From LA Times:
You can’t control it like they did in Korea. In Korea, they tracked every single infected person through their phone location and published the data in a tracking app. Everyone knew where the infected were and to avoid them. If we do that from the start, we are probably in a much better position now. I can’t even get info on where the infected person in my township had been before quarantine. The media likes to have it both ways. If the gov tried what Koreans did, there will be a riot.
Bringing in Katarina from 20 years ago also baffles me and in some ways racist. Katarina affected racial minority a lot. Many pictures show racial minority in distress. That looks like third world? As if it is some kind of wisdom not latent racism.
I don’t know what the outer limit is, but I’m sure it isn’t more than 8 weeks. Some unpleasant choices are going to have to me made.
It might help if we had leadership that was good at “the inspiration thing”, but we don’t.
Heck, rescind HIPPA for coronavirus cases. Then all of us can do our own public health tracing and figure out if we’ve been exposed.
No idea who is eligible and how to get this in place if one has loans. No info on the $10k loan payoff. Nothing. I doubt calling is going to help at this point. Those administering likely don’t know yet and the phone lines will be jammed. Some I know with loans are still getting reminders to pay.
Does anyone remember the days right after 9/11? We faced a sophisticated, mysterious, unknowable enemy, who could move across the world undetected, and adapt almost instantly to any countermeasure we devised?
We were doomed.
Except it turned out not to be true. It was mostly planning and luck.
And then there was the anthrax, which oddly enough had nothing to do with it.
Hope is not a strategy, but my memories of those times are a big help now.
We can start with NY’s 7,000 infected individuals 
So we started an SBA loan for our business. Well the first few pages are basic demographics. Then it got into the nitty gritty and will finish it today. Have to get tax forms etc proof of income and corporate papers etc. We expected that. The person on the phone picked up after like 20 minutes. Again we expected that. The site is slow but a warning states it would be due to the amount of people trying to get one.
I wake up each day looking at CC then flipping on CNN saying to myself… “Yep, this is real”
You don’t need to track it. Everybody just needs to assume they have it. Stay 6’ apart, wash your hands for 20 sec. with soap and warm water regularly, use sanitizer before and after you touch objects in public spaces, disinfect high touch areas, etc etc
https://coronavirus.ohio.gov/wps/portal/gov/covid-19/home/COVID-19-Checklists/
Edited to add: trying to ‘get it’ to beat the rush is idiotic - there are already enough people with it that hospitals will struggle to cope.
Why don’t we already start the construction to build temporary sites to house covid patients in hot areas already? No one in the trump respond team suggested that?
Would be nice, if everyone actually followed through. The problem is we have a small % of people who are stupid and/or stubborn and just won’t follow that advice (or probably any other sensible advice), and we have a much larger % of the population who think they are being careful enough and they really aren’t (it’s OK to go to the gym during quiet time, or go to church and not shake hands, or go to a small wedding and not hug anyone, or keep working in the office if I use Purell, etc.).
Even in times of pandemic, HIPAA entitles you to privacy.
HIPAA laws are a PITA to me professionally but they should never be trampled in the name of public health.
Assume you and everyone else has it and live your life accordingly.
The struggle we see at hospital now will be nothing compared to what’s to come. One study sees about 500K fatalities in the best case scenario meaning if we lock down everything, schools, group gatherings, etc. 1 million if we track the infected and quarantine them. Left alone, it can reach 2 million. How many hospitals are in the US? Let’s say recovery rate from a severe case is 50%. It means if 500K cases are fatal, about 1 million people needed hospitalization. It seems to take a while to reach the end point, successfully or not so. Let’s say 30 days. That means by the time it is over, we would have needed 30 million days of hospitalization. Let’s assume in a year it will be over one way or other. If it is evenly spread out over the year, we need about 100,000 beds every day. Of course, it won’t come steadily. They will surge in and out…
We may find a simple cure shortly. I heard some promising research on it. Or the virus may mutate to something less threatening. Or the weather may inhibit the virus. Let’s all hope we get lucky and one of these happen.
https://www.washingtonpost.com/nation/2020/03/20/coronavirus-elective-surgeries/
As the U.S. government calls for hospitals to suspend elective surgeries amid the spread of coronavirus, health-care workers say patients and staff members are being put at risk at both hospitals and outpatient clinics across the country where surgery schedules are filled with breast augmentations, nose jobs and bone spur removals.
Health-care workers, particularly anesthesiologists who must insert a breathing tube during sedation for surgeries, known as intubation, have been asking institutions to end elective surgery for much of the month, according to interviews with more than a dozen health-care workers nationwide, some of whom spoke on the condition of anonymity. The anesthesiologists raised concerns about scientific reports that found covid-19 can be aerosolized during intubation and spread from patients who have not been tested.
They describe facilities with barely enough surgical gowns to go around, masks in short supply and doctors discussing how to reuse single-use N95 masks. One doctor put maxi pads inside to make it last longer. They also said there are shortages of drugs, including propofol, used for sedation, and saline. One nurse said it is “immoral” that the drugs are still being used for elective surgery.
Jonathan Zenilman, a prominent epidemiologist who is professor of medicine at Johns Hopkins School of Medicine, said the practice of continuing elective surgeries without proper protections of medical workers and patients is “ethically repugnant.”
“If you need your boobs done, why can’t that wait?” he said.
He added that dropping these procedures is a real conundrum for hospitals that are facing dire financial straits from the coronavirus crisis.
On Wednesday, the federal government issued voluntary guidelines, calling on surgeons, physicians and dentists to limit nonessential surgery and medical procedures.
The guidelines are not mandatory. They leave final decision-making authority to state and local health officials, as well as physicians and patients.
“The reality is the stakes are high, and we need to preserve personal protective equipment for those on the front lines of this fight,” said Seema Verma, administrator of the Centers for Medicare and Medicaid Services, which issued the new guidelines Wednesday.
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Now that tests are more available, can they mandate testing everyone undergoing a surgery?
The Atlantic.
Why the Coronavirus Has Been So Successful
We’ve known about SARS-CoV-2 for only three months, but scientists can make some educated guesses about where it came from and why it’s behaving in such an extreme way.
ED YONG
MARCH 20, 2020
EMARYS / GETTY
One of the few mercies during this crisis is that, by their nature, individual coronaviruses are easily destroyed. Each virus particle consists of a small set of genes, enclosed by a sphere of fatty lipid molecules, and because lipid shells are easily torn apart by soap, 20 seconds of thorough hand-washing can take one down. Lipid shells are also vulnerable to the elements; a recent study shows that the new coronavirus, SARS-CoV-2, survives for no more than a day on cardboard, and about two to three days on steel and plastic. These viruses don’t endure in the world. They need bodies.
But much about coronaviruses is still unclear. Susan Weiss, of the University of Pennsylvania, has been studying them for about 40 years. She says that in the early days, only a few dozen scientists shared her interest—and those numbers swelled only slightly after the SARS epidemic of 2002. “Until then people looked at us as a backward field with not a lot of importance to human health,” she says. But with the emergence of SARS-CoV-2—the cause of the COVID-19 disease—no one is likely to repeat that mistake again.
To be clear, SARS-CoV-2 is not the flu. It causes a disease with different symptoms, spreads and kills more readily, and belongs to a completely different family of viruses. This family, the coronaviruses, includes just six other members that infect humans. Four of them—OC43, HKU1, NL63, and 229E—have been gently annoying humans for more than a century, causing a third of common colds. The other two—MERS and SARS (or “SARS-classic,” as some virologists have started calling it)—both cause far more severe disease. Why was this seventh coronavirus the one to go pandemic? Suddenly, what we do know about coronaviruses becomes a matter of international concern.
Read: What will you do if you start coughing?
The structure of the virus provides some clues about its success. In shape, it’s essentially a spiky ball. Those spikes recognize and stick to a protein called ACE2, which is found on the surface of our cells: This is the first step to an infection. The exact contours of SARS-CoV-2’s spikes allow it to stick far more strongly to ACE2 than SARS-classic did, and “it’s likely that this is really crucial for person-to-person transmission,” says Angela Rasmussen of Columbia University. In general terms, the tighter the bond, the less virus required to start an infection.
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There’s another important feature. Coronavirus spikes consist of two connected halves, and the spike activates when those halves are separated; only then can the virus enter a host cell. In SARS-classic, this separation happens with some difficulty. But in SARS-CoV-2, the bridge that connects the two halves can be easily cut by an enzyme called furin, which is made by human cells and—crucially—is found across many tissues. “This is probably important for some of the really unusual things we see in this virus,” says Kristian Andersen of Scripps Research Translational Institute.
For example, most respiratory viruses tend to infect either the upper or lower airways. In general, an upper-respiratory infection spreads more easily, but tends to be milder, while a lower-respiratory infection is harder to transmit, but is more severe. SARS-CoV-2 seems to infect both upper and lower airways, perhaps because it can exploit the ubiquitous furin. This double whammy could also conceivably explain why the virus can spread between people before symptoms show up—a trait that has made it so difficult to control. Perhaps it transmits while still confined to the upper airways, before making its way deeper and causing severe symptoms. All of this is plausible but totally hypothetical; the virus was only discovered in January, and most of its biology is still a mystery.
Read: Should you take Advil for COVID-19?
The new virus certainly seems to be effective at infecting humans, despite its animal origins. The closest wild relative of SARS-CoV-2 is found in bats, which suggests it originated in a bat, then jumped to humans either directly or through another species. (Another coronavirus found in wild pangolins also resembles SARS-CoV-2, but only in the small part of the spike that recognizes ACE2; the two viruses are otherwise dissimilar, and pangolins are unlikely to be the original reservoir of the new virus.) When SARS-classic first made this leap, a brief period of mutation was necessary for it to recognize ACE2 well. But SARS-CoV-2 could do that from day one. “It had already found its best way of being a [human] virus,” says Matthew Frieman of the University of Maryland School of Medicine.
This uncanny fit will doubtlessly encourage conspiracy theorists: What are the odds that a random bat virus had exactly the right combination of traits to effectively infect human cells from the get-go, and then jump into an unsuspecting person? “Very low,” Andersen says, “but there are millions or billions of these viruses out there. These viruses are so prevalent that things that are really unlikely to happen sometimes do.”
The Atlantic part 2
Since the start of the pandemic, the virus hasn’t changed in any obviously important ways. It’s mutating in the way that all viruses do. But of the 100-plus mutations that have been documented, none has risen to dominance, which suggests that none is especially important. “The virus has been remarkably stable given how much transmission we’ve seen,” says Lisa Gralinski of the University of North Carolina. “That makes sense, because there’s no evolutionary pressure on the virus to transmit better. It’s doing a great job of spreading around the world right now.”
Read: The U.K.’s coronavirus “herd immunity” debacle
There’s one possible exception. A few SARS-CoV-2 viruses that were isolated from Singaporean COVID-19 patients are missing a stretch of genes that also disappeared from SARS-classic during the late stages of its epidemic. This change was thought to make the original virus less virulent, but it’s far too early to know whether the same applies to the new one. Indeed, why some coronaviruses are deadly and some are not is unclear. “There’s really no understanding at all of why SARS or SARS-CoV-2 are so bad but OC43 just gives you a runny nose,” Frieman says.
Researchers can, however, offer a preliminary account of what the new coronavirus does to the people it infects. Once in the body, it likely attacks the ACE2-bearing cells that line our airways. Dying cells slough away, filling the airways with junk and carrying the virus deeper into the body, down toward the lungs. As the infection progresses, the lungs clog with dead cells and fluid, making breathing more difficult. (The virus might also be able to infect ACE2-bearing cells in other organs, including the gut and blood vessels.)
The immune system fights back and attacks the virus; this is what causes inflammation and fever. But in extreme cases, the immune system goes berserk, causing more damage than the actual virus. For example, blood vessels might open up to allow defensive cells to reach the site of an infection; that’s great, but if the vessels become too leaky, the lungs fill even more with fluid. These damaging overreactions are called cytokine storms. They were historically responsible for many deaths during the 1918 flu pandemic, H5N1 bird flu outbreaks, and the 2003 SARS outbreak. And they’re probably behind the most severe cases of COVID-19. “These viruses need time to adapt to a human host,” says Akiko Iwasaki of the Yale School of Medicine. “When they’re first trying us out, they don’t know what they’re doing, and they tend to elicit these responses.”
Read: We were warned
During a cytokine storm, the immune system isn’t just going berserk but is also generally off its game, attacking at will without hitting the right targets. When this happens, people become more susceptible to infectious bacteria. The storms can also affect other organs besides the lungs, especially if people already have chronic diseases. This might explain why some COVID-19 patients end up with complications such as heart problems and secondary infections.
But why do some people with COVID-19 get incredibly sick, while others escape with mild or nonexistent symptoms? Age is a factor. Elderly people are at risk of more severe infections possibly because their immune system can’t mount an effective initial defense, while children are less affected because their immune system is less likely to progress to a cytokine storm. But other factors—a person’s genes, the vagaries of their immune system, the amount of virus they’re exposed to, the other microbes in their bodies—might play a role too. In general, “it’s a mystery why some people have mild disease, even within the same age group,” Iwasaki says.
Coronaviruses, much like influenza, tend to be winter viruses. In cold and dry air, the thin layers of liquid that coat our lungs and airways become even thinner, and the beating hairs that rest in those layers struggle to evict viruses and other foreign particles. Dry air also seems to dampen some aspects of the immune response to those trapped viruses. In the heat and humidity of summer, both trends reverse, and respiratory viruses struggle to get a foothold.
Read: How you should get food during the pandemic
Unfortunately, that might not matter for the COVID-19 pandemic. At the moment, the virus is tearing through a world of immunologically naive people, and that vulnerability is likely to swamp any seasonal variations. After all, the new virus is transmitting readily in countries like Singapore (which is in the tropics) and Australia (which is still in summer). And one recent modeling study concluded that “SARS-CoV-2 can proliferate at any time of year.” “I don’t have an immense amount of confidence that the weather is going to have the effect that people hope it will,” Gralinski says. “It may knock things down a little, but there’s so much person-to-person transmission going on that it may take more than that.” Unless people can slow the spread of the virus by sticking to physical-distancing recommendations, the summer alone won’t save us.
“The scary part is we don’t even know how many people get normal coronaviruses every year,” Frieman says. “We don’t have any surveillance networks for coronaviruses like [we do for] flu. We don’t know why they go away in the winter, or where they go. We don’t know how these viruses mutate year on year.” Until now, research has been slow. Ironically, a triennial conference in which the world’s coronavirus experts would have met in a small Dutch village in May has been postponed because of the coronavirus pandemic.
“If we don’t learn from this pandemic that we need to understand these viruses more, then we’re very, very bad at this,” Frieman says.
ED YONG is a staff writer at The Atlantic, where he covers science.
Here is that study: https://www.imperial.ac.uk/media/imperial-college/medicine/sph/ide/gida-fellowships/Imperial-College-COVID19-NPI-modelling-16-03-2020.pdf
I read through it yesterday, and found it somewhat reassuring. In an uncontrolled pandemic - meaning literally nothing is done to “flatten the curve” - the researcher sees 2.2 million dying, and the virus completely passing by August 2020 (see Panel A, p. 7). That would be a death rate across the entire population of 0.65%. Again, though, this is in a totally uncontrolled scenario.
Table 1 on page 5 estimates infection to death ratios by age bracket. People should really look closely at those numbers. Keep in mind that the numbers must be adjusted downwards by the probability that one catches the virus in the first place. Probabilities are vanishingly small for all age cohorts under 50, and what I consider acceptable risk (others may disagree) for all cohorts under age 70. Median age in the United States is approximately 38 years old. It is difficult to see the vast majority of the population sacrificing for too long (say, more than 4-6 weeks) and literally shutting down the economy to protect groups of people who have an alternative: self-isolation during a virus sweep.
Just to counter the narrative that all people who think this way must be “selfish,” keep in mind that my wife and I are over 50 and we have four parents who are in their early 80s and early 90s, two with health conditions (one of whom has very serious ones involving lung function).
Italy has universal health coverage, so has the UK. Over 90 % of the money spent in healthcare comes directly from the government. Did not help.
At least the survivors there don’t have to pay tens of thousands in medical bills once they recover.