I don't think that HN is a good venue for discussion of specialized preprints that have highly surprising results, in topics that are moving extremely quickly.
Too few people in this community are able to evaluate the information contained, which leads to lots of pointless speculation, and lots of misinformation. Despite working in biology for 20 years, I would not trust any of my own interpretations of this pre-print.
The only people who I would trust are named specialists in this field, that are willing to stake bits of their reputation on what they say.
The only venue where that is happening in the public is on Twitter.
I'm going to throw in my two cents as a medical student. There's no way that I could give you a lucid digestion of whether or not this paper has any significance after studying medicine for thousands to tens of thousands of hours. These topics are highly nuanced and incredibly specific to a certain domain of medicine/virology.
Your point on disinformation is also salient. I've noticed that many followers on here are intelligent, but being able to synthesize the Wikipedia article gives one the basics on a topic. There are medical theories and philosophy that contradict normal thinking, but are the fundamentals of practice. I've engaged multiple users on another account about medical principles but was shocked at how resilient people are in their claims when they seriously understand math/statistics but don't understand the medical application of those statistics; the example I can think of is I know what ARDS is, the treatment guidelines for it, how intense the nursing care is, but how many people here have ever watched someone be intubated, let alone do it themselves? There are a lot of intangibles that aren't directly written in a Wikipedia article or cannot be fully realized without actually experiencing them.
I remember learning about the 10,000 hour rule, in that spending 10,000 hours doing something one becomes a master of that domain. After my experience I can say that is not the case with medicine, which has shown me serious humility.
> but was shocked at how resilient people are in their claims when they seriously understand math/statistics but don't understand the medical application of those statistics;
> but how many people here have ever watched someone be intubated, let alone do it themselves?
I am not sure I understand the connection you are trying to make here. Are you saying that just because someone understands statistics they cannot understand medical application of statistics b/c they have no experience physically working in the field? Just looking for a little more clarification on the point you are making.
I am genuinely interested in learning about multi-disciplinary disconnects in real life, because these seem to be the some of the biggest problems we face in progress today.
I want to start by saying, I appreciate your curiosity :)
I think my point above was talking about COVID. The specific example was where I was describing how at scale COVID was going to be a massive problem and have an increasing case fatality ratio as the virus spread. The reason for that is because ~19% of people, I'm probably out of date here and frankly don't feel like looking at Uptodate, go into ARDS. ARDS usually requires high flow oxygen therapy or mechanical ventilation. High flow oxygen essentially means you're hospitalized on a standard medicine floor costing ~$5k per night whereas mechanical ventilation is $10k with crucial nurses managing. A tertiary care hospital in your local probably has between 50-200 ICU beds. Rural hospitals will have 10-30.
Now the the disconnect here is with the statistics. Early estimates were putting COVID at 2-4% CFR because when you have practically unlimited resources you can save the overwhelming majority of patients. But as incident rate increases those supplies become saturated. ARDS is an intense symptomology to treat, this isn't just a cold and it is a tonne of resources. Also, the recovery times from pneumonia that leads to ARDS is usually measured in the months from initial hospitalization. Then on top of all of this COVID has a reproducibility number of 2.5-2.7, but now we're thinking it's actually around 3. Influenza is ~1.3 for reference.
So the key points of why I was afraid:
1) ARDS is life threatening
2) ARDS requires intense nursing/intensivist (ICU doc) care
3) ARDS takes months to recover from
4) COVID has a crazy reproducibility number
Here on Hacker News there are many mathematicians and statisticians who have done centuries of work, so I was told that making an assumption this early was a fools errand because the numbers were not painting the picture that I was describing: a very bad pandemic. I think I was told that because the consequences of a viral pneumonia are not common knowledge and there is a lack understanding of what entails a viral pneumonia. But the main crux of my argument was that the CFR was going to rise from the reported 2-4% all the way up to 5-10% based on the percentage of complications that were occurring. In Wuhan the CFR is 5.9% and there's still 2-3k people on ventilators months later (on top of the fact that in the American medical community there's accusations of a manipulation of those numbers....). The CFR in Italy and France at ~10% at the moment, if not higher.
I hope this explains the entire crux of what my point was earlier. I didn't want to get into too many specifics so as not to offend anyone.
It’s like if someone came to you and asked you to deploy some software so that if someone calls 911 from a cellphone their location shows up on the dispatcher’s terminal. In 2006.
“It’s just software” they say, “I’ve already written it, how hard can it be to deploy it? It’s only a few thousand lines of code!”
There has never been any "10,000 hour rule". In his book Outliers, Malcolm Gladwell misinterpreted and oversimplified the research into learning and training.
Honestly, I never really thought that the 10,000 hour thing was that lucid to begin with. Certain things are mastered in hundreds of hours while others are "never truly mastered". When I say I learned of it, it was reading the New Yorker article and then hearing it from my favorite kind of philosopher: stoned ones.
Twitter is often extremely useful for scientific fields, and in many ways is perfect for it. You can post a figure and legend, tag people that may find it interesting, and start threaded discussions. It's all in the public, with no invitations or closed doors, so it is open to discovery by that dozen or two dozen people in the world that may be interested.
Science is the ultimate long-tail of super-specialized interests with extremely small audiences, and Twitter is perfect for connecting those people with extremely esoteric interests.
There is a lot of crap, but science Twitter is also the only reason I'm on it. Sadly, my own biases against Twitter Kept me off it for 8+ years, but after I started finding the right people to follow, a whole new world opened up, and it is now a vital tool for me to navigate the literature and learn quickly which new tools are best.
>There is a lot of crap, but science Twitter is also the only reason I'm on it. Sadly, my own biases against Twitter Kept me off it for 8+ years, but after I started finding the right people to follow, a whole new world opened up, and it is now a vital tool for me to navigate the literature and learn quickly which new tools are best.
That's really interesting, I've been avoiding Twitter for the same reason, but I can see how it'd help keep up with fast-moving niche fields. Maybe I'll give it a try, thanks!
I don't know of anybody that uses Facebook for science discussion, but I did know many that were using Twitter for science, which is what finally drew me in.
Facebook seems like a much worse fit than even Twitter for discussion, but I would potentially check it out if somebody I trusted had found it useful.
There are plenty of blue checkmark specialists in these fields on Twitter who are ready to go to critique and contextualize their field. Of course the issue on Twitter is A) finding them B) filtering the low effort and bad faith trolling in the replies.
Other than twitter, I'm not sure where else you can find that audience that is accessible to a layman.
Slightly off topic but I once had a question at work on a very niche corporate finance topic. So I logged onto Twitter and tagged Aswath Damodaran in the question and had the world's foremost authority in Corporate Finance respond in like 30 minutes with a detailed answer. Twitter can be amazing for finding specialized expertise if you know where to look.
That is indeed the magic of Twitter. I’ve mostly avoided it since the last presidential election but prior to that my ability to connect with people doing interesting things all over the world was incredible.
I don't know, I find pseudo-anonymized, but (mostly) civilized and on-point debate that touches varying spheres of sciences as well as degrees of accuracy on them, quite valuable, too. It could probably be more "valuable", if all posts were anonymized, but then it might entail all the dangers that 4chan reminiscences about.
Sometimes, reputation blocks science too, e.g. applied in reverse, the reputation-seeking prevents many false-hypothesis confirmations, because they're less likely to propel a career (or damage it).
EDIT: ...come to think of it, the scientific method is in itself reputation-agnostic.
EDIT2: ...imagine a world, where all science was public, open, but anonymized. No patents, no proprietary research. It's a dystopia for some, and possibly a utopia for others.
> The only people who I would trust are named specialists in this field, that are willing to stake bits of their reputation on what they say.
That is basically the antithesis of the enlightenment and the whole idea of the scientific method. You should not trust experts because they say so, you should trust because they are able to present evidence which is persuasive and reproducible. Even experts are wrong, and the history of the N95 mask illustrates this in the case of a relatively unknown Wu Lien-teh being correct over the objections of the prominent French Mesny. In less contemporaneous things, it took a long time in North America for gluten to be recognized as the cause of Celiac's disease because too many people there trusted the expertise of Sydney Haas who asserted that eating bananas would cure the disease.
I trust evidence and citations to evidence. Experts are generally willing and capable of providing those easily and so experts generally quickly earn my trust. Assertions based instead only on claimed or even actual expertise do not earn my trust and often arouse my suspicion.
That is very useful information, and explains why this preprint got so much traction here, I guess. I would have rather seen a post that's aimed at a more general audience, perhaps from the company blog or similar. It would have been able to provide the proper context to this audience, which is not an audience that is monitoring MedRXiv or has the skills to understand what this preprint means.
> I don't think that HN is a good venue for discussion of specialized preprints that have highly surprising results, in topics that are moving extremely quickly.
Then close the site, it is useless.
But I thing the premise is 100% wrong.
People are absolutely able to evaluate reputation and evaluate comments amongst the internet and collate them here.
Currently this as a working model is not happening for C19 though and needs to be fixed.
Or you are right HN is just a Reddit clone and pointless.
Well, yes. Even areas of the world with high levels of testing and low levels of infection are going to be missing some cases. Here in MA where a full 30% of tests are coming back positive[1] it would be surprising if actual infections weren't a multiple of confirmed cases. But things are probably much better than they were in February where estimates of the ration are that we were factor of 100 or more behind actual cases.
On the graphic it's "29% of todays tests were positive", not of overall tests which indeed stands at 19.94% positive (18941/94958). The graphic is incorrect with 16% of all tests positive.
EDIT: Creator of the graphic is /u/oldgrimalkin who posts these each afternoon in /r/CoronavirusMa
I live in MA and got very sick on Feb 26, then had a horrible cold. My wife is a doctor, and she thought I just had one of the many things going around.
I asked her if it was COVID-19 and she looked at the CDC's web site and said she didn't think so. Then a week later she flew out of Logan to spend a weekend in LA. I also went skiing in New Hampshire twice, and went to two networking events!
Throughout March I had symptoms that I never had in my life... I couldn't get a test! The symptoms went away after 4 weeks.
Did I have it? I have no idea, but if I got it, it most likely came from her or my kids, who all felt kinda wonky in mid February. My wife had a very bad headache two weeks before I got sick.
In Germany, the lead virologist in Berlin said that in the beginning they went after cases like yours, testing people who had weird symptoms in February, or even late January, because the hypothesis that the virus had been circulating in Europe for quite some time seemed plausible at the time. None of these cases tested positive.
I'm not saying you didn't have COVID-19, just that it's very unreliable to draw any conclusions from anecdotal evidence like this.
Absolutely, I also had a strange flu that could have been it in early to mid February. First I dismissed Covid,but later I did find a one hop link with someone who was tested positive. But until I can get tested (or my intermediary) its just guesswork.
None of those cases tested positive, but what kind of test did they have? PCR only identifies an active infection. Need antibody testing if not currently infected.
I don’t know. I can only assume they took this into account. I don’t want to be condescending, but do you really think that you just thought of a rather trivial catch that a bunch of expert virologists didn’t think of?
If they did PCR tests, and didn’t consider that N days (I don’t know the number) after infection you don’t have virus RNA anymore, they’re stupid. Really stupid. If they did think of it and now the guy claims this proves there was no virus flying around, he’s simply lying. Until shown otherwise, I will assume that the leading virologist in Germany and a respected public figure is neither stupid nor lying.
Same! In mid-February I went to a party. A couple of my friends were getting over "a really weird cold" that "everyone in the office had". A few days later, I was sick with the same symptoms, mostly a dry cough. I thought nothing of it except that it was very unusual for the kinds of colds that I usually get (I am a sore throat and aches guy, so I was thrown off by not aching and having a cough). I had this for a couple weeks.
I wasn't working at the time, but it was minor enough that I would have gone to work. That is also very rare for me, usually I am out of commission for a week when I get a cold.
Was it Coronavirus? I have no way of knowing. But looking back, it seems very suspicious. An extra-infectious cold with the same symptoms of Coronavirus going around the New York office populated by people that travel internationally extensively? You have to wonder.
I kind of assume that Coronavirus cases are massively underreported. Given that 20% of cases are people without symptoms, what would prompt them to get tested? And all the advice I've read is along the lines of "if you think you have it, don't get tested, just stay home and get over it". With that advice, I have to assume that many cases are not accounted for in the official data. It does seem strange to me that if Coronavirus was circulating in New York in mid-February that it didn't show up at all until early March "officially", though. It's unlikely that not one person would have severe symptoms. For that reason, I assume I'm not immune and am self-isolating like everyone else... but if I can get an antibody test, I would love one. I am very curious as to what happened there.
One thing about case reporting is that they tend to ignore the denominator, the number of tests.
I've been tracking DPH reports in our state since they started, and one thing I've noticed is that although the case counts have gone up, the probability of testing positive has remained roughly constant. It's increased slightly here in the last week or so but not a lot.
One thing this suggests to me is that at least here, the virus was present in significant numbers before they started testing, or at least in similar numbers.
If you combine that with consistent reports of substantial fractions of asymptomatic carriers, it seems very plausible to me that the virus was circulating before authorities in the US started tracking it.
Even if it wasnt Sars-COV-2, something odd was going around as early as December and January, all over the country. Everyone who got it said it was like nothing they had before. The cough was horrible, and it caused headaches in less symptomatic people.
I'm kind of glad to hear other people reporting similar events. I too had a really weird cold in Jan/Feb that left me coughing and very short of breath after simple activities like running up the stairs. Before the lockdown, I was a 5-day-a-week gym-goer, so this was very unusual.
It wasn't until the shutdown occurred that I read about the symptoms and noted that shortness of breath was a tell-tale symptom. I also worked at a place with offices in Shanghai and many Chinese nationals working locally.
Just chiming in to say I had the same "weird cold" at the end of February, all the way in Israel. I had just a day of a minor fever but before and after I had an exceptionally sore throat, coughing, general lack of focus to really do anything, and somehow no stuffy nose etc. at all. I'm used to some colds hitting worse at first then transitioning to a real cold afterwards, but a week later I only had the cough left. I didn't go to work those two weeks because of that cough, which got better but lingered for another (3rd) week.
And now I remembered 5-7 days before any cold-like symptoms started, I was at a couple work functions that included our entire US office. (So there's the possible trans-atlantic link)
I'm also waiting for an antibody test purely because of that weird experience.
Sounds similar to what happened to me, I had a dry cough come on around March 17 and initially thought it was allergies, but those aren't my normal symptoms (sneezing and itchy eyes). I had heard enough rumblings about asymptomatic cases that I decided to completely isolate until it went away just in case. The cough got moderately bad the following weekend and then slowly cleared up over the next week and a half. The only other thing that was any different than normal was that my appetite was roughly half of what it normally is but I chalked that more up to just being home all the time and not doing a whole lot.
My mother-in-law had an awful fever and dry cough unlike any I've ever seen in mid-February that lasted for ages. Chalked it up to the flu. Went to the doc and everything, but this was before Covid-19 had officially landed anywhere near us.
It's certainly possible that it's been around longer than expected, growing exponentially, hidden in the flu season, but we just recently reached the exponential turning point that makes it a big problem. It only starts killing when it's saturated enough of the population that the at-risk start dying in greater-than-usual numbers, which might take quite a while even with a relatively fast doubling rate.
The same here. I maybe had the virus. Symptoms that felt different, but nothing to worry about, a little headache and a little cough.
So I never got tested.
My wife and kids also had this but also nothing to worry about.
And at the same time other Carona types are going around with mostly the same symptoms. So who knows what we got.
But when it turns out people get resistant after having COVID-19 I would like to know if I had it. Because then I don't have to worry anymore about infecting others.
I had a similar experience and I really would love to know if I had COVID-19 or not.
I did some work traveling in the US Minnesota <-> North Carolina late January into February and came down with a flu-like thing.
I say flu-like because I had some symptoms you'd just say was seasonal flu except I had a few other things going on that were unusual. Shortness of breath and dry cough with low fever.
The condition was persistent but mild, it lasted about two weeks except I _STILL_ suffer shortness of breath.
After I came home I'm pretty sure I passed this along to several people despite usual "I'm sick, stay away" considerations (pre social distancing days), several coworkers and my wife got sick.
Antibody tests can't come fast enough. I'm sure this thing is/was far wider spread than thought.
My family lives in MD, and same thing happened to us in Feb. A child in our daughter's daycare came down with severe pneumonia and ended up in the hospital, our daughter was sick with diarrhea and fever for a week, and my wife caught a bad cough that lasted for weeks and had trouble breathing.
Thing is, we cannot know at this point whether everyone already has covid-19, since there are no anti-body tests. It is a live possibility, but meanwhile we are shutting down the world's economy.
We know when Coronavirus entered the US and the serial interval, and can estimate via phylogeny how big the population of the virus is. The phylogenics+excess deaths are ruling out a mass infection that no one died from.
How do we know when covid-19 entered the US? How do we know the R0? R0 is continually being estimated upward and death rate downward. We don't seem to have much clarity on any of this.
Another problem is if covid-19 was already widespread, it would have been misclassified before the huge spotlight. So, increase in cases and deaths could be misattributed.
If there is an overall increase in excess deaths, we still have a question of causality. Could the measures we are instituting themselves contribute to deaths? Just a lot of questions and lack of clarity in this matter.
In terms of tracking all the chains, because of the dearth of testing in the beginning, I would suspect any shorter chains of transmission that didn't end in a super-spreader could easily be missed.
It is hard to get tested even now. It was essentially a catch-22. You could only become tested if you had contact with a proven case. But there were almost no proven cases, because you can only become a proven case if you had contact with a proven case.
I don't know what the glass infiltrate is, but morgues overflowing could be a symptom of the government shutdown. For example, in Ecuador, there are bodies just lying on the street because the shutdown and general alarm about the virus means there are less people removing the deceased. The deceased are themselves not necessarily dead from covid-19 (although the news article headlines are worded ambiguously in that regard...).
In general, I see a lot of confusion and lack of clarity, along with cherry picking stats and stories to support a catastrophe narrative.
It is very unlikely COVID-19. Stanford did a study and showed that the prevalence was very low in the early period even if you had respiratory symptoms and common viruses had been ruled out: https://news.ycombinator.com/item?id=22824878
People do lots of stuff sick. That is why we have pandemics. Do airlines refund your ticket because you're feeling a little under the weather? Nope. So you infect the entire plane-load of people. Do bosses or customers like it when you're gone for two weeks because of a cold? Nope. So you go to work sick and a week later, everyone in your office is sick. The incentives are always aligned towards loading yourself up on cold medicine and going about your day. No company is willing to take the financial hit for public health.
If people disappeared into self-isolation whenever they had a sniffle, many diseases would be completely eradicated. They don't, so they aren't. (Yes, I know the flu can jump between humans and birds and back, so isolation wouldn't eradicate the flu. But a lot of other diseases would be completely gone.)
I don't think this is right. Getting sick significantly more or less can be a drawback at the individual level. Your hypothetical self-isolating people would be more sickly.
Most of the work humanity does against a given pathogen is in getting sick. We've recently automated that. But our immune systems are still out there fighting the good fight every cold/flu season.
The ideal season for an individual is one where you get exposed but don't develop symptoms, not one where you never get exposed. Not getting exposed is like missing a ski trip-- a terrible outcome to be avoided at all costs.
My wife occasionally works in an emergency room, so the advice she gave me is the same advice that anyone else with the same symptoms would have from a doctor following the CDC's instructions.
She just thought it was a seasonal virus.
Edit: It wasn't until mid March that we (MA residents) suspected it was in the wild. Basically, there was a reported case that came through Logan airport in February, and then when it came out that the incubation period was 2 weeks and many cases just resembled a bad cold, everyone started to suspect that there were a lot of asymptomatic cases in the state that we didn't know about.
I had this too around the same timeframe. I have a condition which lets me "feel" ferritin spikes and it was the biggest one of my life. It took me 4 weeks too and then another 4 weeks to get over the ferritin feeling.
I dismissed it as the flu because of a runny nose (not a typical COVID symptom). But apparently a lot of flu patients have COVID because it's more contagious and why wouldn't they?
My plan is to continue self-isolating and try to nab one of the serological tests (if they ever do come out) which will tell you if you've had it.
How did you get rid of the excess ferretin? Just waiting it out?
I'm trying turmeric because something is making me not get rid of this thing and the excess ferretin it dumps in the blood seems plausible. I've had on/off fevers for weeks.
The other reply nailed it. There is a sort of calcium "hack" your body has for binding to the iron. Try IP-6, colostrum or milk/dairy. At some point your body just stops being able to do it, though. IP-6 to me seems to work even past that point.
Past that, mitigating absorption with green tea seems to help a bunch. And avoiding breakfast cereals. And boxed pasta. I haven't tried turmeric. Despite hearing good things, it seems difficult to source. Everything else pales in comparison to phlebotomy. Of course, you can't donate if you've got on/off fevers.
Also there's some relationship between vitamin D and iron. I'm not clear enough on that to recommend it just for iron, but I will say I do supplement with it, especially through the darker parts of the year.
If you want to drop your ferritin levels, lower your iron (if that is safe for you). The body has no way of dropping iron levels apart from chelation. So, drinking/eating foods that act as natural chelators (ie. black tea) will help. Or, if you're feeling particularly generous, give blood.
(not a doctor, just someone who has hemochromatosis.)
> MM and NG are cofounders of Biobot Analytics. EJA is advisor to Biobot. NE and CD are employees at Biobot. All these authors hold shares in the company.
Another comment suggests that Biobot is YC. As far as I can tell, Biobot has never posted a Launch HN, but they did post a Covid page 3 weeks ago:
They were in the news in 2018 for testing wastewater to measure the opioid crisis, but I can't find any HN discussions about any link or story that I can find myself, or from their list of media posts.
According to the Heinsberg Study in Germany, the infection rate was as high as 15% and the mortality rate in the town would be as low as 0.37 per cent.
Germany launched the Heinsberg Protocol study to examine the rural town of Gangelt in the region of Heinsberg, where the first virus fatalities occurred.
During recent weeks, his team completed substantial research conducted through surveys and investigations in homes across the Heinsberg region - where more than 1,400 confirmed cases had been reported. Heinsberg has an approximate population of 250,000 inhabitants and has confirmed 46 coronavirus-related deaths.
These research findings have already provided some indication on how the virus works, as Streeck clarified:
“There is no significant risk of catching the disease when you go shopping. Severe outbreaks of the infection were always a result of people being closer together over a longer period of time, for example the après- ski parties in Ischgl, Austria.” He could also not find any evidence of ‘living’ viruses on surfaces. “When we took samples from door handles, phones or toilets it has not been possible to cultivate the virus in the laboratory on the basis of these swabs….”
“To actually 'get' the virus it would be necessary that someone coughs into their hand, immediately touches a door knob and then straight after that another person grasps the handle and goes on to touches their face.” Streeck therefore believes that there is little chance of transmission through contact with so-called contaminated surfaces.
There is substantial criticism mounting directed at the Heinsberg study [1]
- Immunity tests used might have shown false positives. So the 15% might be too high.
- Results of the highly infected town Gangelt are not transferable to whole Germany with lower infection rates.
- The author of the study is inflicted with a marketing agency, which is at least uncommon in science.
Own comment: The danger SARS-Cov19 remains in the speed of spreading due to missing herd immunity (in contrast to the common flu). 0.37 per cent is still a lot. USA: 327,200,000*0.37% = 1,210,640. Social distancing remains the single most effective tool.
There is always substantial criticism of any minority position in science, it's a subculture full of bullshit politics like any other. Also see my other comment - 15% could just as easily be too low:
Just to add a bit more context regarding the now often cited study of Gangelt (some questions where raised re methodology and esp the policy conclusions):
it is a good start & germany is doing now many more serological studies (also to monitor over time) and hopefully we'll soon gain more confidence re status quo and what it means
The recent case of 45/60 choir members contracting coronavirus after actively practicing social distancing contradicts this unusually confident assertion that it's hard to contract the disease.
That seems consistent with GP's claim. I'd classify 2.5 hours of choir practice in the same risk category as a ski party, considering that the choir members are standing next to each other, constantly ejecting virus particles, and taking deep breaths.
There's not some magic involved where the virus gives up after exactly 6 feet.
6 feet was chosen as a matter of policy because it was the most you could reasonably get people to stay apart. Sidewalks, store aisles, elevators, etc, are all about 6 feet wide and so it's a good number to convince people to cross the street or wait for the aisle to clear. 100 ft would be a much safer number but that's just not really physically reasonable (and so the guidance would have been dismissed by the public).
And crucially, the context of the shared space makes a large difference. You simply cannot compare 6ft. outdoors with lots of ventilation vs. indoors and forced air vs. indoors and no ventilation.
The choir practice should not be an example of how easy it is to spread; rather, it should be an example of the unreasonable intuitions people have about 'distance'.
Remaining in close contact, indoors, while singing, for a long period of time is not a good idea. It is quite reasonable to expect that to lead to transmission.
Similarly, two people passing by each other on a sidewalk, with nose breathing and mouths closed, even if it's closer than 6 ft., is a very small risk. Still good to maximize space, but nothing to get worked up about.
Singing is also likely to expel more droplets further.
I don't have a source, but a microbiologist I know was saying that safe distances, based on droplet physics, depend on activity, e.g. standing in a single file line vs walking vs hiking vs running.
Where did the article (https://www.latimes.com/world-nation/story/2020-03-29/corona...) say they maintained a 6 foot distance? If anything it suggests they were closer (foot between chairs, people weren't spread throughout the room but close to front).
Regardless, doesn't matter. Singing/shouting/chanting with a high density of people inside a closed setting is dangerous for any repository disease as viral concentration just keeps building up. Same thing happened with Shincheonji on a far larger scale.
"Members of the choir were already aware of the COVID-19 outbreak in their state, particularly around the Seattle area, which is about an hour south of Skagit County by car. Hand sanitizer was dispensed at the door of the practice that night in March, no one shared sheet music, and people were conscious not to stand too close to one another or engage in their huggy greetings. Also, no one remembers anyone coughing or sneezing, and no one present felt ill at the time. Nonetheless, a huge percentage of people present later tested positive for the virus."
My point is that the original article said that it's hard to get infected. Assuming that everyone was asymptomatic, and there was no coughing or sneezing, and everyone stayed away from each other, it's actually not that hard to spread the infection. In fact, if there was a single person who was asymptomatic and they infected 45 people, that means it's very easy to get infected.
From the LA Times article: "At one point the members broke into two groups, each standing around separate pianos to sing.". If you've ever watched a choir practice, this likely meant everyone facing inward toward the piano, and you can't stand too far apart because you need to hear everyone else to harmonize and adjust your volume. Singing loudly is probably only second to sneezing in terms of projecting atomized 'stuff' from the respiratory tract into the air. So there were 30 people standing in a circle spraying droplets directly at each other.
It may very well be that it's very easy to spread this virus, but I don't think this incident is a good indication of that. It seems more an indication of how poorly even well-intentioned people understood the contagiousness and what exactly social distancing meant at the time this happened (1 month ago).
I suspect that the risk increases the longer you're in an enclosed space with someone shedding the virus. Thought experiment, if spending two hours in the church with people singing meant 50% got infected. Then spending 5 minutes assuming it's linear (and it likely isn't), is only a 2% chance.
Brings up the difference between public health risk and personal risk. Public health perspective you want contacts to be infrequent and importantly short.
I'm not sure how to interpret hard vs. easy in this context. The measures they took to protect people (not touching) has no effect on the real risk (shouting/singing in a crowded room), which again should have already been known at this point in time to be a major risk factor (Shincheonji).
That is this evidence doesn't contradict Streeck arguing that formate transmission is unlikely and that it is long term exposure to breathing people that is the real risk. (Or that being in a relatively empty grocery store provides little risk)
(I don't have a clue one way or the other, just commenting on applicability of evidence)
Walking 6 feet past someone has a low risk of transmitting the virus to them.
Standing 6 feet away from someone for an hour... Is another story.
Also worth noting: My wife has worked with a lot of community choral groups. She is convinced that they took all reasonable precautions, but doubts that their rehearsal space was sufficient to accommodate everyone standing 6 feet apart from eachother for the entire exercise... Or even for any part of it.
I leave it as an exercise to the reader to work out what this means for the typical tech firm's open office layout.
They mention “certain distance” which I suspect is 3-4 feet at best but frankly even 6 feet probably isn’t enough for people singing loudly in a confined environment for a long period of time.
But it's not the same as a ski party, where people are mingling together. My entire point is that the original article downplayed how contagious it is, but even following social distancing guidelines, there was an enormously high infection rate.
Getting into a large room with a bunch of people and singing isn't in my mind following social distancing guidelines, even if you're not as huggy as usual.
Also this is self report of behavior after people did what was in retrospect a very stupid and risky activity.
When you’re singing loudly, full-throated, with deep breathing... that seems like an ideal scenario for a respiratory illness that might not mean much for the general population.
I am not sure if it’s even possible to give the fatality rate before everything is over because we don’t know if an infected patient eventually dies from the disease with a long delay. This is why I totally expect a fatality rate that is higher than we can observe today.
An asymptomatic infection should still count as an infection, so it should lower the infection fatality rate. I don't have expertise in this area, but I think both infected fatality rate and symptomatic fatality rate are useful.
For the study, they tested a representative sample that includes asymptomatic cases. Hence, one can assume a known, constant number of infected cases. And to complete the study they should, as far as I understand it, wait until they know how many of those infected die in order to calculate the fatality rate. I don’t think it’s relevant here if further people are infected after testing for the illness, and there shouldn’t be a need to monitor the new cases or even check if they die (it shouldn’t be necessary for the study).
That quote about shopping being safe doesn't seem to have much support, and frankly sounds very dangerous if taken too literally.
In fact existing outbreaks COVID-19 are notably NOT solely due to "people being closer together over a longer period of time". Cases of completely untraced community infection are everywhere with this disease.
> “To actually 'get' the virus it would be necessary that someone coughs into their hand, immediately touches a door knob and then straight after that another person grasps the handle and goes on to touches their face.”
This is just simply not true. Fomite transmissibility was demonstrated back in January. I think what he's trying to say is that the chances of static infectious surfaces seem low and that close proximity to an infected person is still the most common vector. But the way you quoted it makes it sounds like you can't get it from a surface, and we know that's not true.
Seriously, wash your hands, folks. And beware of selectively quoted articles telling you not to take obvious mitigation steps.
In early April 2020, Streeck and his team reported that they had "carried out an intensive search of the home of a family infected with the coronavirus but found no trace of it on surfaces."[18]
“We did not find any live virus on any surface. Not on cellphones, not on taps, not on doorknobs.”
One study of one family does not a public health policy make, was my point.
Again, we know that this virus can be transmitted to surfaces by the infected. We know that it lives there for days and can be cultured. We do not know the fraction of real-world infections that take a fomite route vs. inhalation, and this study seems like evidence (albeit somewhat limited) that the number is very low.
No one should be interpreting this as "you can't get sick from touching things". We don't know that. Even given this one study, that's not an appropriately conservative way to understand the disease, given the known stakes.
The WHO report out of China made it clear that the majority of transmission was happening within households (ie outside of Wuhan; in Wuhan it makes sense that this would be the primary route). Most people weren’t transmitting by casual contact, and “asymptomatic” transmission was essentially never happening. The media has blown the risk of these things way out of proportion.
While “social distancing” is a logical thing to do because of what we generally know about respiratory viruses, there’s actually little/no evidence that “shopping” is a thing that we need to specifically be worried about. It’s likely that we hit the point of diminishing returns once we shut down large gatherings like concerts and restaurants.
Any claim without sufficient data and reproducible results that the virus is unable to transfer via a surface, to me, borders on criminal negligence, given real research shows this is inaccurate.
As a counter to claim virus is “unable to live on surfaces”:
First link is ambiguous as to if the samples taken were “toxic” enough to result in infection, but the second link makes it clear that virus survives on surfaces for days in quantities large enough to infect someone.
> SARS-CoV-2 RNA was identified on a variety of surfaces in cabins of both symptomatic and asymptomatic infected passengers up to 17 days after cabins
Unless there’s more to this, it doesn’t seem very useful to me. It seems obvious to me that you’ll find some RNA. However it would likely be damaged/fragmented.
I’m not sure about the second reference, it would be interesting to dig out the original study.
— Research found that SARS-CoV-2 was detectable in quantities large enough to be infectious in aerosols for up to 3 hours, up to 4 hours on copper, up to 24 hours on cardboard and up to 2-3 days on plastic and stainless steel.
Human coronaviruses can remain infectious on inanimate surfaces for up to 9 days. Surface disinfection with 0.1% sodium hypochlorite or 62–71% ethanol significantly reduces coronavirus infectivity on surfaces within 1 min exposure time. We expect a similar effect against the SARS-CoV-2.
This meme in the media is the real negligence. This is the biggest blurred distinction they've used to sensationalize headlines. It's like digging up a graveyard and using it as proof that humans can survive for 300 years underground.
I'm quite happy to be over cautious until there's better evidence. It's fairly simple to change my behaviour and with a relatively low cost compared to the risk related to uncertainty over ease of transmission.
I'm not talking about whether to stay indoors or not. I'm talking about the precautions one should take in public spaces. I still need to go shopping but whilst there I'm going to assume all surfaces are potentially contaminated.
Likewise groceries, parcels and deliveries either go into quarantine for 2 or 3 days or they are washed.
Do you believe the point of isolation is to stop the spread or slow the spread? If the point is to slow the spread but ultimately for everyone to be exposed, wouldn’t it make sense to do that as quickly as possible without overrunning hospitals?
At this point new hospital admissions are significantly down from their peak. If the point is to slow the spread but acknowledging that it cannot be eliminated, we’ve in fact over-corrected.
The further you get the cases down, the slower the spread when things open back up, especially if it gives you time to ramp up other mitigations like PPE and test production during the lockdown to bring the R0 value down significantly.
The unmitigated doubling time is approximately 3 days. So for every halving in the overall prevalence you buy yourself 3 days of unmitigated growth in a population with no immunity.
On the testing and PPE front, again I wonder if this is just a feel good notion or if there’s even napkin math to show what scale of PPE and testing is theoretically being deployed and what impact that may have on R0.
But returning to the core point, how long until COVID has runs its course, and at what cost? Can we admit that herd immunity must be reached? As Dr. Birx repeatedly asks, are we at the tip of the iceberg or 25/50/75% of the way through?
No one wants to think about it because I guess it would make an uncomfortable choice obvious. Better to just self-flagellate so we can feel like we’re doing something.
> Saying that live virus is there because viral RNA was found is like saying I must be holding a meatball sub because there's a marinara stain on my pants.
There is no such a thing as a “live” virus. They are just a bundle of RNA in a protein/fat shell. If the RNA was identified it means the shell was intact.
Also they measure active live viruses, and has been shown that some viruses can go dormant and come back to life so measuring an area for a virus may not pick up dormant ones and lead to a result that is a false reassurance as the potential for those dormant virus to come back into life is still there.
But so much we don't know about this new virus strain, hence big rush to learn all these details about this virus as with better understanding, better management and approaches come about.
As for its survival rate on surfaces, we still don't know all the details, but does no harm to just treat all surfaces as infected outside your home and work with that - hence hand washing and not forgetting the details like tap, keys, phone, things you can't avoid touching up to the point you actually get to wash your hands. I'd hate to think how many have clean hands and then turn the tap off with the same hands that turned it on when potentially contaminated. That will be the small oversights that catch people out more.
Hence until we get that data to know for sure science wise, presume the worst and hope for the best is always the only prudent approach.
Dormancy refers to when a host is infected but the virus is not replicating.
There is no "dormant vs. live" distinction for viruses outside of a host as they have no function / biological processes outside of a host. They are just molecular robo-syringes that inject RNA/DNA.
Also refers to viruses dormant without any host, for example https://www.bbc.co.uk/news/science-environment-26387276
whilst an edge-case and it does show that enviromental factors and how a particular virus responds and reacts are still things we are learning about this one.
Heck, may find out that frozen good with contaminated packaging can put the viruses into dormant mode and when you take them out of the freezer, and temperature and humidity level kick it into life. Details like that unlikely, yet still not been ruled out and much science still ahead upon this virus and caught many off guard and on the backfoot, but we love solving problems and the science is starting to get more detailed a bigger picture every day. But still, mindful of not eliminating aspects that have not been totally ruled out is a balance of risk/caution and fair judgement still plays a part.
Dormancy isn't really proper biology jargon, the correct term for what I referred to above is latency.
However, outside of the cell, neither of those terms mean anything.
A virus outside of a cell does nothing, period. It is essentially a USB flash drive with a computer virus in it. Saying a USB flash drive can "lie dormant in a drawer for days" is just silly.
> Heck, may find out that frozen good with contaminated packaging can put the viruses into dormant mode and when you take them out of the freezer, and temperature and humidity level kick it into life.
We won't though, because we thoroughly understand how these things function. There are things that function like that: bacteria.
They just found RNA of the Virus not an active Virus, there is a huge difference. Same goes for Virus in stool, you can detect the RNA but it’s not active anymore. Source: Webasto Study
It's a two page summary. Note that this, and the accompanying press conference (with professional PR team) are it. That is the entirety of the details they have released.
I think it's absolutely crazy and irresponsible to do a press conference on a paper that you haven't even released a preprint of. I really hope that there aren't any issues with the actual publication, because if there are, they're going to cause a great amount of damage to scientific credibility, which so incredibly important right now.
Despite it opposing their previous stance on it? They're now mostly backpedalling, and discrediting the study. Or, at least, how it was presented - but can anyone blame them for that?
— Research found that SARS-CoV-2 was detectable in quantities large enough to be infectious in aerosols for up to 3 hours, up to 4 hours on copper, up to 24 hours on cardboard and up to 2-3 days on plastic and stainless steel.
AFAIK it remains unknown how many viruses are required and where in the human body to get an infection. So 'quantities large enough to be infectious' is probably false.
There are very well defined scientific protocols for what an infectious dose is, used in this research. You can put your “probably false” argument against the contents of the paper.
I was not referring to anything like that, but to the fact that a different amount of different viruses is required to cause an infection. E.g. in this paper it is estimated that influenza A (in aerosol form) requires around 2000-3000 viruses to infect: https://www.hindawi.com/journals/av/2014/859090/#conclusions. On the other hand Noro-viruses can infect a person in much smaller quantities (don't bother finding a reference but you'll find it quickly). All I'm saying that it's unlikely that we know such numbers at this point for SARS-CoV-2 so in the paper you linked they must have used some other definition for an 'infectous dose' than what you'd intuitively think.
Edit: Now that I actually read the paper that OP posted, it seems that they're estimating the half-life of SARS-CoV-2. It really depends on the initial amount of viruses how long it takes to go below some fixed 'non-infectious limit'. So numbers such as '3 hours' quoted in the paper are pretty much meaningless in practical situations where the inital amount of viruses might be much different. It's not that they're trying to emulate a cough or something.
The CDC is currently saying that this virus has an R0 of 5.7. Couple that with the many cases of casual spread (e.g. people who have gotten it with people they have barely interacted with), and the contrarian claims by this German study seem farcical.
More generally: will you please stop posting unsubstantive comments and flamebait to HN? You've done it a lot, and we ban accounts that do it, because it destroys the spirit of curious conversation, which is what the site is intended to be used for.
It took a couple of months for the Robert Koch institute to figure out what masks are good for. Let's give Dr. Streek some time to figure out how fomite transmission works.
This study and its conclusions have seen close to universal dismissal. It can't even demonstrate that it is actually detecting SARS-CoV-2 immunity (it was claiming results before anyone had even demonstrated effective tests for relevant antibodies), and not any of the many variations of coronavirus that spread during the colder months (yet which offer no immunity to SARS-CoV-2).
The claims about shopping are...unsupported and go contrary to an enormous volume of evidence (namely the high R0).
It isn't a good example of anything except that junk science has a moment to shine in a crisis.
EDIT: LOL, -2. This is the moment I delete my account and find slightly less stupid venues to participate in. Cheers.
Streeck studied medicine at the Charite University, Berlin and obtained his PhD from the University of Bonn, which he performed part-time at the Partners AIDS Research Center, Massachusetts General Hospital, Harvard Medical School.
After his graduation Streeck started to work as a postdoctoral fellow at the Ragon Institute of MGH, MIT and Harvard. In 2009 he was promoted to Instructor in Medicine and in 2011 to Assistant Professor at Harvard Medical School. In September 2012 he was recruited to the United States Military HIV Research Program, Bethesda, where he became the Chief of the Cellular Immunology Section as well as Assistant Professor at the Uniformed Services University of Health Sciences and adjunct faculty of the Bloomberg School of Public Health, Johns Hopkins University.[3] In 2015 he became the Chair for Medical Biology at the University Duisburg-Essen and founded the Institute for HIV Research in the same year,[4][5][6][7] though he still maintains the status of "visiting scientist" with the US Military HIV Research Program.
In 2018 Streeck was appointed to the advisory board of the German AIDS Foundation (Deutsche AIDS Stiftung).[8] In April 2020, he was appointed by Minister-President Armin Laschet of North Rhine-Westphalia to a 12-member expert group to advise on economic and social consequences of the 2020 coronavirus pandemic in Germany.[9]
Coronavirus research
In early April 2020, Streeck and his team reported that they had "carried out an intensive search of the home of a family infected with the coronavirus but found no trace of it on surfaces."[18]
“We did not find any live virus on any surface. Not on cellphones, not on taps, not on doorknobs.”
There are some red flags about this study though. German press is reporting that a PR firm founded by the notorious yellow-paper journalist Kai Diekmann is involved in publicizing the results. Diekmann was recently involved in a scandal where researchers in Heidelberg wrongly claimed to have developed a blood test for breast cancer. Streeck appears to be a personal friend of one of the other founders of the company. In any case, using a PR agency is pretty much unheard of for a German research institute.
I'm reminded of that time a Nobel prize winner used the "authority" he generated from winning the Noble prize to convince everyone that Vitamin C was a magical cure-all for all disease.
Being an amazing HIV researcher does not mean Streeck has an appropriate background in coronaviruses to be an authority in that field, especially given that his team has (a) found outlier results at odds with every other study thus far published and (b) is making a broad policy pronouncement based on studying a single family's household without considering confounding factors, like say the family cleaning the house before the researchers visited.
This is comforting, but I'd rather still be cautious. I wear gloves when I go shopping. I wash my hands frequently anyway, and now I wash them even more. Worst case, I've wasted some time.
Junk science can come from people not known for junk science. And in the end we rack it up to a technical fault (e.g. a test for coronavirus antibodies that cannot distinguish between many of the several other coronavirus infections that spread during the winter), the way participants were enrolled, etc. That's why there is a peer review process.
And this study bizarrely was released with a press conference and a press conference, yet perilously little actual methodology or useful information for the scientific community to critique. Oh and with a professional PR firm. And it uses this to promote significant changes in public policy! (e.g. relax the restrictions because our two page summary gives some conclusions that are entirely contrary to the entire world of experts)
It's all extraordinarily weird.
And again, it has only made waves online. Among the medical professionals, virologists, etc...crickets.
Just to be clear, HN would normally laugh nonsense like this off the site -- a PR "study" that has zero peer review, that goes against all conventional wisdom, that is not acknowledged or credited by any other expert in the field. Has this site gone absolutely stupid?
> The claims about shopping are...unsupported and go contrary to an enormous volume of evidence (namely the high R0).
Honestly? An R0 of 2-3 is frankly not that high.
If grocery shopping were a huge risk, and people spread the disease before being symptomatic, you’d expect a single sick individual to infect way more than just 2-3 people on average.
Severe acute respiratory syndrome coronavirus 2 is the causative agent of the 2019 novel coronavirus disease pandemic. Initial estimates of the early dynamics of the outbreak in Wuhan, China, suggested a doubling time of the number of infected persons of 6–7 days and a basic reproductive number (R0) of 2.2–2.7. We collected extensive individual case reports across China and estimated key epidemiologic parameters, including the incubation period. We then designed 2 mathematical modeling approaches to infer the outbreak dynamics in Wuhan by using high-resolution domestic travel and infection data. Results show that the doubling time early in the epidemic in Wuhan was 2.3–3.3 days. Assuming a serial interval of 6–9 days, we calculated a median R0 value of 5.7 (95% CI 3.8–8.9)
Calling it Junk science is a bit harsh. I would say that the sponsoring entity (one of the German states) did force an intermediate result. This might turn out to be a bad idea, but is needed to steer the political decision process (the German states and federal government want to convene to make decisions about the lock down on April 14th).
The study has been widely critiqued, but dismissal is too harsh. I don't think anybody really has said that the main finding is wrong. It just might not be as strong. Instead of 15% immune in the area, it might be just 12% or 10%. Fatality rate might be 0.5% rather than 0.37%.
The study goal itself is correct and it is a shame that not every epidemiologist is doing exactly the same study right now all over the world. That the German CDC did not think to run such a study themselves since Covid-19 turned bad is a scandal.
Austria has just published the results of their first representative study on about 1500 randomly selected people [1]. They found 0.33% infection rate (confidence interval 0.12% to 0.76%). While this figure is somewhat larger than the previously known numbers (still within the confidence band), it pretty much rules out that a large fraction of the population is already infected.
I don't think this rules anything out, because this study was done on throat swab PCR tests. It's entirely possible a much larger percentage of the people in this study had already been exposed and cleared the virus. Not saying that IS the case, just saying it's entirely possible.
I don't see how this theory would be compatible with the rapid rise in hospitalizations and deaths that was observed in the last weeks. If many people had been infected a long time ago, why are they only now starting to get sick?
There's a logical inconsistency here. If we assume that the total number of cases is much higher than reported, then the hospitalization rate per infection is driven down by the larger denominator. There's a point at which there are so many total cases that the number of hospitalizations is problematic and noticeable. If we continue to assume that the total number of cases is much higher than reported, the death rate per infection (IFR) is also driven down by the larger denominator.
But if we had a large number of undetected cases in the past, then we should also have a large number of undetected cases now, contrary to the study. (Unless we already have herd immunity, but there is no data at all suggesting this.)
Perhaps in the past, earlier in the virus's exponential growth, many people had it but still an order of magnitude less than now. And that order of magnitude is the difference between a slammed hospital and a regular day. And because an order of magnitude people less had it, groups like the elderly were an order of magnitude less likely to be exposed en mass.
I'm not necessarily saying people got infected a long time ago. If anything I think we're just missing way more cases than people assume at this point.
A giant outbreak that had already passed weeks ago would be inconsistent with the shape of the curve of symptomatic cases, though. We know for sure that the bulk of people who have ever had this disease are still sick
> "We know for sure that the bulk of people who have ever had this disease are still sick"
Most people who contract Covid-19 fully recover by around 7 days after showing symptoms. Severe cases that go to hospital? Yes, recovery may take a long time.
The bulk of people who got sick enough to get tested and/or go to the doctor are still sick. Remember, the hypothesis is that there are a large number of infections mild enough to not be reported, tested, or hospitalized.
Yes, but if they are the same disease, then the asymptomatic/symptomatic fraction of cases must be the same over time[1]. So a bunch of people who had the disease asymptomatically weeks ago should have shown up in a spike of people with symptoms, and it didn't.
[1] Or if they weren't, that would be a BIG result and very surprising. It's absolutely not something you can assume to make an argument.
Actually SARS-CoV-2 has been found to have a comparatively low mutation rate. But my point was that now you're not just positing a very large undetected outbreak of COVID-19, you're positing a very large undetected outbreak of an itself-undtected variant strain of COVID-19 that just happens to have the properties needed to produce the overmeasurement that you want to see in the case fatality rate.
> Actually SARS-CoV-2 has been found to have a comparatively low mutation rate.
Compared to what, a rhinovirus?
> you're positing a very large undetected outbreak of an itself-undetected variant strain of COVID-19
From the linked study, it appears that at least one variant has been detected:
"Population genetic analyses of 103 SARS-CoV-2 genomes indicated that these viruses evolved into two major types (designated L and S), that are well defined by two different SNPs that show nearly complete linkage across the viral strains sequenced to date."
How would PCR test results give us any sense of the relative spread of these two strains (or indeed others)? Is it possible that you're motivated to dismiss ideas that challenge your understanding? I'm not convinced that it's the correct explanation for these observations, but the argument that it's impossible seems pretty weak.
I'm not saying it's impossible. I'm saying it can't be simply assumed to make an unrelated point about case fatality rate. If you want to cite me a study showing a separate, weaker strain of COVID-19 that explains how the CFR is much lower than we think you need to show me the actual science, not just assert that it exist.
Because the obvious hypothesis is that it's one disease and one outbreak and the CFR is what we measure and not something else.
Different hypotheses are obvious to different people. You're hearing one of the scariest ones - partly because it's great business for the media and political industries, and partly because it supports the belief that we can accurately measure an in-progress epidemic of this kind with our modern technology. Here are some very experienced folks with less-scary "obvious" hypotheses:
The exponential curve is consistent with the exponential increase in testing.
If a stable 30% of a pop has X at any given time, and you test 10 people for X the first week, 100 the next week, 1000 the next week, etc. you will have a nice exponential curve of the number of cases while, in reality, nothing all that exciting is happening.
Have you seen a scary graph anywhere in the media that normalizes for the number of tests given? I haven't.
The exponential curve in deaths and ICU admissions is independent of testing (and wouldn’t exist if the virus had been endemic in the population before March).
The exponential curve in deaths would be reflective of exponential testing/ Once again, if you have a stable X percent of people dying from Y, an exponential increase in testing for Y will give the illusion of an exponential increase in Y deaths.
As far as ICU admissions, that is an extremely subjective number, based on individual hospital policies; from my conversations with local HCPs, of two patients in the same degree of distress, the one who tests positive will have a greater likelihood of being put into a quarantined ICU for covid cases. There is no sinister reason behind this; its just that the covid patient has a much greater chance or taking a rapid turn for the worse.
Anyway, my statement (now downvoted) isn't meant to be controversial. It's just a fact. We have had an exponential increase in testing in many parts of the countries... posting the results and then having a newscaster say, "Look at the scary exponential curve" is absurd. There could be -- and most likely is -- an exponential rise in the number of cases. But, using the graphs without backing out the curve in the testing would get you an F on a freshman statistics quiz.
Very few positive PCR tests, very few positive blood tests, so not as interesting as blood tests in a region with more positive PCR tests, but it demonstrates there's not a big group of people in the county that have immunity.
Just a note, no evidence of how much immunity yet. We are hoping that is the case but there are also a few loose stories of people getting covid a 2nd time. We should know more in a few weeks to a month...
The blood test looks for antibodies, so it detects whether the person has had an immune response to the virus.
The GP is pointing out that having an immune response to a first infection has not been riguorsly demonstrated to prevent future infection. If we are unlucky, immunity may only persist for a short period of time.
I believe in those "recovered patient tested positive again" cases, they are talking about PCR testing (which detects virus RNA), not blood antibody tests.
Antibodies (Immunoglobulins) will fade over time, and may not be detectable in the blood after a while. So a negative antibody test for Covid-19 wouldn't necessarily mean you're not immune.
However, immunity should persist for a long time, perhaps even for life. That's because the immune system retains memory of past pathogens and knows how to make new antibodies quickly if needed.
The reason we seem to keep getting infected with cold and flu, year after year, is because these are actually different viruses each time.
You are carefully explaining the mostly true generality.
The fact remains, we simply don't know how long immunity will persist for a given novel virus. We will find out over the next months and years, but at this time, we do not have concrete knowledge about SARS-CoV-2.
It's explained on the page I linked earlier in the thread. A founder of the company that developed it is paying to have the county where he lives tested.
Correct me if I'm wrong, but this used PCR testing to determine the number of _currently_ infected people. It says nothing about the number of people that _were_ infected, but fought off the virus and are now potentially immune.
Simple exposure is not enough to become immune. You need a significant infection which triggers a strong immune system response to build long term immunity. Thus in the initial stages of an outbreak you can basically ignore people that became infected weeks ago, had a significant infection, and are now immune due to the exponential growth curve.
It’s only after the rate of infection stayed the same or falls for a month+ that you need to adjust for such people.
>You need a significant infection which triggers a strong immune system response to build long term immunity.
I don't think this is true. I get the flu shot every year and have never had a strong immune response to it, yet I'm still immune to the major flu strains each year.
Point being, it's possible for your body to create long term immunity to a virus without suffering from a severe infection.
I am specifically referring to COVID-19 where we don’t have a vaccine. Vaccines fake a significant infection to get that same strong immune response. This is also why some vaccines require multiple doses over a short period.
If we did know the true current infection rate (which this report does not give, as there are too many unresolved assumptions), then could we not, with some reasonable assumptions about the rate of spread and the duration of an infection, estimate the number who have recovered from it?
Indeed PCR tests only test for the presence of the virus itself. Their big advantage is an extremely high specificity. Antibody tests are plagued by large numbers of false positives.
I realize that your comment is tongue-in-cheek, but if the situation were so (or just if there are a great many asymptomatic cases), then the continuing rapid increase of symptomatic cases would indicate something rather unusual, including, if I am not mistaken, little immunity, in many cases, from a first infection, and second infections being more serious than the first. I vaguely think that there are some diseases like this (or perhaps I am just thinking of allergen sensitization.)
> and second infections being more serious than the first. I vaguely think that there are some diseases like this (or perhaps I am just thinking of allergen sensitization.)
You might be thinking of dengue (which is endemic in my home region). There are four strains of the dengue virus; if you are infected by one strain, and had in the past been infected by a different strain, it increases the risk of the more serious hemorrhagic dengue.
Thanks, that is interesting. As far as I know, we are only dealing with one strain here, though there have been enough mutations that it is clear that most cases in New York came via Europe.
Yes, this is Antibody Dependent Enhancement[1], which is also something that any vaccine will have to rule out through human trials. These sorts of immune system traps and pitfalls are why vaccine testing takes so long.
My dad caught dengue. It was nasty. Fortunately not the hemmorhagic variety. It's at least as scary as malaria, but with much less research devoted to it.
There was some data from Iceland that showed about 50% of cases being asymptomatic. That's more optimistic than we saw originally, but not as optimistic as the most optimistic scenarios proposed.
Please note that how useful the results of that study are is widely debated. Not much detail about the process has been published, it's unclear how reliable the tests used are (other experts say they will likely also trigger for other Corona-viruses) and how representative the sample is (e.g. they did look at individuals, not households).
There was also this report from northern Italy, where 40 of 60 asymptomatic blood donors were found to have antigens (incorrectly described as antibodies in the article, from what I've been told):
I truly doubt the asymptomatic carrier and spreader myth. People lie to their doctors all the time. Why wouldn't they lie to a stranger taking a poll of their health?
Sure, the virus will hit some people much harder than others. There's a component there yet to be discovered. But those exposed must have some sort of response, even if it's just a series of stronger than usual headaches. Stuff like that goes under reported because "oh that was just a random headache". Said person might drink a lot and deal with hangovers so headaches are expected. Whatever.
My point is that these studies are not very thorough in following up on the response quality or even a requery 2 weeks later when symptoms got much worse.
Lies,damn lies, and statistics from personal health studies.
I'll follow up my own post with anecdata rather than edit.
My father was pretty good at giving differential diagnoses. He always said, "everyone lives, you just need to figure out what they're hiding and not focus on the why." I laughed when "everyone lies" became a meme on "House MD". The even more sardonic truth is that my father even lied after being diagnosed with a bad version of pancreatic cancer! (squamous cell carcinoma of pancreas) They asked him how much he drank and said, "A little bit, not too much." I stopped him and said, "Dad, you drink at least a bottle of wine every night." Oncologist replied, "OK heavy drinker". When asked about smoking he said, "No I haven't smoked since I left the Air Force 50 years ago." I corrected him and said, "Dad, you smoke at least a cigar a night while drinking. That's a lot of second-hand smoke." Oncologist replied, "OK, smoker." Everyone lies, and doctors make especially bad patients.
Next bit is personal, about me. One day I had a headache. Slightly off from a normal headache, hard to explain. Not wildly off like a migraine...just slightly. I rarely get headaches. I didn't think too much of it but left work to go home and rest. Two days later, I woke up with the same headache. No drinking the night before (honestly). Said, hrmm that's weird. I'm going in to get checked out. Long story short, I have intracranial hypertension and it's starting to manifest in new symptoms (exact cause unknown). It's good that they caught it now because it can lead to irreversible blindness if not caught. My point is, even big things can have minor symptoms -- even if they're "everyday" symptoms. (Pancreatic cancer symptoms are upset stomach)
I've personally observed two households where one member had some sort of very nasty flu thing with a dry cough, fever and breathing issues (likely covid but no test available) and other members were just unusually tired and with a tickily throat. The later could be classed as asymptomatic and would never have considered covid but they clearly had some symptoms.
> "I truly doubt the asymptomatic carrier and spreader myth."
I partially agree. If you're infectious, then the virus is multiplying inside your body. Eventually your immune system is going to react to that and you'll feel it.
But it's also quite possible that you can be infectious before you feel ill.
Definitely! That's why I mentioned no lack of requery 2 weeks later. "Oh I was fine then, but now I feel horrible." That is missed in these studies. They're flawed!
Why is there being asymptomatic patients unbelievable? You believe some people can die from this virus, and some people can just have headache; but you don't believe some people may have no symptoms. I'm following your reasoning.
My family lives in Maryland, and we're pretty sure we caught covid-19 back in February. A disease suddenly came out of nowhere in our daughter's daycare, put one child in the hospital with severe pneumonia, and our daughter had diarrhea, upset stomach, and fever for over a week. My wife caught a cough that stayed with her for many weeks, and at times had trouble breathing. This was before we even knew much about covid-19, nor were taking it seriously.
The LabCorp test is not FDA cleared or approved and is being used under an emergency act.
"Testing was performed using the cobas(R) SARS-CoV-2 test. This test was developed and its performance characteristics determined by LabCorp Laboratories. This test has not been FDA cleared or approved. This test has been authorized by FDA under an Emergency Use Authorization (EUA). This test is only authorized for the duration of time the declaration that circumstances exist justifying the authorization of the emergency use of in vitro diagnostic tests for detection of SARS-CoV-2 virus and/or diagnosis of COVID-19 infection under section 564(b)(1) of the Act, 21 U.S.C. 360bbb-3(b)(1), unless the authorization is terminated or revoked sooner."
"It is possible for this test to give a negative result that is incorrect (false negative) in some people with COVID-19. This means that you could possibly still have COVID-19 even though the test is negative."
"This test is not yet approved or cleared or authorized by the United States Food and Drug Administration (FDA)."
Due to this, it's hard to trust test results. It's a best effort and not perfect.
Well, each test is different though. More so, testing wastewater is also a totally different story than testing humans. Although I find your comment interesting, I don't see how this relates to the topic of wastewater analysis.
This reminds me strongly of the methods used in Neal Stephensons's novel Zodiac, where they follow sewerage pipes to determine where the source of an infection is.
The whole avenue of analysiing waste water when you have centeralised procesisng of the inhabitants as a finger in the air feel upon things is already used in some avenues and like this, many more avenues of potential. Sure it won't be exacting, but does give a feel for things in a way that is very cost effective over alternatives in so many area's.
For example, drug usage - measuring the waste water for levels of cocaine, etc etc etc is already used to some degree and proven in many studies.
Sure it won't say who, what or exactly were and with that, also anonymised and ticks a few privacy box's in that respect. Let alone the aspect that your fecies and urine and property that we all happily sign away to the water/waste company and even pay them. They can do with it what they like if it comes down to it, but in this approach, nobody is identified and it is more a finger in the air measure of things and a good indication of any shifts/change overall for the costs and speed of doing so.
Though personal toilets that will do some serious analysis of your waste for health reasons may well be a big in japan joke phase, but certainly at some level they do have merit and whilst the waste treatments today may be a good overall feel, the market and technology will gradualy filter down into the homes for those that want to be ontop of their health or just want that extra level of safty.
Certainly a good initiative and practical approach, though such an approach does depend upon a good waste/water infrastructure and that will be mostly modern area's, towns cities and the like and for some area's, may not have that high a percentage using such centralising waste management.
Though when we start tracking area's health media wise like we do weather and get the poo forecast, that's when I know reality has caught up with my darkest of humour.
If the number of cases are really as high as this paper suggests (5% infected) then we are one or two weeks away from a death wave like nothing else. However let's pay attention to the many caveats the authors point out about their calculation, including the assumption that there are no particular individuals who are shedding especially large quantities of virus.
Note/Tangent: A quick search shows the black plague killed an estimated 25 million people over a century. Less than Spanish Flu, but a much higher percentage of the population at the time. Up to 95% of Native Americans died from diseases introduced from Europe. That's the largest percentage of a population to ever die from disease that I've heard of, and is the primary reason Native Americans are not the dominant population in the Americas today. Whether there's potential for an unprecedented amount of deaths really depends on how you measure things.
With you 100% that in relative terms we're not facing anything close to the black death. Everything past this point is just me enjoying my day off by learning about random things, and wanting to know what the actual answer is.
My original number was from a search for "How many people died from the black plague.". The first result was a National Geographic article which stated the 25 million number occurring over a century. [1]
The linked Wikipedia article states 75 to 125 million, so the two disagree by a factor of 3 to 5.
The Wikipedia article cites an Australian Broadcasting Corporation news article for the 75 million number[2], and thus cites 'Anomalies and Curiosities in Medicine' page 617 for the other number. The edition of AaCiM available online -published in 1906- actually has the information on page 893. [3] The information there doesn't match the Wikipedia article. The largest number stated there is 75 million, and cites 'Le Moyen Age Médical', which appears to have been published in 1896. [4] I found an English translation, and the only number I saw was 25 million over 4 years. [5] It's not clear if the author is referring only to Europe, but it seems likely. At this point, I really need to take my dog out, but it seems to me that the vague answer is that tens of millions of people died, many in a specific four year period. Which, goes back to the idea that, in relative terms we're not dealing with anything like the black plague, and that how you measure things is important.
That would be infection fatality rate, case fatality rate is what we think it is by definition. (A case is a known case, an infection is an infection.)
Quibbles over wording aside, I think the Icelandic data showed us that the percent asymptomatic is about 50%, insufficient for boundless optimism.
Indeed - there is nothing here to indicate a sudden jump (faster than the already high rate of propagation), while there is good reason to believe that the incidence has been systematically undercounted, on account of the shortage of testing kits. The fatality rate is less likely to be under-counted, if we assume most fatalities are preceded by hospitalization (and often testing.)
The problem of course is lack of testing. The same factor censoring observations of the disease among the living censors even more strongly among the dead. AFAIK, no one is trying to test the dead.
Ultimately though society became aware of the existence of plagues long before we knew about germ theory. So sticking our heads in the sand won’t save anyone from realizing what’s going on during a pandemic. It’ll just result in potentially many more dead.
5% is the larger of two estimates given in the paper. The other estimate is 0.1%. These aren't an upper and lower bound, just two very different estimates.
As the paper itself details, there are currently too many unknowns for these numbers to guide policy or expectations. But it is an interesting approach that might yield useful conclusions eventually.
I'm hoping that, regardless of the absolute number, this method can give us a good handle on the relative number and let us know when infections are going up or down and by roughly how much. Right now the rate of new official infections has pretty much plateaued. My guess would be that actual infections are also plateaued but I can't rule out that just testing has plateaued.
>we are one or two weeks away from a death wave like nothing else
As of now in many countries the average death rate hasn't even gone up at all. Risk is not additive, many people die with covid-19, not of covid-19.
So for a realistic estimate of the disease burden one has to compare the total increase in fatalities across some time all other factors held equal. This will be higher in some regions struck particularly hard like Italy, but not by as much as the plain number suggests.
It's been 15 days since March 25. Most of these people are likely already sick, and if their disease will progress to severe, they're already in hospitals. Massive death wave might be coming, but it'll hardly be unexpected, they're all factored in the models.
For any of those studies, look for the specificity of the test, which is basically the false positive rate. A serological test with 2.5% false positives is considered a pretty good test. If the test used in Stockholm were similar, they could have zero cases and get that result.
A Danish study recently concluded that actual infection rates could be 30x-80x higher than what is shown by positive test results. This could easily explain the higher levels than expected and is potentially a good thing and bad thing. It means that mortality is much much lower that expected.
4.1.2. Revised planning basis Statens Serum Institut informs on the basis of antibody studies in 1,000 blood donors in the Capital Region, lost in the period 1-3. In April, 2.7% had been detected with antibodies, which, with a sensitivity of 70%, corresponds to 3.5% of those examined had already been infected with COVID-19. Statens Serum Institut states that if this figure is transmitted to the entire population of the Capital Region, it is equivalent to approx. 65,000 people may have been infected as early as 26 March. At this time, 917 confirmed cases of infection were found in the region. This means that there can be up to 70 times more infected in the community than confirmed cases.
In the work of the State Serum Institute in modeling the development of the epidemic in Denmark, on the basis of studies in, among other things, Iceland and Germany, it has been decided to work with the real number of infected in Denmark being 30-80 times higher than the number that remains. ver proven.
It is therefore estimated that the dark number is significantly higher than in the first planning scenario, and it is estimated from the State Serum Institute that for every detected infection case up to March 28, there may be 30-70, which are actually infected. This ratio will be affected by the number of people who will be infected in the future.
Thus, there is probably much more widespread contagion in society than previously thought. This does not have a direct impact on the planning basis for the health care system, as the increased spread of infection is in a part of the population who do not need hospital treatment and probably only to a very limited extent have sought medical attention. It should also be noted that it also means that the mortality rate of infection with SARS-CoV-2 (infection fatality rate, IFR) is lower than the mortality rate of registered case fatality rate (CFR) and possibly lower than that of WHO have evaluated. The WHO has estimated that the IFR is between 0.3-1.0 with wide variation across age groups. With more precise knowledge of the dark figures, the IFR for the COVID-19 epidemic in Denmark can be clarified and the expected mortality will be accurately estimated.
The State Serum Institute states that over the coming weeks they will be able to continuously monitor the development of immunity in the population through cooperation with the blood banks, focused sample studies and testing for the population's immune status in general.
The above also means that the previous assessment of the mortality in connection with COVID-19 in Denmark is no longer true. When a more accurate assessment of the actual prevalence of infection is obtained on the basis of the epidemiologic surveillance and a precise IFR for the Danish epidemic is estimated, a new and true mortality prognosis can be estimated.
The need for ordinary beds and intensive beds is evident from the modeling, which will be continuously qualified.
TLDR: blood donor antibody testing indicates true infection rates are 30x-80x higher than confirmed cases in Denmark and that 1.5 weeks ago ~3.5% of Copenhagen’s population may have already been infected by Covid-19.
The relationship between the number of infections and the number of confirmed cases is going to be hugely dependent on the number of tests and how they are distributed. 80x higher is very plausible but the ratio is going to be very country dependent. I'd be rather surprised if South Korea was more than 2x off, but I could easily see Ethiopia being 5000x off right now.
Looks like South Korea has administered fewer tests per capita than Denmark, but you're right that their numbers could be closer if those tests were more effectively targeted.
While what you are saying is logically coherent but it does not work in the real world. How are you going to track all the people the infected people has to contact with? How about asymptotic cases?
You don't have to be perfect, just good enough to get R under 1. It's been working pretty well Taiwan, Singapore, and South Korea when combined with moderate social distancing measures.
Good to see that these results are starting to come out. Eagerly awaiting results of the Stanford serosurvey and others. I'm an optimist but maybe we can hit 100x!
My wife's close friend works at Stanford. Her sister was recently contacted by Stanford, because she donated blood a few weeks back, and they detected antibodies for SARS-CoV-2 in her blood. The levels of antibodies were high enough that they requested that she donate plasma to help with other patients.
She has zero symptoms. So the case that the infection rate could be much higher than expected is definitely plausible.
The title of the article is deceiving as virus itself was never isolated from wastewater. The authors used RT-PCR to test for the presence of a 150bp segment of the SARS-CoV-2 genome. Although the presence of nucleic acid implies that virus is there, infectious virus was not isolated in this study.
That is how you detect and characterize the biota of a water source quickly and efficiently- quantitative pcr or rtpcr to detect viral load levels. What would you expect they do instead?
This is neat, but a little scary. If I'm understanding it correctly, they are checking sewage for evidence of the virus, and estimating how many people have it based on that. This would be really cool if it were common place, and tested for all known viruses, drugs, fungus, bacteria, lead, whatever they can find. This could be used to track the health of the population over time and as it spreads. If it were publicly available this would be a great resource.
The scary part is what if they start making the sewage sites smaller and smaller, or even just the collection locations to where its testing fewer people. Then use that information to enact quarantines or investigations.
If covid-19 is much less harmful than we originally thought, why were, and still are, medical experts proposing such draconian measures without a clear understanding of the true threat? Dr. Fauci, advisor to the president, proposed the other day that no one should ever shake hands again, in order to prevent spread. It is bizarre.
Even when the disease first started to spread, there were people making these same points. In fact, most people thought the disease was no worse than a bad flu or cold, hence the difficulty to institute lockdown type measures in the first place. This is certainly not going to build trust in institutional expertise on these matters. So, once the medical experts are actually right, then they'll be ineffective at persuading people.
Too few people in this community are able to evaluate the information contained, which leads to lots of pointless speculation, and lots of misinformation. Despite working in biology for 20 years, I would not trust any of my own interpretations of this pre-print.
The only people who I would trust are named specialists in this field, that are willing to stake bits of their reputation on what they say.
The only venue where that is happening in the public is on Twitter.