I think everybody should carefully read the short section that says "Does the amount of exposure affect the severity?".
Some people are looking at antibody studies that show that large parts of the population are somehow affected and then doing back of the napkin math and deciding that this is really not worse than the flu in terms of death rate. They are further encouraged by the fact that people that die tend to be older and with pre-existing conditions. Then they say we should open everything up and get everything "back to normal", and sometimes they add that this is just a way to winnow out the old and the weak.
As problematic as the latter statement is, the above thinking is actually dangerously optimistic. Experience shows us that in specific situations with prolonged/repeated exposure, the death rates are much higher. Also young and healthy people may get seriously sick and die due to high level of exposure.
This has already been happening in hospitals that did not have sufficient protective equipment/procedures.
If we open everything up and get into a situation where the virus is all over the place we can get into a horrible spiral of increased exposure and increased death rates etc.
> Some people are looking at antibody studies that show that large parts of the population are somehow affected and then doing back of the napkin math and deciding that this is really not worse than the flu in terms of death rate.
i feel like a lot of people are ignoring that a ton of people have relocated outside of NYC. i don't think the 25% antibody positive study in nyc is accounting for that
Already 0.2% of NYC has died of COVID19. That's completely consistent with the very initial, very dire infection fatality rates of 0.6%-1.0%. (Which is different than the case fatality rate.)
When you combine this 10x increase of the IFR along with the 5x-8x increase in suspected attack rate of flu, one would have to quite ignorant of reality, and perhaps an unknowing tool of others, to somehow look at the NYC study and think that it supports the silly "flu" conflation.
(And for that matter, flu kills a ton of people every year, are we going to add another flu to the world without fighting back at all? What sort of wimpy, defeatist person looks at the world that way?)
It's such a breath of fresh air coming on HN where most people are numerate and capable of understanding data.
I actually agree that most parts of the US should carefully open up - the lockdowns have a significant portion of the population in dire straights. Our society can't survive a long-term lockdown intact, I'm convinced.
But that doesn't mean the virus isn't extremely dangerous. It's far worse than the flu. It's irresponsible for folks on social media to insinuate that it's "not even has bad as the flu" based on a few memes they've read.
We have to take great care, or more areas will end up like the Tri-state area. As the GP pointed out, the viral load is extremely important in determining mortality among the younger ages. If there is tons of the virus everywhere, the < 60 mortality rate will increase, possibly dramatically.
Glad to be on HN where most people understand things like CFR vs IFR (as opposed to a vague "death rate" most of social media talks about) along with issues of bias, etc that can affect any of these studies.
There are some interesting stories on this. A lot of deaths are occurring that are outside of the 'normal' and not accounted for by deaths attributed to covid alone:
> And for that matter, flu kills a ton of people every year, are we going to add another flu to the world without fighting back
I feel like they're realistic limits. People are not gears and you cannot turn humanity off like batteries. There is unrest in Ecuador when cities began running out of morgue space. There's unrest in parts of the world where people haven't seen paychecks for two months. Most high income countries have been overproducing food for years, but we're still losing a lot of food quickly. We're depending on that overproduction slack to hold.
Combined with the difficultly of creating coronavirus vaccines. I've read people attribute the lack of a good SARS1 vaccine due to the economics/capitalism, but there seems there more to it. Animal and human trials have produced vaccines that may not provide long lasting immunity and have dangerous side-effects:
A vaccine in less that 5 years feels very unrealistic, not for a safe one. I have a feeling humanity may need to come to the realization that our life expectancy may have been significantly lowered for the next several years, if not decades.
> Combined with the difficultly of creating coronavirus vaccines. I've read people attribute the lack of a good SARS1 vaccine due to the economics/capitalism, but there seems there more to it.
Yes. The reason there is no SARS1 vaccine is because SARS1 burned out after a year:
"The SARS global outbreak was contained in July 2003. Since 2004, there have not been any known cases of SARS reported anywhere in the world." [0]
I read that there was visible lung tissue damage forming the characteristic broken glass pattern on CT scans of 58% of the infected but asymptomatic carriers on the Diamond Princess cruise. That to me adds a sobering footnote to the process of developing herd immunity. Most of us won't die, but do we walk away with long-term impairment of our lungs and possibly other organs?
This was also confirmed by a physician from Innsbruck, Austria that looked after healthy young adults that were divers and got the virus - all of them had only mild symptoms but most lost the fitness to dive anymore and lack lung function.
It's been discussed in the linked article (a translator should work reasonably well). For the physician the look of the lungs in the scans indicate it's non-reversible but only time will tell.
Yep. Lung damage rarely heals, which has life-long consequences. IIRC, a BBC report mentioned a 30% average decrease in lung function in survivors. Heart, liver, kidneys and possibly other organs are also affected.
I'm not equating Covid-19 to the flu, but ground glass opacities are common among people with influenza. They're also not uncommon in older folks with no history of smoking etc. Right now the evidence of long term or permanent damage to lungs is very muddled and often anecdotal.
And how many strokes, kidney disease, and other problems were caused by other respiratory system viruses before COVID-19? We don't know because we've never really looked.
I don't think this is a foregone conclusion by any means. Many countries have gotten growth rates low enough that even after 2 years, their whole population won't have gotten it. Some countries might opt to infect everyone (as the US seems to be doing, due largely to chaos and incompetence), but I don't think it's the only option.
Source? It depends on the intervention, but my understanding is that that is not required to be true on the 18mo timeline. I.e. I think the original Imperial College study was calling for for suppression, rather than just avoiding overwhelmed hospitals
There are a lot of useful interventions that we're figuring out that will help even before we get a vaccine. Lots of antivirals are being studied and those that work will probably be best given in the first few days after symptoms show up, which requires more testing. Figuring out when to give steroids or IL-6 inhibitors after the first week when the virus starts to fade but the danger of cytokine storms gets worse. Figuring out when to flip people onto their stomachs (proning) and how low blood oxygen levels can get before intubation is actually necessary.
If we can keep this thing suppressed for another month summer might provide us with a bit of breathing room to figure out what works and stockpile supplies. But even if not I'd rather get this thing with the medical state of the art a month from now.
A vaccine isn't the be-all-end-all. We can still potentially hold out until there's an effective treatment. Famotidine? Remdesivir? Anything that would reduce the severity of the infection would lead to a better outcome than you're facing currently.
Yes, but they're workers. People generally retire at 65, and in the MTA, I believe you can get a full pension at 55. The population that pushes up the mortality numbers are 70+, and they're not driving a bus or a train anymore.
Age is relevant here. I don't recall the numbers, but I read that a disproportionate amount of younger people who have died from covid-19 or had sever cases, were healthcare workers. And the theory was that viral load plays a part.
The Chinese doctor who blew the whistle on covid-19 died from it, and I believe he was an otherwise healthy 30-something.
The NYC subway system has me concerned. Not only is it filthy, but there is zero air circulation. This means that anything airborne will stay put, possibly in high concentration for a long time. Given the amount of people going thru these spaces, there is a high chance your going to be exposed to something. My concern is that I haven't heard anything on making the stations and cars cleaner or safer.
As someone who hasn’t followed, and I understand I’m asking a random internet user this and not a scientist, but what is the definition of ‘prolonged exposure?’ Are people who contract the disease less likely to die that someone who is in close contact for a prolonged period of time? How long is that period? 15 minutes? Two hours?
Not a scientist, I can only attempt to retell what virologist Prof. Christian Drosten from Charité Berlin told in in his podcast[1]:
It's not really clear at the moment but it could be due amount of dose (more virus particles, faster replication) and where the virus makes contact with the body (if you are unlucky you are breathing a high dose directly into your lungs i.e. coughing patients in a hospital) - your immune system does not know the virus and it takes a while until it's able to fight it off and if the virus is directly in the lungs or you've got a high dose it has less time to do so. If you have it only in the throat it takes a lot of time, like multiple days until it goes into the lungs (if at all, this is also not clear when and when not this happens) and he suspected that in this time period you already have a better immune response.
Besides that (not from the podcast) I've read that the virus can induce inflammation that can can cause blood clots and other nasty things - so you may die from stroke or heart problems and not pneunomia.
There was also a paper that hypothesized that the virus can either replicate in the throat and go the lungs but it's probably also possible for the virus to use the nervous system to reach the brain via the olfactory bulb.
China did isolate ill patients from their families and it was hypothesized that sharing a bed/room with a sick person is a bad idea because the virus is in high doses in the air. So you can read that you should keep fresh air flowing in and possible avoid too much direct contact.
Being around a positive person continually for several days at home would mean a lot more exposure than many people would get when encountering others in public.
Maybe? No one knows for sure. We can't directly measure the dose of virions each person receives. There is a huge variations in contagiousness between patients based on factors that are still unclear. Proper use of PPE by caregivers can also have a huge impact.
It’s dose. So you get a higher dose the longer you are exposed. A smaller dose infected less cells are initially infected and maybe you get less sick. Higher dose may mean you get more sick.
That's the idea behind "variolation", which was used before there were vaccines. It's risky, since you might get infected anyway, or perhaps the dose isn't enough to work.
Making strong guarantees that people will become immune and won't be infected is part of what makes coming up with a vaccine hard. It's apparently pretty easy and quick to come up with vaccine candidates.
It was a controlled infection with Smallpox, by scraping the skin with pus or scab powder from an infected person. Cowpox is what makes the smallpox vaccine.
If we have a vaccine candidate that is safe, is there any reason not to give it in mass before knowing if it works? The only thing I can come up with is it takes longer to prove safety than effectiveness, but I don't much about this.
Also, during the H1N1 scare a vaccine used in Europe caused some people to develop narcolepsy (though perhaps more would have gotten it from the virus itself without a vaccine). It can be hard to determine that something is “safe” quickly.
SARS-CoV-2 is also at a really awkward point in the fatality curve (with the best estimate of the IFR being around 1%) that you really want to do something, but you also can't really accept a significant chance of that something having a significant side effect.
Dosing is a thing. There are high dose and low dose influenza vaccines for example. But even then immunity isn't guaranteed, you need neutralizing antibodies to develop as well. Lots of things have to go right to get a sustained safe and effective response which is why vaccines take so long to develop.
I can't agree with this enough. People are failing to account for viral load. I think that's part of what may be happening in areas like N. Italy and NY where the health system gets overloaded and the death tolls are high. People are getting such high initial inocula that they get really, really sick.
Nurses and doctors work in close proximity to people who are sick. So 50 cm compared to 2 meters.
This is why their viral load would be more.
Given a default R of 2 to 2.5 what model are you implying makes this worse in terms of viral load given a reduced R? How would this work?
This bit need explaining because it sounds like you are implying with a R of 2 to 2.5 then the average person might get a higher viral load than if R was .9 lets say.
I don't think a room would have 10 people with mild cases.
So this needs to be modelled realistically.
I think there's a small chance one person in the room has it for R0 = 2.5 compared with a not quite as small chance one person in the room has it for a lesser R.
Also I also don't think being in a room with multiple people effects load.
I think it's distance. A cough from a person within 50cm is far far worse than 2 people breathing.
So this is my junk science claim, this needs to be backed with numbers. It's not logical R effects load exposure to me, where is this evidence from?
Else this is dangerous information, exactly the same as saying it's just the flu.
I've also been wondering if this is a factor in the high death rates of people who've already been hospitalized, or in their rapid/unexpected deterioration. In a quarantine unit there must be a large amount of the virus all over everything.
Like most people I'm 1) not a specialist at all and 2) still have an opinion.
One thing I'm looking at is the excess mortality in a country like Sweden, which had an outbreak (in the top 25 countries by cases) but has not done any lockdown.
> In practice, however, this strategy, which was rejected in the United Kingdom, is leading to a much higher death rate in Sweden than in other Nordic countries.
and they cite a CNN source. But then I look at this data plotted on a log chart and it appears they're leveling out:
The IHME model has been really interesting for Sweden. While Sweden is saying they have it under control the growth rate of their expected deaths is rising faster than any country. It was projected at about 10k by Aug 4 just a couple of weeks ago, but it is now over 17k expected to die in Sweden. Although they seem to be more OK as a country if their senior citizens die.
Assuming it’s about as bad as the flu, fine, but we have herd immunity to the flu via vaccines and antibodies, plus people with the flu are symptomatic relatively quickly. Infect the entire US population with covid-19 and you lose ca. 0.5% of the population in one swoop, or about 1.5 million people. Just like the flu, but not, and the full consequences of the infection won’t really start showing up for a couple weeks.
In a good year the flu vaccine is 50% effective, and that’s pretty rare (though getting better). That’s not enough for herd immunity, and flu viruses mutate enough where we also don’t get it from naturally formed antibodies.
It is my understanding with some viruses that one doesn't become infected with a single virus particle, but rather with a population. That's because the viruses mutate enough that no single virus has all the machinery necessary for replication. Only when a cell gets hit a few times to get all the parts does replication kick in.
I don't think the mutation rate of this particular virus is very high, though, so this situation doesn't seem as likely here.
My understanding is that viruses don't have replication machinery at all - it's one of the defining features of viruses. Their host cells are essentially tricked into producing copies of the virus.
That is incorrect. The virus particles are mostly identical. The reason the dose matters is because each individual particle doesn't have a 100% chance of infecting an individual. That is partly due to the https://en.wikipedia.org/wiki/Innate_immune_system
> In cats, for example, infection with feline enteric coronavirus may last for months or longer. When this happens, the virus mutates so much that its very nature seems to change. What starts out as a relatively mild gastrointestinal infection eventually causes serious peritonitis (inflammation of the membrane lining the abdominal wall) in some animals. Examining the virus at this point in the infection, researchers found that the mutations had resulted in the emergence of a related virus, feline infectious peritonitis virus — and this one has a higher fatality rate.
Can someone explain this to me, are they saying that the virus mutated into another virus? What conditions would it need to be a new virus rather than a variation of the original one?
> What conditions would it need to be a new virus rather than a variation of the original one
The Carl Woese (Woesian?) [0] definition that's been taught for a while is that when a certain sequence within two organisms exhibits a similarity score of < 97%, then it's new species. The certain sequences is generally 16S rRNA. That definition has its problems, but it's even more complicated for viruses: I think it differs for each virus family (e.g., Filovirus [2]). I just messaged a virologist and they said it's too complicated to explain over G-chat.
That's recently been narrowed down to 98.7% and really only applies to microorganisms, definitely not the definition used for species with sex. Furthermore, the DNA-DNA hybridization technique is considered outdated at this point so one has to take it with a grain of salt. Also, viruses aren't even organisms so I'm not really sure you can even talk about species with them. I have heard the term quasispecies used for them however.
These are two forms of virus. My guess would be that they were isolated and named separately, and retained their original names even after it was discovered they were the "same" virus.
The mechanism sounds similar to what happens with HIV. Simplifying wildly, there are M-tropic strains that infect macrophages, and T-tropic strains that infect T lymphocytes. People tend to get infected with M-tropic strains, because it's macrophages that come into contact with invading viruses. However, over time, the virus can mutate to become T-tropic. It's the T-tropic strains that cause immunodeficiency, and hence AIDS.
Virologists often take a functional definition of how much mutation is required to make a new virus. If two different strains have changed so much that immunity to one strain doesn’t provide protection from the other strain then they are considered different viruses.
On the plus side, a compound closely related to remdesivir (the drug to which remdesivir is the prodrug) showed great promise in curing this disorder (also known as FIP, Feline Infectious Peritonitis). Gilead stopped the trial because it might have interfered with marketing for human diseases, but if remdesivir goes into large scale production, as now seems likely, cats and their owners will benefit.
iirc there's a sort of black market for concerned cat owners getting an experimental (but apparently quite effective) drug for feline leukemia. there's Facebook groups you can join where they'll check you're not a fed and they'll direct you to a supplier.
Basically, taxonomy isn't all that meaningful for viruses.
If a given cell is infected with multiple ~related viruses, various chimeric viruses will be produced. Then there'll be selection on the basis of infecting other cells. And then the process repeats, until the host recovers or dies.
As others note it's super complicated with viruses. If you want to track the mutations in real time, check out the Nextstrain project (https://nextstrain.org/). The main person behind it, Trevor Bedford, is also a good person to follow on twitter for these topics and had a brief thread on mutation rate and immunity. (https://twitter.com/trvrb/status/1244750382338719745?s=20) TLDR: Though there's some uncertainty, given what we know today, it doesn't appear to be mutating in a way that will substantially affect immunity or morbidity.
I agree. I certainly won't be sending mine back in a rush, not until I am confident they have a manner of control rather than just "well the health services won't be overwhelmed by the dying"
> Does the amount of virus exposure affect disease severity? It looks that way.
Besides reducing the transmission rate, social distancing measures could also be reducing the initial viral load of each exposure, leading to milder disease profiles, lowering population hospitalization and fatality rates.
I mean "corona virus" is a extreme corse category of viri which contains all viri of which the outer shell has a certain kind of structure which looks like a corona (crown).
While this puts some constraints on how the virtual can survive outside if the body and similar thinks it still does say hardly anything about e.g. what cells the virus hijacts, what syntoms it causes, etc.
The plural is virus is viruses, or "virus" if you insist on its Latin form. It's a Latin word, but it only occurs in Latin as a singular collective noun:
Coronavirus is the name given to a family of related RNA viruses. The family is named for the spikes. The family is not defined by the spikes. The family is defined by genetics and evolutionary relationships. So yes, we can infer plenty. The covid virus is actually so closely related to another one of the coronavirus (the sars virus) that it's considered just another strain of the sars virus (hence the name Sars-cov-2)
Idk but my impression is SARS-CoV-2 was named that way because it causes a SARS, Severe Acute Respiratory Syndrome, though it’s not the SARS. “SARS” include SARS-CoV SARS and other “SARSs” like COVID-19.
Probably the SARS was too generic of a name... in complete hindsight, SARS should have been named as “SARS COVID-02” and MERS as “SARS COVID-12” or something like that.
I can see where that impression came from since it is a generic sounding name, but SARS is not a generic symptom name like "fever" or "cough." There is only the SARS disease, caused by the SARS-cov virus, and the related COVID disease, caused by another strain of the SARS-cov virus. the strain of virus causing covid is of the same species as the virus that caused SARS. In general, biology names are just really annoying and nonsensical, so I totally see where it's easy to be led astray by these annoying, generic sounding names, the reuse of the word SARS for a specific disease and a species of coronavirus strains, all of which are the same single species and are related and are called SARS-cov viruses, but where only one of them causes the disease called SARS, while another one causes the disease called COVID-19. And to add to the confusion, people just refer to COVID-19 as COVID, but all COVID stands for is "Coronavirus Disease." So the coronaviruses are a family of genetically/evolutionarily related viruses, but only one of them, a strain of the sars virus species, causes coronavirus disease. And while lots of diseases cause respiratory issues in the middle east, only one specific coronavirus gets to cause Middle East Respiratory Syndrome
"Taxonomically, SARS-CoV-2 is a strain of severe acute respiratory syndrome-related coronavirus"
The official paper announcing the name of SARS-COV-2, Titled: The species Severe acute respiratory syndrome-related coronavirus: classifying 2019-nCoV and naming it SARS-CoV-2
The classification of virus is difficult, but it is not based only in the shape. The shape may give some hints, and help to get a friendly name, but it is not the only property. Moreover, in the last (10?) years it is easier and easier to sequence the genome of them, and understand the relations.
For an more familiar example, think about the distinction of rabbits and hares. I can't for the life of me distinguish them, but they are not very related and biologist can classify them and get the more related species of them (specially if the rabbit/hare is dead and they can open it and look at the inner parts and bones, or even better, make a genetic analysis).
Another example is sharks vs dolphins. Both live in water and they look somewhat similar. (I think I can distinguish them.) Why are sharks a type of fish, but dolphins are not?
"This deletion likely hindered its ability to bind effectively, making it harder to produce severe infections. Such evolution by deletion is actually a common feature of these viruses."
Is this really the case?, how would that be a common feature?, how are the strains where this deletion takes place more successful than those where it doesn't happen?, is it because it favors faster spread and somehow the organisms infected by these strains with deletion become inmune also to strains without deletion?, or there are other mechanisms that come into play?
Deletion is an easy mutation to occur in the process of replicating a genome. The reason these strains would be successful is because they dont kill or hurt their hosts that badly. If the infected person is bedridden, they're not going to be out and about spreading the virus, while a less severe infection would make it easier for them to mingle amd infect others to pass on the gene pool.
So from what you are saying the explanation for the paragraph from the article would be that a more severe infection would be more likely to have R0 < 1, so on aggregate viruses would "commonly" evolve this way. I understand this, but thank you for the reminder of the mechanism :)
However if the the R_0 of COVID-19 is between 1.4 and 5 (https://en.wikipedia.org/wiki/Basic_reproduction_number), how likely would it be that another mutation more lethal would appear and still be successful?, that is with R_0 > 1. I think that's a more relevant question than whether most successful mutations will be less lethal. Specially knowing that one of the characteristics of the virus is asymptomatic spread which could invalidate the point of a more lethal strain having much lower R_0.
I've linked at the bottom a great video from minute earth with some food for thought on this that I recommend watching, I found it really helpful/interesting.
R0 is not necessarily inherent to the virus (although I think australia might use a more restrictive definition that makes it more inherint to the virus), it's based on our behavior to a large extent. MinuteEarth has a great video (i'll link it below) that discusses how Cholera, for example, stayed very severe and yet had a high R0 because it spread through sewage and the sanitation system was not so great, so it didn't matter whether people stayed home since their fecal matter ended up in drinking water anyway. But after sanitation systems improved, cholera's R0 dropped and the less severe mutation meaning higher r0 thing kicked in since you needed more human interaction to get it to spread again.
So with coronavirus, if it mutates to become more severe, maybe it'll mutate back to a SARS like form where it's super lethal which also means it doesn't spread really far. Both SARS and ebola are on that end of the spectrum. But let's say people get overconfident and think they've beat it and don't stay home in the earlier days of the infection when they're not bedridden yet, you could still get a lot of spread. Or, let's say it becomes more severe, but also gains the ability to survive on surfaces for weeks and become airborne when dislodged. Now, your santation procedure for your instacart delivery is no longer enough and the virus could keep spreading through a lockdown. And then there are diseases like HIV, which are ultimately incredibly severe, but have a latency period that allows for infection to keep occuring even with a mechanism of transmission that is a lot more effortful than accidentally coughing near someone. As you mentioned, the asymptomatic spread aspect has echos of htis, where even though the mutation could be severe, it might not have the chilling effect on transmission you'd expect because of asymptomatic and presymptomatic spreaders.
So long story short, I don't know how likely it is that a more lethal mutation appears, but I do think you're right in intuiting that it is possible. Perhaps there are ways to estimate a probability by running simulations on the genome of the most common types of mutations to see what sort of effects we can anticipate. SARS-COV-2 is very closely related to SARS-COV after all, it's just a slightly different straing, even though the SARS outbreak and the COVID outbreaks look so different. I don't think it's impossible that COVID could mutate to have SARS' severity while maintaining COVID's presymptomatic shedding and asymptomatic spread. Maybe as we learn more about it we'll discover that both come from the same mutation and it's a fundamental tradeoff, but I think it's possible that that's not the case.
Scientists speculate that while this change slows down reproduction and decreases virulence it also makes it harder for the immune system to track down virus infected cells, so it basically slows down the infection. In the long run zoonotic viruses tend to become less deadly. But I wouldn't expect this sort of mutation to be selected for when the number of cases is increasing exponentially.
Q: How close we are to achieving herd immunity?
A: To achieve herd immunity we need 60-70% of the population to carry antibodies to the virus. The results of antibody tests suggest that in Europe and the US, in general, we are in the low single digits
Why does it seem like both sides seem to be so sensationalist about Sweden. They have middle of the road all-cause mortality and most recently their sero studies suggest an extremely low IFR but that got pulled due to bad randomization of test subjects so that might go up to middle of the road for Europe for Sweden too. They haven't performed great and not poorly either. It's strange to see people so polarized over them.
Unfortunately I think that in the US at least the decision to lock down or reopen has become very highly politicized and we are starting to see virtue signalling enter the equation. People now have a vested personal interest in seeing Sweden's approach fail or succeed, in order to reinforce their own political opinions and/or sense of morality.
I find it very frustrating to see the way it's being spun. Firstly, social distancing is not a binary thing that you either do or don't do. Sweden has certainly implemented some social distancing measures and will continue to make adjustments to their strategy as new data comes out. And second, what works for Sweden may or may not be applicable in other countries. The virus spreads differently in different places, and different cultures may have differing attitudes about what constitutes an acceptable risk. I suspect that if Stockholm saw the same sort of explosive growth that was seen in New York, they would have reacted with stronger social distancing policies.
It's certainly good to look at what other countries are doing in their response to covid-19 and ask if there are things that are worth adopting. But I think it's much more important for countries (and states and cities) to be paying attention to their own data... and that is what should be primarily driving their response.
But isn't that the point? They accepted more deaths up front, but over the long-run those countries should average out about the same per capita, while Sweden avoided immediate negative social/economic impacts.
South Korea was extraordinarily well prepared, and it is yet to see if they'll be able to keep this up with international travel resumed.
I am extremely pessimistic about any country's ability to usefully maintain low infection rates while opening up international travel again. Sweden isn't close to being able to do this in terms of tech infrastructure or cultural mindset.
(That being said, if anyone is going to do it successfully long term, it's going to be south korea)
We actually don't know that. Korea has avoided it, for now. People were saying the same thing about Japan and Singapore. But both had outbreaks that flared up. They'll have to keep doing what is working until a vaccine occurs or the disease dies.
But even if its possible to prevent an massive outbreak that doesn't mean its possible to undo a massive outbreak. Korea has prevented large scale community spread by testing and tracing. That has been a successful and preventing an outbreak. But nobody has ever successfully used it to remove a virus from a population after it was already widely in the population.
As stated by others, they are further along in the pandemic in terms of number of people infected. They also have rather large long term care homes and more than half their deaths are in those.
We won't know if that is a winning strategy until a year from now but there is a strong appeal in having not locked everything down. They will be resuming football games with fans and everything at their large stadiums come June.
Whether Sweden is doing well or badly is a big question for the overall debate about how to handle the virus. While I aim my discussion to always be calm, cool and collected as a general rule, who ever claims approach X for dealing with a deadly pandemic is good has to claim some other approach is bad and I don't see how that can avoid being a strong statement if not "sensationalist". Inded, if Sweden had just an average death rate without a lockdown, their approach would be a win, would be preferable. But they don't have an average death rate, they have a much higher rate than comparable countries and their deaths basically continue exponential growth whereas things in Norway seem relatively under control.
-- Fair warning, Italy's death are higher still, of course but Italy isn't really comparable. Even more, Sweden's in the exponential phase and so we don't know how they will go - they providing a laboratory for the world but I don't think human beings should be volunteered for such experiments.
The death rate is clearly not growing exponentially. Try switching the scale to logarithmic in your link. It's basically linear right now based on some other graphs I've seen, but it's hard to tell due to reporting delays. Since the number of people in hospital has been stable for about two weeks now, I would be very surprised to see the daily deaths increase by a lot.
Because lockdowns aren’t sustainable, it’s unfair to compare Sweden’s short-term death rate to countries in full lockdown. Let’s see what happens once the lockdowns are lifted and the next wave of infection takes off.
Netherlands has a much higher density than Sweden (densest country in Europe and one of the densest countries in the world, dense places don't do well once the virus is released, sadly), so it's clearly not as comparable as the countries in the chart (originally put together by Vox). Nonetheless, if you add Netherlands, you'll notice while it has a higher per-capita death rate, Sweden has been approaching it over time.
What kind of density are you looking at? The majority of cases in Sweden are in the capital, so the whole area of the country doesn't matter for anything.
Many (if not most) people have "picked a team" so to speak, and they want to be correct. If Sweden's way proves to be better in the long run, many of those people will have been wrong. Nobody wants to be proven wrong, hence the passion.
First there is definitely propaganda from Sweden or from its sympathizers who see the failure in this crisis as being an example of being wrong in other issues like immigration.
Secondly there are people who try to use Sweden as an example to advance their local economical or political goals.
Third there are people who see this nonsense though and do not want to be in the chain of stupidity.
Re: Sweden, it couldn’t have been a thought-out “herd immunity” strategy because otherwise they would have locked down nursing homes and they admit they didn’t until very recently. Tegnell simply didn’t take it seriously until it was impossible to do otherwise. Not so different from Trump, even if his motivations were very different.
It is interesting to see how "saving the face" is so important in Sweden when other countries around have been much more flexible to adapt to the evolving situation.
> "Could SARS-CoV-2 become endemic among humans and just never go away? What then?"
I really don't see how we can avoid this. I think it will take too long to create a vaccine, and there will be mutations and recombinations that reduce vaccine effectiveness. I'd love to be wrong though.
Just like the normal flu and H1N1 I imagine it may just become part of the yearly flu-shot - I imagine giving a large proportion of the population resistance changes the math considerably on how much it affects us.
Well, anyone who has regular visits to a doctor at all, or has prescriptions filled regularly at a pharmacies, will probably pestered about getting flu shots yearly, at least.
If you are young and healthy, I don't think they are pestering you for your sake, but to build immunity and prevent its spread. Healthy people should really look at flu shots as a kind of duty to their fellow citizens, who may be more vulnerable.
I'm sure it depends a lot on your location and peer group. In San Francisco, where I live, it's very common for healthy 20- and 30-somethings to get the flu shot every year. I try to remember to get it every year, and there's always friends or coworkers reminding everyone about it every year.
Lots of people, I think. My extended family group chat always has a "did you get your flu shots?" thread around October of every year. Last year when I took my family for the shots, there was a line of probably 100 people on a weekday afternoon.
Oversimplifying, it is recommended for people with more than 65(50) years, people with chronic diseases or HIV, and pregnant women and babies from 6 month to 5(2) years. Also people that work or live with them. But each country has it's own rules and recommendations.
I read about the 2017 and 2018 US vaccination rates on the CDC website recently, those years we got an estimated low 40% range vaccination on adults and in the 60% range for children vaccinated.
Last year I was told that we were at risk of, or no longer had, herd immunity due to that. I don't recall if it was specific to our university, city, or other geographical region.
I stopped getting the flu shots in my 20s because I would always get sick despite the shot. I was convinced in my mid-30s to start getting them again. I still get sick, but it's not as bad as when I skipped the shots.
(I know at least a couple times I ended up getting the shot that prevented a variant that we didn't get. There's enough of a time gap that the shot isn't causing the symptoms.)
Some viruses just peter out, but I don't assume this one will just because it's possible. Some virus become endemic, but why would we assume that about this virus either?
There are a handful of endemic coronaviruses, and historical respiratory disease pandemics have consistently become endemic, so it seems like a reasonable assumption.
We're not seeing much in the way of mutation in the SARS-CoV-2 structural proteins. And for other coroanviruses where we've developed vaccines, for dogs and pigs, we haven't had the same sort of problems with having to produce new vaccines that we do with the fast mutating flue.
Now, resistance does fade and to keep your dog protected you need to give it a booster shot every year or two and it might very well be the same with humans and SARS-2. But at least we wouldn't have to play the game of guessing which strain would be dominant in an upcoming season.
We can avoid it by developing a vaccine and vaccinating everyone. It would no longer be endemic in the population by the next generation. If there are no susceptible hosts because everyone is immune either from having it or from being vaccinated against it, it will die out like smallpox.
This really hinges on whether the vaccine confers long-term immunity. If it works like the flu vaccine, then being endemic is inevitable.
It's worth noting that while we have eradicated smallpox, we have only eradicated smallpox. We have not managed to eradicate any other infectious disease of humans.
It's the rapid mutation of the flu virus that undermines the flu vaccine.
People often have differing immunity to a flu based on their past exposures. People that had been exposed to the 1950s strain were not hit as hard by the H1N1 that emerged in 1977: https://mbio.asm.org/content/6/4/e01013-15
Even if we create a vaccine how are we going to vaccinate people in conflict zones? If we can’t immunise everyone with the oral polio vaccine, then we have no chance of immunising everyone against SARS-Cov-2.
There is a possible ecological solution - we drive the dangerous strains to extinction by deliberately spreading a harmless strain. Unfortunately few people seem interested in investigating this idea.
The solution is to use a harmless strain that has gene deletion(s). These sort of mutations are very unlikely to back mutate as the information has been lost from the viral genome.
The harmless strain doesn’t have to spread naturally better than the dangerous strains and it is likely any harmless strain would not spread better. We can artificially spread the harmless strain around so even if it is less contagious than the dangerous strain we tip the ecological balance in favour of harmless strain. This is really how an attenuated vaccine like the Sabin polio vaccine works from an ecological perspective.
The risk of the virus mutating is there right now. It is much less likely that a harmless strain becomes very dangerous than a dangerous strain become very dangerous. This would be a bigger jump in evolutionary space.
Ultimately as the immediate downvoting of my OP suggests this idea doesn’t appear popular. This doesn’t mean that it is not a scientifically valid approach that could work.
There are many more coronaviruses in the wild and we will continue to see pandemics until unsanitary practices like wet markets with exotic animal products are outlawed.
Simian Inmunodeficiency Virus (SIV) could jump to humans, becoming HIV, through the manipulation of raw meat from infected apes.
We have immunity or at least some control over diseases coming from more common species of cattle.
There are many potential sources for serious zoonotic diseases. As long as we keep large number of pigs and chickens in farms there'll be the possibility of a flu pandemic caused by viruses going from humans to animals and back.
I don't believe a 'wet market' is any worse than a confined animal feeding operation in terms of breeding pestilence.
CAFOs have continued to exist through indiscriminate use of antibiotics, but the potential future impact of their practices seems like it's even bigger than the impact of bush meat in a wet market
(Also, the wet markets are not the definitive source of sars-2. I thought the pangolin-as-pets trade seemed to be the more likely source?)
> we will continue to see pandemics until unsanitary practices like wet markets with exotic animal products are outlawed
I'm really no expert and don't know what to think, but Wikipedia asserts that as of April 2020 investigations are still trying to determine whether the Huanan market was really the source of COVID19. Even if it was, can we even conclude getting rid of these markets would solve pandemics as a general problem?
So at this point we can't really say the "fix" is to remove these markets, can we?
Epidemics are a statistical game, not a black-and-white one.
We aren't realistically out to completely eliminate high-mortality pandemics, but reduce the changes. E.g., perhaps we can make the hundred year event a thousand year event, and the population mortality 1-2% rather than 10-20%.
The question is not whether the Wuhan wet market was definitively the origin of SARS-Cov-2/Covid-19 in humans, but whether it, and similar markets significantly increase the chances of a similar event in the future.
> So at this point we can't really say the "fix" is to remove these markets, can we?
Yes, I think we can. Given what we know of how viruses evolve, mutate and the mechanisms by which they move from various animals to humans, we want to minimize the points where people come into contact with large amounts and variety of raw animal matter in highly unsanitary conditions. Wet markets are probably the lowest hanging fruit in that category.
I'm unconvinced that minimizing contact with raw animal meat markets -- in what you call "the lowest hanging fruit" -- would "fix" the problem with these kinds of pandemics. Not until we know they are the major factor in spreading the infection. Maybe it would help, or not, but "fix"?
Note I'm not disagreeing better sanitary conditions are desirable. I'm disagreeing -- or rather, casting doubt because I'm unconvinced -- that [quote] "we will continue to see pandemics until unsanitary practices like wet markets with exotic animal products are outlawed".
If there is a firm conclusion that this was indeed the major factor, sure. My comment was that, according to articles linked to from Wikipedia, the jury still seems to be out on this.
It is known it comes from certain animals, like bats.
So, how can the virus jump from a bat to a human, either directly or indirectly?
Sure, you can randomly run into a bat anywhere in the world. I know a person that found a bat in her balcony some weeks ago.
But the probability that the virus jumps across species is low. You have to increase the odds, and a good way of doing that is creating a wet market full of them.
And it has been known for a long time that those markets were a disaster waiting to happen.
Maybe it happened like that, maybe it didn't. The Wikipedia page on the (possibly) zoonotic origins of SARS-CoV-2 mentions lots of questions and uncertainties, including whether the Huanan wet market was the source at all (because of the raw meat) or simply a place where infected people spread it:
I'm not going to quote every paragraph casting doubt, but take a look at this (from Wikipedia):
> The first known infections from the SARS-CoV-2 strain were discovered in Wuhan, China.[12] The original source of viral transmission to humans remains unclear, as does whether the strain became pathogenic before or after the spillover event.[18][57][15] Because many of the first individuals found to be infected by the virus were workers at the Huanan Seafood Market,[58][59] it has been suggested that the strain might have originated from the market.[15][60] However, other research indicates that visitors may have introduced the virus to the market, which then facilitated rapid expansion of the infections.
Note that "facilitating rapid expansion" may simply mean that because it was a place with a lot of people grouped together, the infection could have spread more easily -- the reason we need social distancing now -- but it doesn't automatically mean it has to do with raw meat of exotic animals.
Now, it can be the problem is raw meat after all! But it seems to me research is still ongoing about whether this was the real culprit. That's all I'm saying.
> Serological evidence for SARS CoV in human beings working in these markets, taken together with the earliest cases of SARS in restaurant workers, supports the contention of a potential zoonotic origin for SARS. WHERE NEXT? Will SARS reappear?
I'm not saying we should discount this, and in fact it's a reasonable hypothesis.
But the fact remains it's still under investigation; we do not (yet) know where and how it originated for certain, or whether the origin was an exotic meat wet market.
Even that bats were involved is not certain.
If we do not know this, we cannot know whether closing exotic meat wet markets is a major thing we can do to stop these pandemics.
Ah! The blame game. I'm uninterested in the obsession with blaming the CCP for everything. This and similar pandemics are mankind's problem. China and the ruling party want to solve it too, regardless of how they initially (mis)handled the situation.
We may or may not find patient zero and/or the root cause of the pandemic, but blaming the CCP is pointless.
It's not like other huge parts of the world don't have raw meat wet markets with unsanitary conditions, either. And that's if they were the cause for the pandemic to begin with.
> There are many more coronaviruses in the wild and we will continue to see pandemics until unsanitary practices like wet markets with exotic animal products are outlawed.
Before trying to find a global definition for "exotic" we could start with washing hands or not sneezing or coughing at people nearby.
Sneezing and coughing, sure, but lots of folks don't have easy access to clean water, a problem that is likely to exacerbate over the next few decades. Excessive hand washing among the people who do isn't gonna help a lot particularly in drought-prone areas.
I don't think it is a bad idea to keep looking for ways to prevent these outbreaks as close to whatever their origin is as possible.
Note that in some very poor countries (India comes to mind) it's not at all clear that more total lives are saved via lockdowns since they will result in famine and all sorts of other terrible consequences.
In Africa folks are worried about a huge spike in malaria that could dwarf the projected CoVid impact in certain populations.
Every country for themselves and the current lockdown strategies are what we are gonna get, and I'm not angry about it since the action-reaction-logic of all of this is pretty straightforward, but it's not at all quite clear to me that it leads to the fewest number of human casualties vs just some local minima.
> Excessive hand washing among the people who do isn't gonna help a lot particularly in drought-prone areas.
I am a European who has been living about 100km north of Western Sahara for a few years now: People here wash hands much more often than Europeans or US Americans and they know how to do so using much less water. More often than not, in restaurants, with European guests, I have to point out that "I am going to wash my hands" before eating so that everyone does it - despite locals and me visibly having done so when entering the restaurant (that all have facilities to clean your hands in the dining room or directly at the entrance).
In Berlin, for 15 years I was pissing people off by pointing out they did not wash their hands after using the restroom. Pro tip: Wait until they are back at their table and then congratulate their friends on having such a close group where nobody minds sharing a bowl of peanuts with the guy who just did not wash his hands...
> I don't think it is a bad idea to keep looking for ways to prevent these outbreaks as close to whatever their origin is as possible.
Not at all, but let's not forget that these markets are the only ones in a lot of places. People rely on them for food and income: Where I live the next proper supermarket is a 2.5h drive either north or south. People from small villages walk to the closest souk (market) once a week to sell their goods.
Furthermore, whenever people in the first world blame "unhygienic wet markets" that sell "exotic food" I am very careful:
* What's exotic for a US-American might be a staple for someone else;
* What the tourist buys might be something the same vendor would not dare to sell to locals (but tourists leave after a few days, so no impact on the customer base);
* Preparation matters: Down here meat is always well done and vegetables are always cooked to death. Notable exceptions: tourists who explicitly order meat medium or medium rare.
So, given that the markets are essential for the locals and that we 1st-world citizens cannot maintain a decent hygiene, I still think we should start with ourselves before banning "exotic" behaviour.
It should be noted, with respect to acquiring immunity, that with SARS-CoV(1), the amount of time after which immunity theoretically could be lost would be => 3 years. If SARS-COV-2 offers a similar level of immunity, that may not be a ton of time, but its not insignificant either, especially if a vaccine could be developed within that time frame.
This is what worries me the most. More research needs to be done, but if you can get reinfected it seems like herd immunity is a pipe dream. If immunity doesn't last long then does a vaccine even work? Now I am very clueless on all this so I could be way off. In fact if someone does know more about virology and could explain to me where I am wrong that would be great!
If you get reinfected, can you expect the same level of severity? That's what I'm wondering. Does having antibodies for a a virus that's very close, but not quite exact result in less severe symptoms and/or a quicker time to showing symptoms? If so, that doesn't necessarily help the spread greatly right now, but it does point towards a time in the future where this virus actually is more like the regular colds and flus we are used to.
Depends on the virus. For diseases like dengue you get antibody mediated enhancement of the infection, making it far worse, so the first time you're nearly asymptomatic and the second time you're on deaths door. For other diseases, even partial binding helps make the disease more mild. Biology is super variable.
It maybe more that immunity within the body fades quickly, not so much that the virus mutates to the point it's different enough. The linked article talks about a sharp drop-off of coronavirus antibodies over time, which doesn't happen with antibodies for some other viruses (e.g. varicella antibodies are lifelong). And it doesn't sound like we really know why this might be.
For coronaviruses subsequent infections seem to be less severe. Some scientists speculate this coronavirus might not be intrinsically any more virulent than the 4 common cold coronaviruses, it's just that with this one we weren't able to train our immune system to handle it in childhood.
Well the article oversimplifies the linked source quite a bit in my opinion:
The article says
>Volunteers experimentally inoculated with HCoV-229E showed a steep decline in antibody response over time, and the majority could be successfully reinfected a year later.
while the linked source for that 1990 study says that while the 10 study participants were reinfected, none of them developed colds a second time, and the virus shedding period was much shorter.
Immunity will presumably last at least a few months, and the problem always reaches its greatest severity in the winter months because people are indoors more. We will just default to the influenza model, where there are circulating betacoronaviruses every season and we try to predict and vaccinate against them. The Middle East deals on and off with MERS.
Presumably immunity goes away once the antibodies are gone, but does the body remember the virus for next time? Assuming the virus does not mutate too much from year to year, at what point will it not be novel anymore to the human body? Will subsequent infections be easier for the body to fight?
From what I understand you build some resistance as you are exposed to multiple variants of the same flu virus so it's quite possible this would hold for coronavirus making refection less likely to lead to a severe infection.
Lets also not forget that there is likely to be well studied effective anti-virals at some point like we have for the flu today.
If you’re not a biologist, it may have flown under the radar that there’s quite a bit of stem cell work going on already.
The development of induced pluripotent stem cells (iPSCs), which can be made from adult tissue rather than embryos, sorta sidestepped much of the ethical debate. They’re not exactly equivalent, but iPSCs have opened the door to a lot of exciting research because you can culture tissue that’s very similar to a patient’s. A few clinical trials were starting to get underway too....
Some people are looking at antibody studies that show that large parts of the population are somehow affected and then doing back of the napkin math and deciding that this is really not worse than the flu in terms of death rate. They are further encouraged by the fact that people that die tend to be older and with pre-existing conditions. Then they say we should open everything up and get everything "back to normal", and sometimes they add that this is just a way to winnow out the old and the weak.
As problematic as the latter statement is, the above thinking is actually dangerously optimistic. Experience shows us that in specific situations with prolonged/repeated exposure, the death rates are much higher. Also young and healthy people may get seriously sick and die due to high level of exposure.
This has already been happening in hospitals that did not have sufficient protective equipment/procedures.
If we open everything up and get into a situation where the virus is all over the place we can get into a horrible spiral of increased exposure and increased death rates etc.