So thinking the worst is over for sure is wishful thinking; and to just resign to "out of the bag" isn't an option either; the worst is only over if we keep at flattening the curve enough to not collapse the system. There are many different parts to it, and one such part might be contact tracking/tracing with an app.
Also, all the talk about herd immunity etc is based on the premise that you actually get a lasting immunity after you had the virus. While it thankfully looks like this may be the case (exceptions like immunocompromised people, apply) - with e.g. blood plasma from cured patients showing good results when given to still severe cases - it isn't certain yet. It could mutate enough (like the flu) and reinfect, or it could "hide" like herpes and hit you full blown when your immune system isn't operating at full capacity. Let's hope not, but let's act at least with that in mind. Contact tracing technology we develop and roll out now may help should there be a second wave.
And yet another also: there have been reports that even after mild progressions some patients end up with damaged lungs, damage that is most likely be permanent. So while these reports haven't yet been verified or refuted, I am not a big fan of "just get it and get it over with, if you're young and low risk".
Humanity has dealt with double-digit-fatal diseases, several of them, for centuries. SARS2 is an ugly bug, but hardly an existential threat to the species.
While not criticizing you directly, I cringe every time I see this reported in the media, and even some TV scientists are not immune from these statements. It is a novel virus, all right. We know almost nothing about it, all right. But it's not a magical Star Trek-like being which does not fit any biological hypothesis.
Other members of the coronavirus family do not exhibit these properties (hiding like the herpes virus that is), so it is at least unlikely that this will happen. And while it can mutate, it will do so at a much lower rate than influenza, which, due to the structure of its RNA, can have plenty of recombination events which cause far more variation.
A nice non technical explanation: https://www.city-journal.org/coronavirus-vaccine
In other words, not all of those people that had a virus are currently infectious. Only the people that are currently actively infectious are the ones that need to be traced.
I'm hearing such a wide variety of claims about this virus that I have by default become skeptical of anything that makes a wide ranging claim. The descriptions range from "highly infections, potentially causes strokes in otherwise young healthy people" to "highly infectious, young people often display no symptoms at all".
Are there multiple strains of this virus out there in the wild? I don't know of another way to explain what I'm hearing from people that work in virology and in hospitals on the front line.
There's probably a lot of other factors that feed into it - median age, pollution, weather/temperature, potentially genetic/ethnic factors... Even things like the prevalence and use of public transit. It's a lot harder to get/spread the virus in LA where most people drive private cars to everything than in NYC where a lot of people spend an hour or more every day in crowded subway trains/stations.
Working out exactly what contributed to the real-world outcomes we're seeing is something we'll probably only be able to guess at, but nothing I've seen so far feels inexplicable.
Both those things can be true at the same time.
I saw one German doctor (from Charité Berlin I think?) who did over 100 autopsies on TV saying in all cases he had on his table there were preexisting conditions (and the older the more likely you have one or more of those). But he also said that the young and "healthy" people he looked at also had preexisting conditions that usually were never diagnosed before.
This reminded me of a buddy in school, who went for the routine mandatory checkup before the mandatory military service (since been abandoned), a jock-type who seriously considered joining up voluntarily to become a jet fighter pilot, and ended up learning he only had one kidney since birth. Something he never knew or suspected and never had any issue with because he was otherwise young and healthy, but which could come back to bite him when he gets old or when he contracts some serious disease (like this one maybe).
In some sense that is pretty high compared to the baseline, but being equal to 10 years of driving isn't apocalyptic.
One of probably a dozen panel discussions on COVID19 he's hosted so far.
UCSF Experts on the Epidemiology, Science, & Clinical Manifestations of COVID-19, and UCSF Response
I think it makes more sense when the density of contacts is less extreme.
If there is no vaccine, or if the vaccine isn't very good, social-distancing and contact-tracing is the only way to win.
One fifth of the global population doesn't yet have it. Like many people around the world are undoubtedly experiencing, an elderly relative died yesterday from Covid-19 in New York. I doubt she will be the last.
Why is herd immunity not a "way we win"?
edit: Ah, yes, concern about the time to get there. Well, let's hope that happens quicker than expected (has any study not shown this?) because from where I'm sitting it looks like lock down is ending.
Hospice patients, and the hospice workers.
People already in treatment, and the healthcare professionals providing them with care.
People who smoke, have diabetes, a heart condition, or are immune compromised, and so on, and everyone they know.
This has got to be millions and millions of people, and this isolation will be extraordinarily porous. Those folks have friends and family too, they will slip up, exposing their contacts and then the virus is on the other side of a firewall. And we've seen how quickly the virus spreads in isolated groups!
New York has six times the per capita deaths that Sweden does. Just extrapolating and multiplying their current number by 3x6==18, that's about 35000 dead swedes until they get to herd immunity.
I genuinely don't understand the alternative world some people live in where Sweden has already beaten this. They're current curve is about 3 weeks behind most of Europe, largely due to the lack of lockdown that allowed the early outbreak to spread for longer.
This isn't evidence. You're reading spin. The article even tells you that.
I have heard R0 estimated around 4. So, technically you would need 3/4 of the population to be immune. The result of this being that R_t drops below 1 thus no longer becomes an epidemic and eventually either disappears or becomes seasonal.
(we also get the benefits of herd immunity if enough people get an effective vaccine)
I know I sound like a broken record every time I say this on HN... but why no one thinks of pharmacological treatment? The first wave of (small) trials will end this June.
Plus I'm confident that the anti-inflammation drugs being tested can help with lung tissue damage.
It would be great though if one of those studies found an effective drug!
Even if the results are bad, it also depends on what they were used for, since the little evidence we have tells us that the sooner we act, the better.
Example: ritonavir was a letdown, but even in the NEJM paper the limitations of the study mention that the trial was done on people with rather severe sympthoms. At this point it was probably too late to make a dent in the infection.
The data on remedisivir (which came from two suspended trials due to lack of enrollment, so no statistical power) showed an almost-identical mortality between the two groups, but I'd argue that those (at least one of them was) were done on patients in severe conditions, so once again late.
Later trials which are ongoing are hopefully better designed (NIH's for remedisivir at least, Gilead's don't use a placebo IIRC) and will get us answers. IMO, even a small improvement on hospitalization rate would be a huge win for the ICUs.
That said, remedisivir is i.v. so this limits applicability to hospitals.
But, that's the larger point I think... Next time.
Let's say this ends up being way better than anyone modeled, it's great practice for a virus that actually has a 5%, or 10%, or etc fatality rate.
They're not.
The NY study is the only one measuring a positive rate much higher than the false positive rates of the tests, and it is consistent with about a 1% infection fatality rate.