with most death and new cases. That’s why they are closing gyms, barbers, bars and indoor dining. Schools not opening in Sept because they don’t have it under control.
California’s problem is that they’ve struggled to put out the fire from the start. Stage 1 of California’s reopening is shelter in place (in other words stage 1 is not reopening); I think the state made it to stage 2 (slight loosening) and I think some select counties were allowed to go to stage 3 (gradual reopening of some high risk activities) — now being rolled back. Essentially they’ve had an ongoing problem that got worse as their biggest population cluster is now getting the worst of it.
Florida on the other hand had cut daily cases from 1,400+ in the early spring to 300+. Texas from 2,000 to 500. Then both appeared to succumb to political pressure and reopen without taking time to examine the effects Texas went from carry out to “75% restaurant capacity and tables permitted for parties of up to 10 people” in weeks. We make a big deal out of Disney — theme parks opened in Texas a while ago.
Arizona gets publicity because they were a canary in the coalmine for this second wave. Numbers seemed to start climbing there before the trend began appearing basically everywhere that wasn’t hit really hard in March / April.
tl;dr - one guy couldn’t put out his house fire; his neighbors quelled their fires, then cracked beers and let them light up again. Who is an observer going to be drawn to?
If we had the CE board to refer to, there were posts in late spring about packed California beaches, and frustrated public officials.
Im certain they weren’t all masked on the beaches — and I’m sure they all didn’t go straight home and social distance after spending an afternoon at the beach...probably not wearing masks at those house parties or backyard bbq. We don’t catch it from friends and family, right? Even when it’s lots of friends...
Masks also help limit viral load transfer. Im not sure if it’s been proven yet or just strongly hypothesized, but viral load exposure appears to be closely associated with severity of illness with this disease. What % of people were wearing masks in March / April vs May / June?
If anecdotes that the hospitalized are not as sick this time around are true, then perhaps masks are partly attributable to the improved outcomes due to less load transferred even when infection permeates the mask.
Just making casual links here — I don’t feel guilty since the counter-argument goes something like: “California has lots of cases; California has lot of libs, libs wear masks. So masks don’t work”
There are far too many examples that bust the 20% theory.
Not really, there are a few. Read the article it discusses that fact quite openly. Pointing to one aged community or prison environments that do not reflect general society is not very scientific.
https://www.bbc.com/news/health-53248660
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Yes, they wrote a highly flawed sentence, saying 20% were infected in Stockholm when only 10% were, revealing a lack of thoroughness in their research, as the data were readily available, so that makes me doubt their other speculations, plus, as I said earlier, distancing is plausible of an explanation, although I would agree there might be something else going on that isn't being figured out. And the "20%" thing isn't even a thing really, if one looks closely at city data, where sections of cities, like NYC, Bergamo, London, etc. have areas with 10-15% with antibodies and areas with over 50%. If there's some magical 20% cap, then >50% shouldn't be possible.
I believe they said 20% because the private lab test of 50,000 showed 14% in late May and they were projecting (as Swedish Epidemiologist Tegnell also did) that the level today is probably close to 20%.
Things that cannot be currently explained make it magical? You do understand why Friston purposely used the "dark matter" analogy right? A small sub-group that does not represent the whole population has 50% and that eliminates the possibility? You could not come up with a list of possible explanations in 30 seconds? BTW, Bergamo has 1 in 4 as over 65 YO as they have a very aged population. Not very representative of the overall population. I would start there. I would also suggest we do not have nearly enough information to explain what we are seeing. But I do believe we will at some point. And when we do, it will make sense and it will explain what we see.
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I'll add a bit to Barnaby's points. California, like almost every other state not part of the DC-Boston corridor, had far less cases/deaths from the March/April outbreak, since they simply had far less cases seeded from travelers from Europe in Feb/March, plus, they have less population density and commuting density, so less "seeds" meant much less "spread." Essentially, the DC-Boston corridor got very unlucky in having far more cases early and then that was multiplied many-fold by the time mid-March rolled around, when we finally had some testing to reveal just how bad the outbreak was in the megaolopolis.
But most states did some sort of shutdown in mid/late March regardless of how big their outbreaks were and it turns out that the outbreaks in CA, FL, TX, GA, AZ, and almost everywhere else, were far smaller than ours was in this region. Those states were "lucky" in that respect. The problem though is those states having far less people infected (maybe 2-5% vs. 10-20% for the megalopolis as per antibody tests) had far more left to infect. So it was not a surprise that they're mostly seeing significant outbreaks when reopening wasn't done as per CDC guidelines, especially in places like FL/TX/AZ.
CA is certainly seeing an outbreak, but only at about 1/3-1/2 the level of new cases per capita (see my post last night on that) as those three states, even though they ostensibly followed the CDC guidelines. As Barnaby said, despite the guidance, they had a lot of non-compliance, especially at the beaches - these states aren't monolithic "red" or "blue" states (just like NJ isn't), so we're going to see gradations of outcomes in all of these states: one shouldn't expect a "blue" state to have 100% mask compliance and no cases, just like we shouldn't expect a "red" state to have 0% mask compliance and cases through the roof.
I understand why they said 20%, but it was a poor scientific choice to select the non-random private antibody test data when there was better data showing 10% in Stockholm and 6% in Sweden. Also, there are at least 7-8 neighborhoods in NYC, alone, with over 35% positive via antibody testing and two with over 50%. Do you think they're all not representative either? And as I posted last weekend, the two over 50% both have IFRs around 0.7%, which is fairly compelling data suggesting that over 50% can become infected (no 20% cap) and that the overall population IFR will be 0.5-1.0%, as most experts have opined, including, now, the CDC, who just raised their estimate from 0.25% to 0.65% for the overall (including asymptomatics) IFR.
We discussed the "dark matter" possibility awhile back and while I said that I understood where it came from mathematically and that cross-reactivity could be a scientific explanation for dark matter, I also said that it all starts to become irrelevant once we start to see decent population subsets reaching 40, 50, 60+% infection rates with IFRs in the 0.5-1.0% range. Even if one took NYC's 1.1% IFR at 21.6% infected and assumed that there wouldn't be any more deaths due to lack of susceptability in the remaining population and still used the 65% herd immunity number (~3X 21.6%), then the eventual IFR would still be almost 0.4%, which is still very bad for the planet. And I simply don't believe there wouldn't be any more deaths in NYC if the virus was left to run its course. It's always possible I'm wrong on this, but I don't think so.
I really hope no one approaches NY and NJ in terms of deaths per capita.
If we call DC a state for a second, 10 of these would be in a ranking of the 15 densest states.
I guess we should expect such an overlap for a disease that needs proximity to transfer, no?
Trivia — Frank Luntz is responsible for the term ‘climate change.’
https://www.sun-sentinel.com/corona...0200714-xcdall2tsrd4riim2nwokvmsxm-story.html
Has anyone talked about this yet?
Has anyone talked about this yet?
Derek Lowe (In the Pipeline blog in Science Translational Medicine) updated his blog from 2 weeks ago on antibodies, T-cells, immunity and more - and what it all might mean, as well as detailing how little we really know.
The fundamental problem is we have snapshots of antibody levels in state and even country-level serology surveys of close to random populations (i.e., those who had a viral infection and those who didn't know they had one) and we have selected data on T-cell levels active against the virus in small populations (dozens to a few hundred, since measuring these is far more complex than measuring antibodies) of infected and never infected people (from pre-COVID blood donations), but we don't know how these antibody levels might change over time, or how someone's T-cell response might change over time, and (importantly) what a protective profile looks like for both of those.
We've presumed that infected and recovered patients will have immunity from months to a few years, but we don't know that for sure and we've assumed unexposed people have no immunity and that might also be wrong if "cross-reactivity" from exposure to other coronaviruses somehow has given people some or total immunity to the virus from the T-cell part of the immune system. A link and excerpt from his blog is below, The 2nd link below is to a fantastic paper in Cell, which he talks about, which also includes the great graphic, below, showing the two main parts of the immune response (antibodies, which typically work to prevent the virus from latching onto and infecting cells and T-cells, which are special white blood cells which target and destroy virus infected cells) and even this is greatly simplified.
https://blogs.sciencemag.org/pipeli...-on-t-cells-antibody-levels-and-our-ignorance
https://www.cell.com/trends/pharmacological-sciences/pdf/S0165-6147(20)30130-9.pdf?_returnURL=https://linkinghub.elsevier.com/retrieve/pii/S0165614720301309?showall=true
We have similar data here in the US: several surveys of IgG antibodies show single-digit seroconversion. You could conclude that we have large numbers of people who have never been exposed – and indeed, the recent upswing in infections in many regions argues that there are plenty of such people out there. But we need to know more. We could have people who look vulnerable but aren’t – perhaps they show no antibodies, but still have a protective T-cell response. Or we could have people who look like they might be protected, but aren’t – perhaps they showed an antibody response many weeks ago that has now declined, and they don’t have protective levels of T-cells to back them up. Across the population, you can use the limited data we have and our limited understanding of it to argue for a uselessly broad range of outcomes. Things could be better than we thought, or worse, getting better or deteriorating in front of our eyes. We just don’t know, and we have to do better at figuring it out.
Time for an update on everyone's favorite topic - T-cell responses and immunity! Lots of talk the past couple of days about the various vaccines and the dawning realization that the immune response is not just about producing the right antibodies, but likely also depends greatly on producing the right T-cell response. In addition, T-cell responses also can have "memory" years after exposure to a virus and can even have responses to viruses never before encountered by that person, i.e., people never exposed to SARS-CoV-2 can have T-cells that have an immune response (in cell cultures) to the novel coronavirus in a phenomenon known as "cross reactivity."
Just as in the quoted post, I'm going back to the well, citing Derek Lowe's In the Pipeline blog and the paper that came out today in Nature, which he discusses/reviews (easier than reading the paper sometimes). Both are linked below. As I often do, especially with immunology, which I'm no expert on, I'm excerpting part of Lowe's blog, which explains things better than I could. Maybe our own @UMRU can stop by and comment, too.
Now comes a new paper in press at Nature. It confirms that convalescent patients from the current epidemic show T-cell responses (mostly CD4+ but some CD8+ as well) to various epitopes of the N (nucleocapsid) protein, which the earlier paper had identified as one of the main antigens as well (along with the Spike and M proteins, among others, with differences between the CD4+ and CD8+ responses as well). Turning to patients who had caught SARS back in 2003 and recovered, it is already known (and worried about) that their antibody responses faded within two or three years. But this paper shows that these patients still have (17 years later!) a robust T-cell response to the original SARS coronavirus’s N protein, which extends an earlier report of such responses going out to 11 years. This new work finds that these cross-react with the new SARS CoV-2 N protein as well. This makes one think, as many have been wondering, that T-cell driven immunity is perhaps the way to reconcile the apparent paradox between (1) antibody responses that seem to be dropping week by week in convalescent patients but (2) few (if any) reliable reports of actual re-infection. That would be good news indeed.
And turning to patients who have never been exposed to either SARS or the latest SARS CoV-2, this new work confirms that there are people who nonetheless have T cells that are reactive to protein antigens from the new virus. As in the earlier paper, these cells have a different pattern of reactivity compared to people who have recovered from the current pandemic (which also serves to confirm that they truly have not been infected this time around). Recognition of the nsp7 and nsp13 proteins is prominent, as well as the N protein. And when they looked at that nsp7 response, it turns out that the T cells are recognizing particular protein regions that have low homology to those found in the “common cold” coronaviruses – but do have very high homology to various animal coronaviruses.
Very interesting indeed! That would argue that there has been past zoonotic coronavirus transmission in humans, unknown viruses that apparently did not lead to serious disease, which have provided some people with a level of T-cell based protection to the current pandemic. This could potentially help to resolve another gap in our knowledge, as mentioned in that recent post: when antibody surveys come back saying that (say) 95% of a given population does not appear to have been exposed to the current virus, does that mean that all 95% of them are vulnerable – or not? I’ll reiterate the point of that post here: antibody profiling (while very important) is not the whole story, and we need to know what we’re missing.
There are still major gaps in our knowledge: how many people have such unknown-coronavirus-induced T-cells? How protective are they? How long-lasting is the T-cell response in people who have been infected with the current SARS CoV-2 virus, and how protective is it in the declining-antibody situation that seems to be common? What sorts of T cell responses will be induced by the various vaccine candidates? We just don’t know yet. But we’re going to find out.
https://blogs.sciencemag.org/pipeline/archives/2020/07/15/new-data-on-t-cells-and-the-coronavirus
https://www.nature.com/articles/s41586-020-2550-z_reference.pdf
I will add a short passage from the Nature paper's abstract, which kind of says it all, especially the last sentence. Is this cross-reactivity at least partly responsible for the vast majority of confirmed positive cases (80-85%) being mild to asymptomatic? And is it possibly responsible for even more, i.e., some % of the population simply never getting infected in any measurable way (and maybe not even showing antibodies? About 50% of the 37 unexposed donors had a T-cell immune response (in cell cultures) to SARS-CoV-2.
Epitope characterization of NSP7-specifc T cells showed recognition of protein fragments with low homology to “common cold” human coronaviruses but conserved amongst animal betacoranaviruses. Thus, infection with betacoronaviruses induces multispecifc and long-lasting T cell immunity to the structural protein NP. Understanding how pre-existing NP- and ORF1-specifc T cells present in the general population impact susceptibility and pathogenesis of SARS-CoV-2 infection is of paramount importance for the management of the current COVID-19 pandemic.
This is what leadership looks like. Stumbled across this story tonight from 5 years ago. The pic is of Dr. Fauci suiting up to treat an Ebola patient back in 2015, as he says he "gets unique insights into disease when you actually physically interact with patients" and he also wanted to show his staff that he wouldn't ask them to do anything he wouldn't do himself.
https://www.sciencemag.org/news/2015/03/why-nihs-anthony-fauci-treating-ebola-patients-himself
https://www.sciencemag.org/news/2015/03/why-nihs-anthony-fauci-treating-ebola-patients-himself
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