IFR slightly greater than seasonal flu * fraction of population susceptible greater than seasonal flu, occurring within a compressed window of weeks rather than months, is very very bad.
Fewer infected with a larger percent of them dying or more infected with a smaller percent dying can leave just as many corpses to bury. New York City’s death rate is compatible with an IFR not much higher than the flu infecting a very large number of people in a fairly short period of time. Might or might not turn out to be but is compatible with.
It is horrific. Sorry if some end up disappointed that much worse than the carnage of New York City and Northern Italy was not to be and are pissed. Me I think that’s nightmare enough.
I think there is no question that we will have a subsequent pandemic that is worse than this one. Will it be next year, next decade, or a generation from now, that’s hard to predict. But, when you have a population density like we have, and increase it every year, there is no question that things will get worse.
And, of course, when this blows over in a few months, or even a few years, those who survive will not take the next one seriously, since they lived through this one just fine. Human nature.
I mean, if we are lucky, hopefully we can use this one as a learning experience. Hopefully the death rate won’t be nearly as bad as expected (I was thinking we’d see 100-200 million deaths globally from this) but we realize that both bioterrorism and random mutations in wild animals pose a serious threat to peoples lives, safety and the global economy and hopefully the world invests far more heavily in pandemic preparedness so we can handle the next one far better and far more smoothly (some nations like Taiwan have handled this whole thing really well).
But another part of me fears if this one isn’t too bad, people assume its all overblown and do even less than we would otherwise.
I’m kind of worried that terrorists will see how much damage a bioweapon can do from all this. Groups like Al Qaeda and islamic groups have a lot of intelligent, highly educated types in their ranks who can probably create a more virulent form of a contagious pathogen. The damage to lives and economies from this pandemic is far worse than 9/11.
On another note, I’m still confused how all this data jives with the princess cruise. I believe 800 got infected there and at least 10 have died so far, showing an IFR of over 1%. Maybe the age group of that particular cruise was higher, but I’ve heard the IFR for those over 70 was around 7%.
This article from over a month ago predicts 15 deaths on the princess cruise. So far I think it has been at least 10.
Bioweapons must be incredibly difficult to produce and deploy because we’ve not suffered biowar attacks.
Effective bioweapons are difficult to develop but they can slip free, like the current situation.
Bioweapons will be developed, will escape control, and turn us all into pink goo.
I don’t expect stateless terrorist bioweapons - too iffy. Much easier (in theory) to carefully pour an ounce of powdered plutonium in a balloon, inflate with helium, and release to be wafted over a metropolis. I’m surprised that’s not happened yet.
Whether or not it’s biowar, humanity should expect increasingly regular and virulent plagues because global density and interconnection. How to prevent pandemics? That’s for another thread. Meanwhile, I could be asymptomatic for all I know. This county has only tested a few hundred and I don’t qualify. Stay away from me.
The overwhelming demands on the healthcare systems of northern Italy and of New York caused by the size of the wave have been very real whether they reflected 5% of the population infected or 70% of it. Flattening that curve is essential everywhere that is in progress.
If verified by more research it informs on how to proceed as surges pass some. We are no better informed as to what sorts of controls or behaviors in what timing were required to achieve flattening.
This is the Sweden page, click on logarithmic death count. You can easily extrapolate it and the final death count you would get is between 5000 to 10,000 => this final death toll for a nation of 10 million people which corresponds to final fatality figures of 0.05-0.1%. remember that Sweden does not have a lockdown so covid-19 has run its full course.
Basically this shows that cold countries will have 0.05 to 0.1% of their population succumbing to covid19, in a hot country lockdowns are not required anyway in my opinion.
We have a thread discussing Sweden and your thoughts on hot cold are expressed elsewhere as well. As the op I request that this thread try to stay related to the topic of asymptomatic rates and what the data on them imply as they emerge.
Only parts of California are a hot area, to use your terminology. The state does have a pretty good distance between its southern and northern borders.
Next, not all of China is a cold area. A good chunk of it is in a hot area.
Thanks to ratatoskK in the Breaking News thread for bring this one to attention. Chelsea MA, population 40,160. Another convenience sample not necessarily representative of the whole and unknown what the false negative and positive of the test is.
Official case count about 1.8%. Confirmed case fatality rate 5.5%.
Percent positive by this antibody test as having had the infection with signs of immunity - 32% resolveds, which would translate to 12,851 cases about half of whom could not remember having even had a single of the non-specific symptoms of COVID-19 in the past four weeks.
Actual infection fatality rate in Chelsea using these as real numbers: about 0.3% … with a pretty wide error bar to be sure. Doing the same sort of calculation with Santa Clara’s much bigger n came up with 0.14%.
More to come I am sure! Hopefully some that are more methodical and breakdown by decadal cohort if nothing else.
Yeah, I would be careful taking these results as gospel. There has been talk of these quick tests for a while, but it seems there is yet to be one that is considered to be reliable. See the UK government’s statements about that the last week or so.
In addition, it is unclear how much antibodies you need for immunity to actually happen. Just this week the Dutch government body for infectious disseases warned that there is a decent chance that people who had mild versions of the infection, will not be immune.
In short, there is still a lot we just don’t know.
Qom - Iran hotbed, Wuhan - China hotbed, all European hotbeds , newyork - basically all covid19 hotbeds are significantly cold.
No hot area has been touched with the exception of Louisiana and there also death toll is small (so is the population). Look at Africa, look at 1.75 billion population strong subcontinent, Look at Asean countries etc. Do the comparison with cold areas, conclusions are pretty obvious. I rest my case.
That’s not exactly the point right now. We’re trying to figure how widespread this disease really is. But “how much antibodies you need for immunity” strike me as a weird way to put the uncertainty. We don’t know how long immunity will last at all.
Never take any single study or even single line of evidence as “gospel”; take it as part of an aggregate.
Yes there will be issues with determining specificity and sensitivity. Early reports are that false positives are uncommon but false negatives not so infrequent. Likely that will vary by product and is the same issue as with RT-PCR testing for acute infections.
Yes the first studies out will mostly be convenience samples. These will give some broad bounds of confidence but cannot be assumed to represent complete populations. Or differences within the population.
Yes it is unknown how specific antibody titers correlate with immunity. There is already (referenced earlier) reason to suspect that fast onset NON-specific coronavirus antibody responses and undetectable specific antibody response may correlate with mild to asymptomatic disease and possible strong and more lasting cellular immunity that titers do not pick up. A different sort of false negative. Or perhaps the resolveds will not have immunity as strong or for as long as most experts expect.
Still the various lines are so far broadly consistent with each other: confirmed case number dramatically underestimates actual syndromic case number by large amounts, asymptomatic cases to never noted as being ill symptomatic cases outnumber symptomatic cases significantly, true IFR is much less than reported CFR, and the fraction of Americans in some areas already having had this disease is likely much larger than many were expecting. And very different than the numbers many of the models used as assumptions in the inputs.
No question that more methodical work is anxiously awaited.
Since there are such a wide range of coronaviruses, is there a chance that the people testing positive for antibodies haven’t caught SARS-Cov-2, but instead caught some common cold years ago and tested positive for that?
How do they distinguish antibodies for this strain from the other coronaviruses? I mean, I’m assuming we don’t understand the topical protein structures or the antibodies produced of the endless coronaviruses that have gone around already, how do we know its an antibody for this particular strain.
