So a more more accurate description seems to be "there is no evidence that thinking of the viruses in terms of multiple strains is scientifically helpful".
You, you are going to be crucified by scientists. :-)
More seriously, I get your point but many discoveries are done by finally observing something which existence has been anticipated, hypothesized but still unproven. A planet that had an effect on nearby objects because of its gravity for instance. Or the Higgs boson.
So, yes, thinking of things that are not proven to exist (yet) is often scientifically helpful.
You've cut the context, was that on purpose? The context is a discussion of improving medical interventions during the current pandemic, in that context, at present the argument is that 'considering Covid19 to be separate "strains" (isolates) will not help to treat patients'.
It’s not clearer, it’s a completely different statement. The idea of the answer to a question being “medically unhelpful” doesn’t seem at all related to “scientifically unhelpful”.
In Canada, our officials said in January that asymptomatic individuals were not main drivers of epidemics.
And while that may have been true with something like influenza, a more accurate statement would've been we don't have evidence _yet_ that suggests asymptomatic individuals could effectively spread the virus.
We proceeded to operate on that assumption by not forcing incoming travelers from infected regions to isolate, unless they contacted health officials with symptoms associated to the virus. We didn't change this stance until late March, well after the virus had infected thousands of people across the country.
In contrast, Taiwan implemented mandatory 14-day self-isolations for incoming travelers from specific regions as early as late January.
In Ontario, we've had cases of airport taxi drivers pass away from Covid-19. Whereas Taiwan recognized that there'd likely be a large number of people coming home with the virus, so they created special airport quarantine taxis equipped with mandatory masks for passengers and isopropyl alcohol for the driver.
Worth noting how some people, including mainstream press, have vilified WHO for saying there was "no evidence yet of human-human transmission" (at the point there was no evidence yet), and for saying (paraphrasing) "it's not a pandemic yet, not until there's community spread across global regions" when it wasn't yet a pandemic.
So, yes, I'd agree with your 3rd para, but press can spin such statements to create reputational damage which is really underserved.
What exactly do you expect? If we can predict a recession, the world wouldn't have recessions. There's a reason why the label "pandemic" is purely an observational threshold and not a warning for what's to come.
Because they in the next breath said it had potential to become a pandemic if no intervention is done? At the same time declaring it an emergency outbreak of a novel virus?
Words have meaning, and pandemic a very specific one. Would you have declared SARS a pandemic when the first cases started to show up simply because it's a scary virus?
A pandemic actually had an incredibly vague meaning. It’s been the topic of heated debate amongst epidemiologists for quite a while. You can read this [0] to get a hint of vague it all is, and if you look, you’ll find plenty of different highly qualified perspectives on the topic. The WHO waited until it spread to over 100 countries before it called it a pandemic. This wasn’t because it had crossed a very specific threshold to become classified as one. It was an opinionated decision. It wasn’t supported by a strict technical definition, or academic concensus. Because those things don’t exist.
The definition of a pandemic is very simple:
> an epidemic occurring worldwide, or over a very wide area, crossing international boundaries and usually affecting a large number of people
Laymen are perfectly capable of understanding this, and forming their own perfectly reasonable opinions about it themselves. It is perfectly reasonable to criticize the WHO’s decision making around this, and they absolutely don’t have a technical definition to hide behind.
They need to change how they communicate this though. It shouldn't be binary. It was clear to me that this would become a pandemic by mid January and hearing them say it isn't a pandemic was disheartening even though it was clinically correct. Perhaps they sound introduce probability to pre-pandemic viruses. Something like the doomsday clock.
"Would become a pandemic" is not the same as "is a pandemic". Why is it disheartening? The WHO wasn't saying this virus was not a threat of becoming a pandemic.
I don't think anyone who wasn't intrinsically sceptical of 'might become a pandemic', or otherwise highly motivated to dismiss warnings about potential pandemics heard the WHO and thought 'absolutely nothing to worry about here'.
How media communication works is that the disease was hyped as a major threat to humanity in January (why would we even be hearing about a disease in China otherwise?), but everybody still downplaying the threat in late March is furiously spinning that they didn't receive any warning
I don't disagree with anything you said. I do think a more defensive approach to communication is warranted though. The world is run by people I wouldn't trust to flip a burger.
There's a lot of grey area within "wasn't saying this virus was not a threat of becoming a pandemic".
It's a problem I see a lot in technical people (often somewhat on the spectrum). They communicate everything technically correct, but with complete disregard for how the nuances in framing alters the perception to other people.
You can argue that the recipient is responsible for assessing everything they hear/read correctly, but I would put equal responsibility on how you choose to communicate yourself.
We're drifting somewhat from the context, but the main one affected by how other people interpret me is me, so I have a lot of incentive to self-reflect on how I'm perceived.
"Falling out of an airplane doesn't kill you" might be technically correct, but it betrays the very concept of communication.
It's not arbitrary though. Genetic variation is common within a particular species. Some humans have red hair. That doesn't mean they are substantively different. What the author is saying is that differences seen in Corona virus are also not substantive.
Sorry to piggy back on your post. I'm not intending to aim this at you, but it made me think. I'm finding a lot of the current reactions to Covid-19 are pretty similar to the stages of grief.
Denial - It's not really a problem. We don't have to disrupt our lives. It will all disappear in a few weeks. It's all a conspiracy theory.
Anger - If (some organisation) had done their job, we wouldn't be in this mess! It's all the fault of the (some country)!
Bargaining - If we get the new cases below X (or wait for X weeks), then we can all go back to our normal lives. I did what I'm supposed to do, you can't tell me I have to shelter in place any longer (well, a little bit of anger mixed in there)
Depression - We are so screwed. That's it. The world as we knew it is over. Our politicians, health organisations, etc are so incompetent that there is no escape.
Acceptance - Yep. It's a bad situation alright. However, it will pass eventually. It will be difficult for people. A lot of people will die. A lot will lose their jobs. The economy will probably be hurting for a very long time, but we will come out of it eventually.
You might find this article on "Adjustment Reactions: The Teachable Moment in Crisis Communication" [0] (1/17/05) interesting. I found out about it through the peak prosperity daily COVID-19 updates [1] back in mid-March.
I guess the important thing is not so much if two viruses differ in any base pairs or in any 'biological property'; but whether immunity to one is also immunity to the other?
If they were two strains of SARS-CoV-2 but your body fights them the same, that's as good as only one strain for most people. But still very interesting for scientists.
Equivalently, if we see lots of differences in base pairs but no differences in biological properties yet, that might still alert us to the possibility of new strains rapidly emerging in the future.
That is certainly a "biological property". Immune response depends on the "outer form" of the pathogen - what does its protein structure look like from the outside?
Based on the difference in virulence of the virus in Western Europe and US versus Asia, it is hard to believe there is only one strain of SARS-CoV-2.
My hypothesis is that while Asia was originally infected by Wuhan originated strain, the Western Europe and US may have been infected by a mutated strain. The differences in impact in different countries is very difficult to explain without the hypothesis of multiple strains.
Edit: There was a decent article recently (I am unable to find now, most probably from NYT, WSJ) that addressed several factors mentioned in replies and showed none of those could explain the discrepancy in cases across countries. For example, high temperature and warm weather don’t explain differences in cases between Singapore, Thailand, Indonesia, Malaysia, and Amazon region of Brazil.
The closest article, I could find using google search is from Brookings.
Could you elaborate on this? How do the effects differ and couldn't a lot of it be explained by the vastly different pandemic reactions (lock-down vs doing almost nothing)?
Because there are too many wildly differing reactions in similar populations.
More than 700 passengers on the Diamond Princess were infected, leading to a total of eight deaths. This would have been an older-than-usual cohort, simply by dint of demographics on cruise ships.
Meanwhile, in New York, deaths in long-term care homes have approached 5,000.
Obviously nursing home residents are a more vulnerable population, but with this kind of disparity in outcomes, I'm not buying it. Nursing homes may have an older clientele, but then, cruise ships aren't staffed by medical professionals.
IMHO it's been obvious that there are multiple strains in circulation for a long time. Otherwise, the medical community needs to explain exactly why outcomes vary so dramatically, not only from one individual to the next, but between populations with similar demographics. When they explain that, then I'll be more interested in their opinions regarding how many strains are out there. If they think the bugs are all the same, they aren't looking closely enough.
Respiratory viruses are very seasonal. Weather conditions matter. Generally speaking temperature, moisture and sun UV radiation decrease the spread of the virus.
Closer to equator you go, less there is seasonal forcing in respiratory viruses.
Not sure what you mean. The differences in impact seems to be trivial to explain given the vastly different measures taken by different countries, and their timing relative to the start of the outbreak. The IFR estimates are very similar everywhere.
Disclaimer: I assume by impact you mean "case fatality rate" (CFR)
This is my hypothesis of lower impact. Both India & Germany have low CFR and we find that in Germany 49% of cases are under the age of 50, while in India 70% of cases are under the age of 50 years. On the contrary, in Italy 70% of Covid infected individuals are above the age of 50, with 39% above the age of 70 and Spain has 69% of cases above the age of 50 with 37% above the age of 70. US case data by age is grouped somewhat differently by CDC but my guess is that close to 40% of infections are in the age-group below 50 years and about 20% are above the age of 70 years, this might partially explain the relatively lower CFR because CFR for ages under 50 is ~0.4% if you are in the age-group of 40-49 & lower below. Median age of the population for these countries are India - 28, Italy - 46, Spain - 44, Germany - 48 & US - 38. Germany seems to have either done something differently here.
This can only partially explain the differences but would be an important factor when looking at overall fatalities.
That would not explain the difference in outcomes between countries with well known cross-contamination. For example, the pandemic spread to Romania from Italy and Spain (there are around 1 million Romanian nationals living in Italy and 3 million in Spain, and constantly traveling between the 3 countries), and yet CFR and R0 are significantly different between them. The difference with Bulgaria is even more stark.
The reality is that government measures seem to have had the biggest impact by far. Western Europe and the US have badly dropped the ball on this issue, whereas Asian and Eastern European nations have mostly handled this much better for their citizens.
For anyone else reading and wondering what the founder effect is:
> In population genetics, the founder effect is the loss of genetic variation that occurs when a new population is established by a very small number of individuals from a larger population.
Yes, I searched the exact same thing. For how clear the article was in general, I was surprised that this bit was surprisingly confusing in the way it was explained.
Did anyone else read this and, experiences colored by startups, immediately begin thinking about an analogous effect in startup organizational developmental dynamics?
Anyways, to be more on topic, I read this quote from the article: "Because of the founder effect, showing that a particular mutation increases viral transmission in humans is very difficult." Does the author here mean that it is hard to determine whether a mutation increases viral transmission in humans or not because that mutation's survival may not necessarily be the result of genetic fitness but founder effect?
Yes, it looks like that, but it isn't. All those distinct lineages are functionally equivalent. That's the point. A detectable difference isn't the same as a functional difference in transmissibility, virulence, etc.
Well you cannot claim either way. There is still circumstantial evidence for a significant difference in virulence and mortality across the globe, so there might be indeed multiple strains, we just do know about it.
You can definitely claim it if, say, a CUA codon is replaced by a CUG codon because both of those code for Leucine and the resulting proteins will be absolutely identical.
That is not what I said. If there is observable difference between two populations, then indeed there might be two different strains at work. If you want to be super pedantic, not all RNAs are mRNAs, and there might be difference between CUA and CUG in tRNA's behavior.
I don't think the article addresses the point right. Yes, there is only one strain of Sars-CoV-2 as the definition of a strain is a strict scientific term. Nevertheless, there are different clades [1] of Sars-CoV-2, which are characterised as organisms with a common ancestor [2]. This doesn't has to imply a changed property, like infectivity or mortality, but it implies common heritage which is of course of interest. You can see it nicely in the the phylogenetic tree of the sequenced genomes [3].
TLDR; use “isolate” not “strain” to describe genomic differences in viruses
Strain implies functional differences. SARS-CoV-2, like it’s Coronavirus cousins, is quite stable. The genomic sequences found on NextStrain.org are a powerful tool to track the spread of this virus but it is wrong to assume that the difference in each “isolate” carries with it a functional difference; it does not.
The blog post comes from the same scientists that create the TWiV (This Week I’m Virology) podcast which continues to be a tremendous source of quality information for me.
>it is wrong to assume that the difference in each “isolate” carries with it a functional difference; it does not. //
Is that what people are assuming?
It's not that every mutation causes a [medically relevant] functional change, it's that a mutation could have. And, AFAIK, we don't have the ability to sequence _and_ relate sequences to differences in symptoms in the general case at present.
Maybe in 10 years someone will have developed an AI to relate RNA sequences, medical history, and functional changes in real time??
>This doesn't has to imply a changed property, like infectivity or mortality
What about the reports of different strains that focus on having found them having different properties (such as "much more infective")? Are they bogus?
That report was from a Chinese hospital (then repeated millions of times by the media) - they were never confirmed with any sequencing, and the paper was never published due to lack of evidence.
This recent preprint certainly did not come from a Chinese hospital. The authors are listed as being affiliated with the Los Alamos National Laboratory, Duke Human Vaccine Institute, and a few Sheffield institutions.
GP was referring to the “L” and “S” strain theory I believe, which was debunked. The paper you linked is new, and the “more transmissible” property they discuss may just be the “founder effect” at work. It needs more research.
It's difficult to know what user coldtea had in mind. He could have meant the L/S (debunked) theory, or the theory that some strains in Iceland are ineffective [1].
In any case, there are multiple credible sources that some of the mutations of the SARS-CoV-2 have a meaningful effect. In which case the claim of this article that "there's only one strain" may be technically correct (based on some obscure scientific definition), but completely misguiding as far as the general public is concerned.
> the theory that some strains in Iceland are ineffective
I don't see any support at all for that theory though. It is also known that "X show no symptoms" could mean many things, depending who says it and when, and certainly doesn't prove anything alone, only in context, compared to something else, and only when comparison is fair.
For example, from many old news, those "with no symptoms" eventually had the symptoms, it was just that the tests were positive before they developed the symptoms. Second, it is now known that the probability of "having" symptoms is very dependent on the age of the person.
This is all correct, but the importance here is to combat the misinformed titles everywhere talking about multiple different "strains" going around, as well as that one damn Chinese paper (now retracted) claiming two different strains with different mortality rates.
Put more simply, two samples of virus can be of the same "strain" even if they aren't _exactly_ the same sequence. This is because replication can sometimes make errors on segments of the genome that do not impact functionality - moreover these same irrelevant loop segments are not error-corrected either, so mutations are common - despite not modifying the properties of the virus. These irrelevant mutations are actually very useful for tracking the virus spread.
A virus mutation becomes a different "strain" when the change is meaningful for the viruses interaction with the host or the environment.
SARS-COV2-2 is a type of virus that does error correction (unlike flu), so the rates of mutation are extremely low. This is good news because if means a vaccine will work, and we won't need a yearly one - like the flu.
For sure. But I think the point the @gewa trying to make is that yes in the strict academic/technical sense it is correct, however in every day English people probably use "strain" to mean Clad. But not everyone is a evolutionary biologist of some sort.
For sure. But the point of the article is that to non-expert readers, the "every day English" usage people are thinking of is misinforming them!
You are literally nitpicking the wrong people here. They're trying (well, I thought, though clearly not well enough to satisfy HN pedants) to explain the distinction in a way that conveys the fact that there are no known distinct outbreaks with different medical properties. How that's for precision?
> This is good news because if means a vaccine will work, and we won't need a yearly one - like the flu.
That's way ahead of the facts. It means we're more likely to be able to develop a vaccine that works and it's more likely we won't need frequent vaccination to be effective.
Vaccine success involves a certain amount of finger crossing, because it's a natural system rather than an engineered one that we're trying to tamper with. If you've ever boggled at a large spaghetti program, the human immune system makes that look like two dozen lines of clearly documented Java by comparison. None of it has to make sense because Mother Nature doesn't care why she only does results, and in the most brutal way possible.
This is why we've got a bunch of different vaccine programmes in different centres. Some of them might work, hopefully at least one does, and hopefully it produces an immunity that lasts a useful amount of time, has minimal side effects and is cheap to produce in bulk. But there aren't any promises without us having way more advanced biotechnology than exists anywhere today.
> A virus mutation becomes a different "strain" when the change is meaningful for the viruses interaction with the host or the environment.
Of course, that also means that detecting different strains is dependent on understanding those interactions and where they differ. If the post-infection cluster of pediatric multisystem inflammatory syndrome in NYC isn't just NYC being better at identifying that effect, it could well be a sign of a different strain with meaningfully different interactions with hosts. (It could still be a variety of other things, too.)
Different groups of doctors around the world are noticing different aspects of the virus. This is normal with a new virus, and does not indicate that there are multiple strains.
I hadn't seen the UK alert on that, but to be clear my point wasn't that that particular this was an indicator of a different strain, but that something like that, if it turned out to be isolated which wouldn't always be immediately obvious, could be such an indicator that would only be recognizable as such in retrospect.
Totally not a molecular biologist, virologist, etc.
Influenza is smaller about 13K nucleotides vs 30K for corona, it mutates about 4 times faster. It can maintain its larger genome basically because it has better tech. (It seems to better integrate with what it can find in host cells.)
"We demonstrate here, at the molecular level, that CoVs have indeed acquired an enzyme able to enhance the overall fidelity, and that this event might have directly promoted the jump in size of CoV genomes"
"Well before the discovery of nsp14-ExoN in the large Nidovirales genomes (22), this observation led to Drake’s visionary proposition that “RNA viruses would have to acquire several host genes and adapt them to RNA substrates to achieve a major reduction in spontaneous mutation rate. The result would be a substantial increase in genome size” "
"Specifically, SARS-CoV-2 seems to have a mutation rate of less than 25 mutations per year, whereas the seasonal flu has a mutation rate of almost 50 mutations per year."
Nitpick, but viruses are not organisms and so they don't have clades. That's why the paper you linked used the term "viral clades". Like how quasispecies is used rather than species for viruses.
I respectfully disagree. Viruses contain RNA, have reproduction dependent on DNA, and are subject to evolution, which is why they're still categorized in their own tree of "life" with kingdoms, phyla, families, genuses, species, strains, etc. There's no reason why you can't categorize a virus under a clade.
Someone reading this might be wondering how speciation can be measured with viruses, since viruses don't reproduce sexually. Well, we don't test whether different species of animals can reproduce with each other. There's no way to conduct such experiments at any meaningful scale. The vast majority of defined species are educated guesses, and in reality has very little to do with whether two groups of organisms can reproduce with each other. In a lot of cases, species are simply determined by the appearance or behavior of one group of organisms over another group of closely related organisms. The term "species" didn't even originally have anything specifically to do with reproduction; the word effectively meant "looks like", which is why the words "species" and "spectacle" share the first 4 letters.
> Well, we don't test whether different species of animals can reproduce with each other.
"They've been in the room an hour, sir. Nothing's happening."
"Hmmm... Ok, looks like polar bears and flamingoes are different species. Mark that down. Next on the list... swap out the flamingo for the barnacle. Be sure to keep watching closely."
That's not the strict definition. You are using an extremely loose definition. You are missing two key aspects. First, this defintion of species only applies to sexual organisms, and it's about sexual reproduction. Not just any kind of reproduction. Second, the offspring of said sexual reproduction itself must be fertile. So no, in no way can you ever say viruses are human with this definition.
They are definitely borderline; categories tend to fail to capture the continuous. But it is general scientific consensus that viruses do not meet all the criteria for life. They meet some, but not all. And no, they are not still categorized in their own tree of "life". We don't use kingdoms, phyla, etc. anymore. Your argument for viruses being life is clearly out of touch with modern biology, and since clades are by definitions groupings of organisms, and organisms by defintion are living things, no, you cannot say that "There's no reason why you can't categorize a virus under a clade". You have to either change definitions or show that viruses meet all criteria. But then if they did they wouldn't be viruses.
The species definition you brought up does not apply to asexual organisms, for them it's a matter of genomic analysis. As for sexual organisms, it is still a good definition because it is stricter and more "correct" than genomic analysis, although bioinformatics has been getting pretty good with the addition of more sophisticated statistical techniques that go past simple DNA-DNA hybridization.
Yes viruses are not alive and speaking strictly there are no clades or specieses. But I stopped beeing to strict with terminology like this on HN. Most people are not from this field and don't have broad prior knowledge and so it would just complicate and confuse unnecessarily.
Indeed, and you can see on nexstrain (The green RNA region labeled S) that there has been a very prolific functional mutation to the Spike Protein RNA. It is possible that the rapid growth of that strain (in Europe and NY) is due to either a founders effect or higher transmissibility (researchers do not see higher mortality, but may see higher viral load). There are possibilities that it changes the effectiveness of immune response, but it’s all under active research. The outcomes are very significant and unknown. Making broad fairly pedantic statements as the OP has, is unhelpful to understanding.
Tbh the most likely explanation is the very strong prevalence of mask wearing in asian cultures which dramatically reduces (but doesn't eliminate) transmission rates.
The jury is still very much out for many Asian countries (India, Indonesia, etc), and there are a plethora of other factors that can explain the difference: demographics, genetics, comorbidities, sunlight (UV-B), heat/humidity, access to testing etc.
Also, the virus originated from one point (Wuhan) and was spread more or less simultaneously across the world. It would be quite odd if one strain hopped on all the west/east-bound planes, while another strain found its way only to the south-bound planes. Not to mention that the 'second wave' of infections in APAC originated largely from Europe.
The hypothesis is the mutation occurred outside of Asia, and countries in Asia closed ports after the initial infections, but before the mutation.
> sunlight (UV-B), heat/humidity
Much of Asia is in the northern hemisphere (e.g. China and Japan); same season as Europe and USA.
Australia is in Asia too, close to China with much travel between.
I agree there are many factors and it's early. But the low cases and deaths over all countries in Asia has a peculiar uniformity - in contrast to elsewhere.
The continent of Australia is massive. It contains many distinct ecosystems.
Referring to Australia as being "close to China" is like saying Russia is close to England. It's its own continent.
To put it in more concrete terms, any (direct) flight you look up from Wuhan to any city in Australia is 12+ hours. That's a much longer flight than New York to London.
Wow, HN is strange sometimes. Have covid19 strains become political/tribal somehow?
I'm just pointing out something interesting in the data I was curious about. It's a pity HN picks out one detail and ignores the interesting thing... but upon reflection, pedantry is typical of today's HN, and partly why pg withdrew.
Regarding Australia, it's often said we are in the Asia region. And for the specific purposes here, of initial transmission, we have much contact with China, through tourism, education, primary produce and trade in general. It's expected we'd get initial infection direct from China (which trwcing shows we did), rather than via Europe.
I didn't downvote you (can't even if I wanted to since you replied to me!), but the difference in outcomes is unlikely to be explained solely by differing strains, and there's no evidence at this time that the mutations have any biologically meaningful difference:
A series of similar events in similar circumstances can be explained by a series of different causes, but it seems worth looking at a similar cause, no? This is at the stage of initial hypothesis.
Gosh, maybe people thought I was saying it was the absolute truth.
Canada has had a unique situation in that a large proportion of the population was out of country when the pandemic went exponential outside of Wuhan. The large number of imported cases represented every isolate found globally. Perhaps this hypothesis has been ignored but it seems that functional change should have jumped out of this dataset.
The author is Vincent Racaniello Ph.D., Professor of Microbiology & Immunology in the College of Physicians and Surgeons of Columbia University(https://www.virology.ws/about/)
In addition, he is possibly the most prolific podcaster of our time. He's started no less than 6 different podcasts over the last decade or so, collectively known as the TWIx podcasts (This Week in Virology/Microbiology/Parasitology/etc. I'm a huge fan of TWIV, but they're all top-notch.
The crux of the argument is showing different strains requires showing different phenotypes, and that that hasn't been supported with enough evidence. D614S is taken as an example, which purportedly increases transmissibility (thus would be a different strain), but most-likely doesn't. Apparently the data in support of D615S is just based on it being found in a lot of isolates-- but that would also be seen in the case of founder effect.
Did anyone else notice the ".ws" domain of the site and, not being familiar with the site, immediately think "that looks a bit shady"? That's been the long-time association of that TLD for me, probably because a lot of cracks/warez/virus (the computer type) sites used it, along with SEO spam and such.
There are several downvoted comments here attempting to express the common idea that this virus has impacted different regions in very different ways. That observation alone is not an argument against there being only a single strain of this virus, but it is a valid observation in its own right. There are plenty of half-explanations that rely on cultural differences (hand shaking, masks), climate (heat, humidity), and various other factors, but so far no one has proven precisely what factors make the biggest differences. That piece of information is one of the most valuable things in the world right now and we do not have it.
The other big factor is the different government responses, but these are all over the map. Specifically, the lack of a lockdown does not always equal a high rate of transmission, and the presence of a lockdown does not always result in a low enough rate of transmission to avoid a crisis. This is something we should all be curious about.
> lockdown does not always result in a low enough rate of transmission to avoid a crisis.
On that topic, Cuomo just declared that among the last batch of infected people in NY, more than 80% were apparently respecting the lockdown and staying at home and we have no idea how they were even contaminated. Puzzling.
That makes sense to me. The lockdown has reduced people getting infected from being out. There are still people getting infected and that is people in institutions (care homes, prisons, hospitals) and people in houses. Ie if one person in a house of 4 gets the virus and passes it on to the rest of the family 75% of people infected were staying at home.
Generally lockdown in the US has been pretty loose. Many people have left their homes, and had the opportunity to be exposed.
I also think there is a likelihood that between presymptomatic/asymptomatic transmission, and the possibility of 2 week incubation this seems like a nightmare to track transmission.
A friend who had SARS-cov2 was sick for 30+ days. So it’s not clear to me that a mild infection would be over in 14 days.
If it's a mild infection, by definition, the immune system has squashed it. If it didn't, the virus would take hold; it's not a latent viral infection like herpes.
Edit: okay, okay, I didn't specify "a mild infection that stays mild and goes away". We know complications can arise and the infection can progress into severe symptoms. Plenty of examples.
The evidence does not support this viewpoint. Also, things are complicated by the evidence that the worst symptoms are caused by cytokine storm, i.e. an auto-immune response.
Perhaps I should have said there is no evidence that I am aware of that supports that viewpoint. Instead, there is evidence that asymptomatic people can transmit the virus. No symptoms does not mean no virus.
There are plenty of cases that start with mild symptoms, and then progress to severe/critical after about a week. Boris Johnson is a perfect example of this.
I've had coughs that have lasted a month or more - including at the start of lockdown [#] (caught from my son, I think, who was coughing for 8 weeks or more). I've always assumed that this is because a virus can be kept at low levels, but can "hide" in the body not coming across antibodies that will harm it, but not spreading enough to create a heightened immune response??
Kinda like when you don't take a full course of antibiotics, the latent infection grows again to problem levels.
You indicate this is wrong thinking (not a suprise as it's just a null hypothesis from someone without biology training): so what is going on when you have a cough/blocked nose for weeks on end?
{# I'm very curious to find if the virus I had was Covid19; it sent me to bed with mild flu-like symptoms, gave a tight chest, had me occasionally [not persistently] coughing for weeks. No noticeable anosmia. Very little phlegm; no snot (nasal/sinus mucus).}
More importantly than the tightness or looseness, we don't really have any facilities set up for if one member of a household gets sick and wants to stay away from the other members and not infect them. I can understand discharging patients back to their families before they're PCR negative because infectiousness in SARS-CoV-2 seems to be very frontloaded. But for people recently diagnosed with mild cases of Covid-19 it would be good if we had places for them to quarantine outside their households even if it was on a voluntary basis.
No, the virus doesn't just float around in the air, at least, not for any appreciable amount of time. It's much more likely that people in these apartments are touching the same elevator buttons and then wiping their eyes and contracting the virus.
> No, the virus doesn't just float around in the air, at least, not for any appreciable amount of time.
Here is a pretty approachable summary of how transmission happens that contains a review of some specific cases where airflow was critical to transmitting the infection: https://erinbromage.wixsite.com/covid19/post/the-risks-know-.... None of these occurred in isolated spaces connected by shared ventilation but I would be cautious about saying flatly that it can't happen.
I didn't say flatly that it can't happen. I said it can't happen at any appreciable distance. Obviously, if someone sneezes in your mouth your going to get sick.
That's not what you said, and why don't you take a look at that article I linked. The restaurant case and the call center case it looks at were hardly in the category of "someone sneezes in your mouth."
> No, the virus doesn't just float around in the air
I'd be interested in any references you can point to that explain why that doesn't happen. A priori I would expect virus particles to be able to remain airborne indefinitely. Viruses are very small, much smaller than pollen grains that I believe are well known to remain airborne over long distances so I would think Brownian motion from collisions with air molecules would suffice to keep them aloft.
The setup of this whole thread is 'trustable data and scientific method'.
Also, please be aware that a name is often not enough to show that a source is relatively trustworthy, some credentials can help; this is a worldwide forum.
Surely that depends on whose tweets they are? If its Jeremy Konyndyk or Scott Gottlieb or such that's a pretty decent source. If it's a celebrity or political figure or some random person less so.
It's precisely because of the way infections cluster in cases like that that we can tell that we're not seeing (much at least) long range airborne transmission. It this was a true aerosol like you see with chickenpox, measles, or TB you wouldn't be seeing such a nice separation as that. It looks like the furthest away you should be able to be infected someone is maybe 20 or 30 feet if you sneeze without covering your nose. That's the significance of Mr. Konyndyk talking about droplets rather than aerosols. Though it was a big deal in the original SARS outbreak that you could generate aerosols via intubation which caused some nurses wearing surgical masks to get sick in that outbreak.
That agrees that the virus is mostly transmitted via droplets rather aerosolized virus particles. A bare virus can float in the air for quite a while but all the evidence we have, especially stuff like form that site, seems to show that that isn't a route by which people are being infected. Instead its being transmitted over shorter distances, generally around 6 feet but longer if someone is shouting, singing, coughing without covering, or just directly downwind.
I think what the parent commenter is saying is that maybe the virus stays in the air like that but it's not a way in which people get infected, otherwise the clusters wouldn't be so tight. Any tracing would be impossible for example. One possibility is that you need a threshold amount of virus to infect you so close contact is necessary.
That plumbing was not in any way up to standard. If you've got s-curves in your pipes you shouldn't have anything to worry about with getting this (or cholora, or norovirus) via your toilet from another unit.
I don't think we've actually had any fecal transmission with SARS-2 either, or even had someone successfully culture live virus from a stool sample. We've seen a lot of virus RNA show up in stool from infected patients but that might be due to swallowed saliva. I'd try to avoid contact with other people's feces in any event but the danger here really does seem to be mostly droplets.
Reference:
"Preliminary data submitted by 113 hospitals over the last three days show most new admissions have mostly been staying home; they're predominantly from the downstate area (57 percent NYC, 18 percent Long Island) and people of color. Most of them are older and non-essential employees; 66 percent were admitted from their own residences.
Of the new New York City hospitalizations, 90 percent have not been traveling by car service, personal automobile, mass transit or even walking around. If they've been working, they've been doing it from home and apparently weren't going out much, the governor said."
There's a strong incentive, if you're going in to hospital with Covid19, to lie. They ask "were you sheltering in place?" and you'd think "if I answer no, will I be denied care?". That's going to make survey almost useless, a secondary survey (eg speak to neighbors) might be better but would still be relatively poor.
* Hospitalizations, not cases and not infections. That skews old/out of the workforce.
* The stat is that 66% live at home and 84% not working.
* That doesn't mean they are 100% to the letter respecting social distancing. Nor does it mean they don't have housemates that aren't working. (That could be the case, but there's no data).
> 66% of the people were at home, which is shocking to us...This is a surprise: Overwhelmingly, the people were at home...We thought maybe they were taking public transportation, and we’ve taken special precautions on public transportation, but actually no, because these people were literally at home.
That chart is titled "Source of Admission," not "Was supposed to be staying home." Someone providing critical services who woke up with a fever and got tested would fall under "home."
There's also nothing to compare it to. What percent of people are in those circumstances?
To what I think he misread and was surprised by, the idea that most people getting hospitalized were sheltering in-place (a stat I haven't seen), with how many New Yorkers who have been exposed to SARS-CoV2, you'd expect essential workers who are going out every day to be more likely to be immune at this point, those sheltering in place aren't. More people are sheltering in-place than out working, they're less likely to have been exposed, so I wouldn't be surprised to see more of them infected. But again, that's not the data Cuomo was talking about with "66%."
I wasn't sure about publishing this but I took some time to go over Worldometers' data and associate a lockdown type to each country in the EU (+ a few more countries). There doesn't seem to be a strong correlation between how strict the lockdown is and the total cases per million people: https://www.notion.so/Lockdown-data-361fe56821d046a787d76535.... So, yeah, I completely agree with you. We should definitely try to find out what's going on.
I'm writing this because I think HN is one of the very few communities able to properly discuss ideas with hard science and facts. So any observation, correction, criticism etc. is more than welcome!
> I'm writing this because I think HN is one of the very few communities able to properly discuss ideas with hard science and facts.
I propose that if you pay very close attention to the nature of discussions, over a long period of time, across a broad spectrum of differing topics, you may notice that the ability to "discuss ideas with hard science and facts" varies greatly according to the topic.
Or to be more specific...when the topic involves issues that are "political or values oriented", as this one does, the discussion and thinking styles exhibited in the comments much more resembles that which you would find within less "logically capable" communities.
The COVID discussions have been the single most frustrating experience for me on HN since I joined. Ever single comment I’ve made downvoted, even accused of contributing to millions of deaths (an account which was thankfully banned for making the remark).
It’s only in the last week or two that it’s started to become remotely possible to have intellectual discussions on COVID, but it’s still overwhelmingly politicized and unscientific.
The problem is that you have every Jane and Joe who's ever put a line through a set of points making graphs and arguments that conflict with the consensus of epidemiologists/social statisticians. It's fine (and good!) to investigate that sort of thing and share your results, but then you should be sharing "I did this sort of analysis, it seems to conflict with all these other analyses, does anyone know why? Maybe X?". Instead you have "OMG when you do this it looks like Y, the powers that be are lying to us!".
For a non-critical issue this would lower the quality of discourse slightly, but it's not an exceptional problem. In the case of critical major issues involving active disinformation this is highly irresponsible behavior.
> For a non-critical issue this would lower the quality of discourse slightly, but it's not an exceptional problem. In the case of critical major issues involving active disinformation this is highly irresponsible behavior.
Assuming your description of "the" problem is accurate (I suspect it isn't - and it's "a" problem, not "the" problem, pardon the nitpicking), what do you propose should be done about it? On an individual basis, a community basis, a governmental basis, etc - what should be do? Because as far as I can tell, we (the citizens of planet Earth) seem to be stuck in this recursive loop of anger, finger pointing, and general failure. And it doesn't seem like anyone else notices.
I'd say that behavior is similar to if an individual in, say, a school or assembly, shouted "FIRE" upon witnessing a chemistry demonstration involving a controlled flame. If that somehow caused a stampede resulting in loss of life they might be held accountable by the courts. These acts on social media can be quite similar philosophically, so one would expect that the legal treatment should be similar (albeit perhaps adjusted proportionately for impact and reasonableness of the held belief).
I don't necessarily think that's what should be done in practice, but it seems consistent with how western society responds to this behavior in other settings.
I don't necessarily think there is a good solution, either - I just mean to say that people who do that, even if they are well-meaning, are behaving unethically. That's because they believe in their own perspective with 100% probability, but that's obviously unreasonable from a Bayesian perspective. If they accounted for even a small probability that they are wrong then their behavior would change dramatically.
> I don't necessarily think there is a good solution, either - I just mean to say that people who do that, even if they are well-meaning, are behaving unethically. That's because they believe in their own perspective with 100% probability, but that's obviously unreasonable from a Bayesian perspective. If they accounted for even a small probability that they are wrong then their behavior would change dramatically.
Completely agree, but I believe this behaviour applies to 90%+ of those who express confident opinions on the matters of the day, and downvote anyone who dares question those opinions when they can't put together a convincing argument for their strong assertions.
Some evidence for the frequency of this behaviour exists, we could have insight into it, but I suspect we shall choose to not discuss such things. Only downvote them.
Not the OP, but one thing that is vital is that those in power are inscrutably honest and value scientific method, IMO.
If a politician stands between the scientific advisors and the people then when they make pronouncements saying "this is for medical reasons" when in fact the reasons are primarily financial, or tempered by the interests of other parties (their personal backers), that needs to be made clear.
When the UK said "we're using different models" they should have been publishing those models, among with the facts they were relying on, published a list of all people who had input to that decision and the context.
A rolling diary of all people any senior politician had contact with; a list of every shareholding by any member of a politician's family; and such information need to be openly accessible in real time.
Basically we need to treat them as an obsessive helicopter-parent would treat their teenage children, they need to have tracking devices, they need to have "friends" (employees of opposition parties) that attend every meeting they go to, they've down they simply can't be trusted.
But of course you can't do any of those things because corrupt politicians won't vote for it. We're stuck at a local minima of democraacy, IMO.
How to progress? I don't see a way, politicians have enough of the population in their thrall (eg using media manipulation) to sustain the current system. Two things that may help are to have bodies parallel to government adopted ones, like UK's SAGE but excluding the politicians, and have media that will report direct from those bodies to the people rather than via a filter of politicisation. Maybe then enough people can get onboard to bit-by-bit elect trustworthy officials interested in government for the good of the people.
> When the UK said "we're using different models" they should have been publishing those models, among with the facts they were relying on, published a list of all people who had input to that decision and the context.
Everything should be published (it isn't), and nothing should be censored, without good reason (not the case today). That so few people seem to realize this is mind boggling to me. But then, it's human nature, so it shouldn't be surprising.
> How to progress? I don't see a way, politicians have enough of the population in their thrall (eg using media manipulation) to sustain the current system. Two things that may help are to have bodies parallel to government adopted ones, like UK's SAGE but excluding the politicians, and have media that will report direct from those bodies to the people rather than via a filter of politicisation. Maybe then enough people can get onboard to bit-by-bit elect trustworthy officials interested in government for the good of the people.
This idea, and others like it, seem like a very plausible way out of this mess. I really see no other way.
But how much effort, in man-hours, is being expended in this direction, as compared to, oh I don't know, people having the same arguments year after year, in thread after thread?
One part of being a community is slowly building values in new members. Many communities, many subreddits as an example, form monocultures and ruthlessly stamp out opinions not aligned to the deigned philosophy (and then being monocultures, they die a slow death).
HN as a community places value on interesting, well informed debates, but that value isn't universally shared outside of HN. It takes regular exposure to build that value in new members but over time they'll either embrace it or wash out of the community as long as we do our best to consistently embrace it positively.
Keep debating and pushing forward on interesting conversations, keep doing it politely and in the interest of meaningful debate.
> One part of being a community is slowly building values in new members. Many communities, many subreddits as an example, form monocultures and ruthlessly stamp out opinions not aligned to the deigned philosophy (and then being monocultures, they die a slow death).
Yes indeed. Reddit is famous for this, and getting worse by the day. But how might we know, for sure, the degree to which that also happens here? And I don't mean that rhetorically. We can all instantaneously generate "an" answer to that question, based on heuristics, but how accurate is that answer? To gain some certainty, it would require looking at actual data, which is firstly dependent on a willingness to look at the data, which is firstly dependent on a willingness to consider the idea that there may be a problem. This last point seems like a rather touchy subject.
"building values in new members" also seems like a well-accepted but heuristically-based idea. Is it, in fact, only new members who lack these values? Luckily, HN profiles contain an "accounted_created" attribute...with a little effort writing some scraping code (something I don't presently know how to do), I suspect some more precise, evidence-based answers would quickly reveal themselves.
What would be even more revealing would be if one had access to voting history. This way, we could get a decent feel for how certain individuals feel about this general topic. But alas, you and I don't have access to that data. But someone does (see: willingness to look at the data). Shall we truly pursue righteousness, or should we just declare ourselves to be, by fiat, as seems to be the most popular approach in broad society?
> HN as a community places value on interesting, well informed debates...
In the abstract, principled[1] sense, sure. But, how well do we "walk the talk"? Once again: what does the data say?
> as long as we do our best to consistently embrace it positively
And consistently. But now we're back to where we started.
> Keep debating and pushing forward on interesting conversations, keep doing it politely and in the interest of meaningful debate.
Despite the obvious unpopularity, and repeatedly inconsistent (again, based on topic) evaluation of "meaningful debate", as well as the HN Guidelines in general, I seem unable to stop lol
[1] "Lord, I promise not to sin!" Inconsistent adherence to an ideology, however strongly held in theory or principle, is not a problem only within the domain of religion, I suspect. Rather, it seems more like something inherent in human beings. Failure rates may vary fairly significantly across domains (or may not!), but this is a difference in degree, not a difference in kind.
You're right that at least large parts of this can be tested and answered with data. Obviously short of a magical classifier for questions like "is this a productive debate" and "is this ideological fighting or a search for truth?" then we're going to need someone to hand classify a bunch of things which is expensive, slow and only as accurate as the person making the judgement call. In other words, we'd just be making ad hoc judgements again, but calling them something else because we made those ad hoc judgements in a csv instead of a comment.
The other issue is that communities are dynamic, and behaviors trend. You're probably not going to see a flat correlation, you're going to see something that resembles a wave function.
> then we're going to need someone to hand classify a bunch of things which is expensive, slow
True. But not impossible.
And I would recommend comparing effort to potential reward. Imagine, just for fun, the possibility that HN could find a way to discuss climate change[1] in a disciplined, truthful, and non-heuristic manner. What might the value of that discovery be? And if we could find a way do it, perhaps others could as well?
> and only as accurate as the person making the judgement call
How deeply have you thought about that? Like, say it was an engineering problem you've been asked to solve - have you put as much effort into thinking about it as you would if it was a paid assignment?
> In other words, we'd just be making ad hoc judgements again, but calling them something else because we made those ad hoc judgements in a csv instead of a comment.
Do you realize you are:
a) predicting the future
b) making several assumptions
c) utilizing loaded terms (which is harmful not only to others, but sometimes also to oneself)
You should double check your definition for loaded language as I agree with the article you linked but not your usage of it. To quote from your source:
> Loaded words and phrases have significant emotional implications and involve strongly positive or negative reactions beyond their literal meaning.
I hope 'ad hoc', 'judgements', 'csv' and 'comment' don't carry any strongly positive or negative reactions, nor stereotypes or implications. (Though I have known a few people to have negative reactions to the idea of csv files...)
> I hope 'ad hoc', 'judgements', 'csv' and 'comment' don't carry any strongly positive or negative reactions, nor stereotypes or implications.
I would very much like for us to have a written language that has the same bandwidth as a long form, in-person discussion. But we have to play the hand we've been dealt, not the hand we wish we'd been dealt.
And to be clear, I don't object to your complaint, or consider it unreasonable - quite the contrary: this is the type of conversation I think we need more of. My comment above could have been improved by adding some disclaimers to make it explicit that I am not intending to speak in an "accusatory" manner, but I reckon the vast majority of people would have read it that way, and for good reason. So, apologies for that.
The ideas I had in mind are somewhat (again, limited by the fundamental shortcomings in our written language) captured in here:
> Loaded language (also known as loaded terms, emotive language, high-inference language and language-persuasive techniques) is rhetoric used to influence an audience by using words and phrases with strong connotations associated with them in order to invoke an emotional response and/or exploit stereotypes.[1][2][3] Loaded words and phrases have significant emotional implications and involve strongly positive or negative reactions beyond their literal meaning.
(The intent, emotional, and exploit parts I do not consider at all relevant to this discussion).
The larger, more abstract point that I'd like to make is: reality is infinitely complex, and we as individuals reason upon it with far from infinitely powerful minds. Now, start layering on all the other complexities, like collective reasoning (hampered by language and a variety of other things), necessities of being forced to make incredibly imprecise/coarse group decisions on a strict timeline (our political systems), complex and imperfect incentive systems, asymmetry and inaccuracy of information, advances in some domains (science, technology, industrialization) without corresponding advances in complementary domains (psychology, consciousness, etc), and so forth...and before too long you've got a bit of a mess on your hands.
Isn't this what Issac Ben-Israel claims in his article[1]? Basically there seems to be a common pattern in all countries, independent from the type of lockdown applied. After 40 days the peak is reached, after 70 days there are almost no new infections.
That’s not a useful comparison though. You want to compare cases now to cases when lockdown or similar measures were imposed. Otherwise a country that wastes 2 months doing nothing and then takes action far too late just gets put in the “lockdown” bin.
While I mostly agree with you, I wouldn't call the comparison useless. I want to add a few additional things as well that add to the difficulty of these comparisons (and why these simple comparisons people are making are potentially wildly inaccurate)
1) Testing is all over the place and mostly done only on people that are hospitalized. This creates a huge selection bias in official numbers, especially when we're talking about a disease where we're seeing claims from 25-80% of carriers being asymptomatic. There's plenty of evidence to show that many people that suspect themselves (i.e. they show symptoms) are not getting tested because they aren't "sick enough". So all we can do is guess that official numbers are on the low side. This is part of why we see wildly different CFR numbers (as opposed to IFR) in different countries. (Obviously there are other factors as well, but this one captures effects like living conditions)
2) Deaths are being attributed in different ways. In some areas any pneumonia death is being counted while in others the person must have tested positive for covid. In America the attribution even varies by state. What makes this more complicated is that when the metric changes these tend to be deaths added on a single day (creating spikes). This makes it difficult to do 1 to 1 comparisons.
3) The disease's fatality rate drastically changes with the victim's age. There's strong evidence to show that if you're healthy and young that you have little to worry. But if you're relatively healthy and old you should be concerned. There are drastic differences in country's age, and thus this makes a big difference in comparisons.
4) The number of cases isn't exactly a bad thing. Let's take Sweden for example. If their method for containment (develop herd immunity in the general population, isolate the elderly and immunocompromised, and social distance strictly to not overwhelm hospitals) is effective you'd expect a faster rate of new cases AND deaths. But if their method is the better solution they will have less total deaths by the end. But are they right? No one knows yet because we need time. Time is a difficult factor to work into these comparisons, which are often single snapshots rather than growth rates and inflections.
I think cases/1M population is a good variable though. Deaths depend on the quality of the healthcare system, number of infected people (per 1M) only by how quickly the virus spreads + number of tested people (assuming the quality of the tests is the same across all EU countries). Would you please elaborate on that?
Cases are a difficult metric because there's a selection bias. Most places, including the US, does not have adequate testing. Especially for a virus we suspect a significant amount of people to show no symptoms. We're mostly testing those that are hospitalized.
Deaths, on the other hand, are easier (but not perfectly) to count because it is much more clear that someone has died. The symptoms are trivially obvious. The difficulty here is that there is no universal attribution (even within the US) as to what constitutes a covid death. Let's show a tricky example. Let's say an elderly patient had a stroke and are in the hospital. You THEN get infected and die. Did you die from the stroke or covid? Is this as deadly as a disease that kills a healthy 60 year old? How do we distinguish this?
I'm just trying to say that without context these simple comparisons can miss a lot of nuance of the reality of the situation. The thing here is that there are a significant number of variables at play and without discussing those variables you can get inaccurate results.
I agree, that's why I published the table and anyone can comment (in Notion itself), therefore contribute. I think such a comparison can at the very least spark the discussion you mention.
> so far no one has proven precisely what factors make the biggest differences.
The problem is in the question itself. Behind it is an expectation that there is just a tiny number of "magic spells" or "a trick" that would "solve" the problem, and that anything else is unnecessary.
The reality is the opposite: all the countries, and where the regulation was weaker, the people on their own, with the time attempted with different levels of success to protect themselves. They all did many things, many real people on many different levels, and with many not identical results. But it's much more complex than the assumption behind the question.
For example, people like to quote Sweden as some "magical other way country" whereas the universities and upper schools were shut down there too, it still has more deaths per capita than the US, the rate of new confirmed cases is not sinking etc.
Also, those who claim that there is an "impact" which "is different" typically don't try to fairly compare the actual impacts which are eventually much more similar when compared properly than implied in such a claim with no correct comparison done.
That is, a lot of such "arguments" are frauds which depend on those hearing it not willing or being able to look at the data properly.
I worked in finance for years, and I can tell you: if those who promote various claims in the news, media and social media would trade while ignoring so much data which is here so obviously available to find and compare, like they do in their claims, they would lose all their money in a blink of an eye.
I don't know how it would be possible to organize that, but if people who claim bullsh.t would have to invest some money behind their claims, and lose it if their claims would be proven wrong, we'd have much less insane conversations.
Just looking at the raw data and comparing can show you that a lot of claims floating around are plainly and completely false.
One page that allows magnificently easy comparison is
Additionally, one should search for the original sources of the information for different countries, and compare the numbers based on that additional information.
I can especially recommend translate.google.com for an amazingly efficient way to read some information from the original sources.
I strongly suspect when we're through all this, two things will probably be true:
-- We will probably be able to make some statements about what practices seem to have various effects for better or worse and what environmental factors (like density and isolation) tilt the results in one direction or another
-- There will remain debate over what we should have done given the benefit of perfect hindsight
-- However, we're also going to conclude that some of the wide variation in outcomes can best be described as luck of the draw
I doubt our hindsight will be perfect. 9/11 happened in broad daylight at 9 in the morning, in two major cities, yet it is almost impossible to suss out what actually happened that day based on the current, publicly available data. SARS-CoV 2 is probably going to get filed away into the "suspicious mystery" drawer, right next to JFK, Jimmy Hoffa, DB Cooper, MH370 et al.
There's a lot of political effort, it seems, going in to ensuring the truth is hidden from the demos. In part this can be considered necessary - some people need lying to in order to keep them compliant and save lives, but largely is about covering up errors of judgement, and decisions that have purposefully been made against population-health advice. That effect is reduced over time, but doesn't d disappear entirely; if a politician -- or political appointee -- is in charge of the output of a scientific advisory group then their filtering will likely obscure content forever.
The authors of the D614G paper do attempt to rule out a founder effect. I'm not saying their analysis is bullet proof, but the OP doesn't address its merits.
To differentiate between founder effects and a selective advantage driving the increasing frequency of the G clade in the GISAID data, we applied the suite of tools that we had been developing for the SARS-CoV-2 analysis pipeline (Fig. 2, Fig. 3, Fig. S2 and Fig. S3). A clear and consistent pattern was observed in almost every place where adequate sampling was available. In most countries and states where the COVID-19 epidemic was initiated and where sequences were sampled prior to March 1, the D614 form was the dominant local form early in the epidemic (orange in Figs. 2 and 3). Wherever G614 entered a population, a rapid rise in its frequency followed, and in many cases G614 became the dominant local form in a matter of only a few weeks (Fig. 3 and S3).
People like to classify things. They like having neat buckets to place things in, give them a name, make them feel like they have a handle on it.
The world is not easily classified. But people persist. So we end up with situations like "is Pluto a planet?" and "is a virus alive?" Then people start focusing on their classifications and definitions when in fact they don't actually matter to the reality of the situation.
I need to dumb this down more if the audience is a 5 year old.
People like to give things names. Like the colors: red, orange, yellow, green, blue and purple. But sometimes a color can't be easily named.
For example the shirt I'm wearing might look blue to me and green to you. Then we start arguing about what color the shirt is when what we really should talk about is if it matches my pants.
Because by themselves, they don't have most of the properties of living things. They have no metabolism, and they do not reproduce, for example. They're kind of like (physical) books. They can affect living things (people), and some books cause living things to reproduce the books, sometimes in large numbers. But few people would regard books as alive in the way that a dog or tree is.
Can someone explain to me like I'm 5yo why a virus is not considered alive?
Because the scientific community carefully picked certain completely-arbitrary attributes with the intent of drawing a bright line of division between viruses and cell-based organisms. This doesn't make the slightest bit of sense to Mother Nature, of course, but it makes sense to the scientists.
A much better definition of "Alive" would simply be, "Subject to the rules of evolution by natural selection." Viruses certainly quality under that rubric.
I'm not an expert in this field or any related fields. I am, however, in a field where I have to frequently communicate on technical topics to a nontechnical audience. The following is a critique of the technical communication in this article, not of the science.
There are some more nuanced claims which are made or hinted at:
1. There's not adequate evidence to prove a difference in mortality between the L and S variations of the virus.
2. There's not adequate evidence to prove increased viral transmission over time of the virus.
And if your definition of the word "strain" is "reserved only for special changes that confer a new property to the virus", then both of those would be arguments that there's not adequate evidence to prove the existence of different strains of the virus.
However, is the definition of the word "strain" really the important point you want to communicate? Either point 1 or 2 could have been made without talking about the word "strain" (note how I sidestepped the whole strain/isolate issue by using the word "variation"). I would argue that either of those two points are much more important than the meaning of the word "strain".
Sure, using the proper jargon is a strong indicator of expertise in a field. But jargon arises from expertise, not the other way around. Correcting people's jargon before they have the adequate mental framework to differentiate between the terms just creates conflict and is counterproductive.
Yes, science can be pedantic at times, but I do believe that it's necessary to describe terms before you discuss why they're important. For me, this article reads exactly as I was taught to write technical papers. It builds upon the definition of "species" to make an argument against the reoccurring claims that this virus is mutating to become more transmissible. Of course, I did study microbiology at university, so I can see how others might find it too focused on the jargon.
What this pandemic has taught me over anything else is that wielding scientific terms without proper understanding is damaging to progress of science itself. It becomes difficult to tease apart legend from fact, especially for those not trained to do so. I go crazy every day listening to half-baked hypotheses and conspiracies that don't understand the foundations for the things they're claiming.
All this said, Dr. Racaniello is very gracious and humble. He has dedicated his life to teaching, both in the classroom and through his podcasts. I highly suggest sending him your concerns about his discourse and subscribing to his podacast TWIV [0]. He and his colleagues respond to every email at the end of each podcast.
> Yes, science can be pedantic at times, but I do believe that it's necessary to describe terms before you discuss why they're important.
Yes, it's necessary to describe terms, but there's a big difference between giving a definition of "strain" at the beginning of your talk, and explicitly correcting everyone who has misused the term. One is necessary for clarity, the other is unnecessary and combative.
> What this pandemic has taught me over anything else is that wielding scientific terms without proper understanding is damaging to progress of science itself. It becomes difficult to tease apart legend from fact, especially for those not trained to do so. I go crazy every day listening to half-baked hypotheses and conspiracies that don't understand the foundations for the things they're claiming.
I don't think that's true. It's not the terms being misused. You can still say the wrong thing with the right terms.
Let's take a summary of the story that was going around for a bit, "There are two strains of coronavirus, the S strain and the L strain. The L strain is more deadly but it isn't spreading as quickly because sufferers are more likely to be identified and treated/quarantined."
That statement is wrong, because there isn't enough scientific evidence to declare any of that. But is the problem the misuse of the word "strain"? I don't think so. Consider the following: "There are two variants of coronavirus, the S variant and the L variant. The L variant is more deadly but it isn't spreading as quickly because sufferers are more likely to be identified and treated/quarantined."
I'm not an expert in the field, but as far as I know, the word "variant" doesn't have any specific meaning that would say it's being misused here. But nothing has changed: the summary is still 100%, completely wrong, because there still isn't adequate scientific evidence to say there are different variants with different mortality rates.
And, critically, even knowing the definition of the word strain, I can still say the first version of this incorrect statement and be wrong, not because I'm misusing the word, but because there isn't adequate scientific evidence for what I'm saying.
> All this said, Dr. Racaniello is very gracious and humble. He has dedicated his life to teaching, both in the classroom and through his podcasts. I highly suggest sending him your concerns about his discourse and subscribing to his podacast TWIV [0]. He and his colleagues respond to every email at the end of each podcast.
I think it's especially necessary to combat this kind of inaccuracy when the word "strain" also has strong non-scientific connotations.
Completely ignoring what "strain" means to a virologist, when you tell a layperson that there is a new strain of something, they generally will worry, and think one (or more) of the following: a) the existing vaccine or vaccine in development won't cover the new strain, b) existing treatments for people who are sick won't be effective, c) it's easier to catch, d) they're more likely to die of it. The fact that a new strain is related to a distinct biological difference doesn't matter; what people care about is what a strain means for their health.
So even if you ignore the scientific-jargon meaning, it's important to recognize the layperson meaning, and ensure that you stamp out inaccuracies based on that meaning as well. As much as you'd like to educate everyone as to the true meaning of some terms, it's a losing battle, so you might as well just recognize how people use a term and speak to that usage. In this particular case, the scientific and layperson meanings aren't exactly the same, but it's just as important in both arenas to clear up misinformation.
I do think they're both important, but it's more important to me to clear up inaccuracies based on what people are trying to communicate, rather than the specific words people are using.
For example, if the narrative were, "The S strain and the L strain aren't meaningfully different", would that be a concern? Sure, but not a big one. Sure, it makes no sense to call them "strains" if they aren't meaningfully different--that's a misuse of the word "strain". But the layperson would have the correct impression of the situation from that statement.
I tend to disagree. I think that the layperson has a generally accurate understanding of the word strain in this context, namely, they are materially different. News stories about new strains pull attention for exactly this reason.
The layperson would have the correct impression of "The S strain and the L strain aren't meaningfully different", but the wrong impression of nearly every other sentence starting with "The S strain and the L strain..."
The article sets out specifically to caution about the misuse of jargon, so I think that probably is the important point that it seeks to communicate. I think that it goes off track and gets bogged down a bit in the details of SARS-CoV-2.
There are two critical weaknesses in what has been written, taken as technical communication rather than blowing off steam.
Firstly, it does not do a good job of providing the reader with an alternate word that expresses the relationship for which 'strain' is being misused (in the author's opinion).
I believe that he himself would describe identical genome sequences as being the same virus 'isolate', but he doesn't explain that well, and the practical etymology of the term — the notion that the same virus isolate could be isolated in two different instances — makes adoption difficult. If this is indeed how 'isolate' would be routinely used (I am not even sure, as he doesn't establish this clearly) then it would be an instance of something that we might call 'deep jargon' or 'cryptic jargon', when normal words have specific meanings in a professional context that require a mental compartmentalization.
Secondly, it does not establish why it is important for a less-informed reader to draw the distinction between a _____ of the virus and a new strain of the virus. We can imagine that there are differences in importance between a mere genetic difference, a genetic difference with functional biological consequences, and a genetic difference with epidemiological consequences. It is probably our expectations for the last of these, based on prior experience, which makes the distinction important; a very critical difference would be if the immune response to one strain was ineffectual against the other. However, this is muddled in an attempt to instead explain why it is difficult to distinguish the founder effect from biological selection.
> The article sets out specifically to caution about the misuse of jargon, so I think that probably is the important point that it seeks to communicate. I think that it goes off track and gets bogged down a bit in the details of SARS-CoV-2.
That's an interesting hypothesis and you're making me think that maybe I was wrong. It certainly was effective in getting me to stop misusing the word "strain".
My argument was based on the idea that they were trying to communicate the fact that there are no meaningful differences between different genetic sequences of SARS-CoV-2, and got bogged down in the semantics of the words "strain" and "isolate".
As a scientist, but not a technical expert in this field, I felt that this article read pretty straight forward. Though I will admit that there could be added clarity for a more general audience (pretty much all work can).
> is the definition of the word "strain" really the important point you want to communicate?
I think in the author's case, yes. If you are unfamiliar with the subject you learn some nuance about the subject and the terminology used. A basic understanding of the science should have already clued you into that viruses don't replicate perfectly, so the reader should question at what point a change constitutes a new strain. The author answers this question in the beginning.
> A virus strain is an isolate with a different biological property, such as binding to a different receptor, or having a distinctly different stability at higher temperatures, to give just two of many possible examples.
So we learn simply that the different isolate has to have a new biological property. More akin to having a third arm rather than a difference in skin color.
The author circles back to this with a clear example:
> The most recent offender is a preprint claiming that SARS-CoV-2 with an amino acid change in the spike glycoprotein (D614G) increases the transmissibility of the virus.
> Until proven otherwise, their emergence is likely due to the founder effect. Let’s say a virus with D614G emerges during replication in a person’s respiratory tract. If viruses with that change infect the next person, and the next, and so on, then the D614G change will predominate. The change is simply __a single nucleotide polymorphism of little consequence.__
I do think here the author could have strengthened their argument by noting what the founder's effect is.
> (via wiki) the loss of genetic variation that occurs when a new population is established by a very small number of individuals from a larger population.
So the author gives a reasonable assertion for this observation. We then apply Occam's razor and we have the author's thesis. (He should have stated this explicitly)
> As a scientist, but not a technical expert in this field, I felt that this article read pretty straight forward. Though I will admit that there could be added clarity for a more general audience (pretty much all work can).
Yeah. My concern isn't that the meaning wasn't clear. My concern was that by focusing on the semantics of the jargon, it comes across as combative and alienates readers over something which is ultimately not important.
I think you and I are at a point of understanding where we're able to receive this feedback on the terminology and correct our own usage very quickly. I've certainly taken note.
Then I mischaracterized your critique. I do think the author is combative. This is an unfortunately common problem in science discussions, but I think within the community is has become normalized to such a point that anyone that isn't a junior isn't really put off from it. I do think this is a thing the community can work on in general that would help bring people in (imo, everyone should be doing "science").
Well we're chimps that can barely communicate with one another even when we speak the same language. We'll always have room to improve. (considering that you're the top comment, I think more people accurately characterized your message. Comments are more likely to happen with a mischaracterization and can be selection bais)
Viruses get small mutations as they multiply. By now, there is likely huge amount if unique viruses, not a single one. But, most mutations don't actually change anything because they might hit non coding part or maybe she mething unimportant so for the purpose of our communication we lump them together and call them strain.
Most of the time we only start discerning differences when they change the virus behaviour in an interesting way, and most of interesting stuff is around how it propagates, what it does to us and what it is susceptible to.
The final thesis thus should be that there's no adequate evidence that there are two strains. Not an affirmation that there is only one strain. Absence of proof vs proof of absence.
This echoed what Peter Kolchinsky (Harvard-trained Virologist turned VC in Life Science)[1] had said why the initial wave of vaccines for SARS-CoV-2 will arrive and will be mostly effective[2]
Vincent Racaniello's[0] YouTube channel[1] is well worth a visit. He publishes his lectures on virology on the channel, updated each year to reflect latest research etc.
His website Microbe.tv[2] also hosts various regular podcasts (which are also published as audio to YouTube) about virology and microbiology, they're very interesting.
It is ironic that this blog post is published just a little after a preprint was posted making a case that the D614G mutation has biologically significant differences. There is an explanation of the paper here: https://chrismasterjohnphd.com/covid-19/why-the-mutated-viru...
The tone of this content seemed a bit off to me. It converted a high degree of certainty, when the purpose was to decry that we are placing a high degree of certainty on a fact that is unproven and likely unprovable, if not totally untrue. Seems ironic.
Anyway, this was the money line to me: "For an amino acid change such as D614S to be positively selected, as opposed to being maintained as a consequence of the founder effect, requires selective pressure. For such an already highly transmissible virus, the nature of such selection pressure is difficult to discern."
This is backwards of what science does. Science doesn't really rule things in, rather it rules things out till there is nothing left. For example, take the discussion about D614S here. The original claim was that D614S makes the virus more transmittable, and the author claims this is wrong. Who has the burden of proof? It is the researchers that claimed D614S made Cov2 more transmissible. The author here points out that there is no selection pressure here and that there is a more reasonable solution to the results. Occam's razor is in play.
So not all arguments need a burden of proof. It is the one that is making the claim that has the burden.
Except the claim was that there are more than one strain and the author is responding to that. The burden of proof lies in the one making the claim that there are multiple strains. The author has no burden of proof.
This would be akin to one person making the claim: "Unicorns are not only real, but are causing a global pandemic" and then someone writing an article titled "Unicorns aren't real, STFU". The second title doesn't have the burden of proof and we wouldn't be having this conversation if these were the titles of the respective articles.
Why is the unicorns title an accurate analogy? Because the science doesn't expect there to be multiple strains in the same way the science doesn't expect unicorns to exist. I'm using the same vernacular here that we use in science. I didn't say "unicorns don't exist" but "we don't expect unicorns to exist". This is how we say things.
That's the thing. Science is a bit of a different language from English. And they get conflated all the time. The strain doesn't exist until it does, and then everybody gets mad and thinks the scientist was lying.
It's speaking different languages that have a high overlap, but key words may have completely different meanings.
And, when you're talking to a regular person, being able to speak English will help you convey your point.
My point is, this post was supposed to be written in English, but its headline only makes sense in science, and actually means something misleading in English
213 comments
[ 2.9 ms ] story [ 161 ms ] threadWhy the impulse to round off uncertainty to certainty? Ed Yong explained it better:
https://www.theatlantic.com/health/archive/2020/05/coronavir...
More seriously, I get your point but many discoveries are done by finally observing something which existence has been anticipated, hypothesized but still unproven. A planet that had an effect on nearby objects because of its gravity for instance. Or the Higgs boson.
So, yes, thinking of things that are not proven to exist (yet) is often scientifically helpful.
You still want to apply Occam's razor of course.
Is that clearer?
In Canada, our officials said in January that asymptomatic individuals were not main drivers of epidemics.
And while that may have been true with something like influenza, a more accurate statement would've been we don't have evidence _yet_ that suggests asymptomatic individuals could effectively spread the virus.
We proceeded to operate on that assumption by not forcing incoming travelers from infected regions to isolate, unless they contacted health officials with symptoms associated to the virus. We didn't change this stance until late March, well after the virus had infected thousands of people across the country.
In contrast, Taiwan implemented mandatory 14-day self-isolations for incoming travelers from specific regions as early as late January.
In Ontario, we've had cases of airport taxi drivers pass away from Covid-19. Whereas Taiwan recognized that there'd likely be a large number of people coming home with the virus, so they created special airport quarantine taxis equipped with mandatory masks for passengers and isopropyl alcohol for the driver.
So, yes, I'd agree with your 3rd para, but press can spin such statements to create reputational damage which is really underserved.
And then, just because a silly observational threshold was passed “PANDEMIC!!!!!”.
Same as “not recession/recession” just because of a silly totally arbitrary threshold...
Words have meaning, and pandemic a very specific one. Would you have declared SARS a pandemic when the first cases started to show up simply because it's a scary virus?
The definition of a pandemic is very simple:
> an epidemic occurring worldwide, or over a very wide area, crossing international boundaries and usually affecting a large number of people
Laymen are perfectly capable of understanding this, and forming their own perfectly reasonable opinions about it themselves. It is perfectly reasonable to criticize the WHO’s decision making around this, and they absolutely don’t have a technical definition to hide behind.
[0]: http://www9.who.int/bulletin/volumes/89/7/11-088815/en/
How media communication works is that the disease was hyped as a major threat to humanity in January (why would we even be hearing about a disease in China otherwise?), but everybody still downplaying the threat in late March is furiously spinning that they didn't receive any warning
There's a lot of grey area within "wasn't saying this virus was not a threat of becoming a pandemic".
It's a problem I see a lot in technical people (often somewhat on the spectrum). They communicate everything technically correct, but with complete disregard for how the nuances in framing alters the perception to other people.
You can argue that the recipient is responsible for assessing everything they hear/read correctly, but I would put equal responsibility on how you choose to communicate yourself.
We're drifting somewhat from the context, but the main one affected by how other people interpret me is me, so I have a lot of incentive to self-reflect on how I'm perceived.
"Falling out of an airplane doesn't kill you" might be technically correct, but it betrays the very concept of communication.
Denial - It's not really a problem. We don't have to disrupt our lives. It will all disappear in a few weeks. It's all a conspiracy theory.
Anger - If (some organisation) had done their job, we wouldn't be in this mess! It's all the fault of the (some country)!
Bargaining - If we get the new cases below X (or wait for X weeks), then we can all go back to our normal lives. I did what I'm supposed to do, you can't tell me I have to shelter in place any longer (well, a little bit of anger mixed in there)
Depression - We are so screwed. That's it. The world as we knew it is over. Our politicians, health organisations, etc are so incompetent that there is no escape.
Acceptance - Yep. It's a bad situation alright. However, it will pass eventually. It will be difficult for people. A lot of people will die. A lot will lose their jobs. The economy will probably be hurting for a very long time, but we will come out of it eventually.
[0] https://www.psandman.com/col/teachable.htm
[1] https://youtu.be/ogf6Hru2trE?list=PLRgTUN1zz_oeQpnJxpeaEkFim... (queued up to when he talks about this article)
If they were two strains of SARS-CoV-2 but your body fights them the same, that's as good as only one strain for most people. But still very interesting for scientists.
Equivalently, if we see lots of differences in base pairs but no differences in biological properties yet, that might still alert us to the possibility of new strains rapidly emerging in the future.
My hypothesis is that while Asia was originally infected by Wuhan originated strain, the Western Europe and US may have been infected by a mutated strain. The differences in impact in different countries is very difficult to explain without the hypothesis of multiple strains.
Edit: There was a decent article recently (I am unable to find now, most probably from NYT, WSJ) that addressed several factors mentioned in replies and showed none of those could explain the discrepancy in cases across countries. For example, high temperature and warm weather don’t explain differences in cases between Singapore, Thailand, Indonesia, Malaysia, and Amazon region of Brazil.
The closest article, I could find using google search is from Brookings.
https://www.brookings.edu/blog/future-development/2020/05/05...
More than 700 passengers on the Diamond Princess were infected, leading to a total of eight deaths. This would have been an older-than-usual cohort, simply by dint of demographics on cruise ships.
Meanwhile, in New York, deaths in long-term care homes have approached 5,000.
Obviously nursing home residents are a more vulnerable population, but with this kind of disparity in outcomes, I'm not buying it. Nursing homes may have an older clientele, but then, cruise ships aren't staffed by medical professionals.
IMHO it's been obvious that there are multiple strains in circulation for a long time. Otherwise, the medical community needs to explain exactly why outcomes vary so dramatically, not only from one individual to the next, but between populations with similar demographics. When they explain that, then I'll be more interested in their opinions regarding how many strains are out there. If they think the bugs are all the same, they aren't looking closely enough.
Closer to equator you go, less there is seasonal forcing in respiratory viruses.
This is my hypothesis of lower impact. Both India & Germany have low CFR and we find that in Germany 49% of cases are under the age of 50, while in India 70% of cases are under the age of 50 years. On the contrary, in Italy 70% of Covid infected individuals are above the age of 50, with 39% above the age of 70 and Spain has 69% of cases above the age of 50 with 37% above the age of 70. US case data by age is grouped somewhat differently by CDC but my guess is that close to 40% of infections are in the age-group below 50 years and about 20% are above the age of 70 years, this might partially explain the relatively lower CFR because CFR for ages under 50 is ~0.4% if you are in the age-group of 40-49 & lower below. Median age of the population for these countries are India - 28, Italy - 46, Spain - 44, Germany - 48 & US - 38. Germany seems to have either done something differently here.
This can only partially explain the differences but would be an important factor when looking at overall fatalities.
The reality is that government measures seem to have had the biggest impact by far. Western Europe and the US have badly dropped the ball on this issue, whereas Asian and Eastern European nations have mostly handled this much better for their citizens.
> In population genetics, the founder effect is the loss of genetic variation that occurs when a new population is established by a very small number of individuals from a larger population.
https://en.wikipedia.org/wiki/Founder_effect
Anyways, to be more on topic, I read this quote from the article: "Because of the founder effect, showing that a particular mutation increases viral transmission in humans is very difficult." Does the author here mean that it is hard to determine whether a mutation increases viral transmission in humans or not because that mutation's survival may not necessarily be the result of genetic fitness but founder effect?
[1] https://onlinelibrary.wiley.com/doi/abs/10.1002/jmv.25902
[2] https://en.wikipedia.org/wiki/Clade
[3] https://nextstrain.org/ncov/global
Strain implies functional differences. SARS-CoV-2, like it’s Coronavirus cousins, is quite stable. The genomic sequences found on NextStrain.org are a powerful tool to track the spread of this virus but it is wrong to assume that the difference in each “isolate” carries with it a functional difference; it does not.
The blog post comes from the same scientists that create the TWiV (This Week I’m Virology) podcast which continues to be a tremendous source of quality information for me.
Is that what people are assuming?
It's not that every mutation causes a [medically relevant] functional change, it's that a mutation could have. And, AFAIK, we don't have the ability to sequence _and_ relate sequences to differences in symptoms in the general case at present.
Maybe in 10 years someone will have developed an AI to relate RNA sequences, medical history, and functional changes in real time??
What about the reports of different strains that focus on having found them having different properties (such as "much more infective")? Are they bogus?
[1] https://www.biorxiv.org/content/10.1101/2020.04.29.069054v1....
In any case, there are multiple credible sources that some of the mutations of the SARS-CoV-2 have a meaningful effect. In which case the claim of this article that "there's only one strain" may be technically correct (based on some obscure scientific definition), but completely misguiding as far as the general public is concerned.
[1] https://english.alarabiya.net/en/features/2020/03/25/Coronav...
I don't see any support at all for that theory though. It is also known that "X show no symptoms" could mean many things, depending who says it and when, and certainly doesn't prove anything alone, only in context, compared to something else, and only when comparison is fair.
For example, from many old news, those "with no symptoms" eventually had the symptoms, it was just that the tests were positive before they developed the symptoms. Second, it is now known that the probability of "having" symptoms is very dependent on the age of the person.
I didn't have a particular paper in mind that I remembered.
Just remember reading several articles in the past month about new strains. Some examples are easy to find:
https://www.abc.net.au/news/2020-05-06/new-coronavirus-covid...
https://www.cnbc.com/2020/05/05/the-coronavirus-mutated-and-...
https://www.usnews.com/news/health-news/articles/2020-05-06/...
E.g. somebody claiming they invented a perpetual motion machine.
Their claims might not include any conspiracy involved, just a bogus idea of what they accomplished...
Put more simply, two samples of virus can be of the same "strain" even if they aren't _exactly_ the same sequence. This is because replication can sometimes make errors on segments of the genome that do not impact functionality - moreover these same irrelevant loop segments are not error-corrected either, so mutations are common - despite not modifying the properties of the virus. These irrelevant mutations are actually very useful for tracking the virus spread.
A virus mutation becomes a different "strain" when the change is meaningful for the viruses interaction with the host or the environment.
SARS-COV2-2 is a type of virus that does error correction (unlike flu), so the rates of mutation are extremely low. This is good news because if means a vaccine will work, and we won't need a yearly one - like the flu.
You are literally nitpicking the wrong people here. They're trying (well, I thought, though clearly not well enough to satisfy HN pedants) to explain the distinction in a way that conveys the fact that there are no known distinct outbreaks with different medical properties. How that's for precision?
That's way ahead of the facts. It means we're more likely to be able to develop a vaccine that works and it's more likely we won't need frequent vaccination to be effective.
Vaccine success involves a certain amount of finger crossing, because it's a natural system rather than an engineered one that we're trying to tamper with. If you've ever boggled at a large spaghetti program, the human immune system makes that look like two dozen lines of clearly documented Java by comparison. None of it has to make sense because Mother Nature doesn't care why she only does results, and in the most brutal way possible.
This is why we've got a bunch of different vaccine programmes in different centres. Some of them might work, hopefully at least one does, and hopefully it produces an immunity that lasts a useful amount of time, has minimal side effects and is cheap to produce in bulk. But there aren't any promises without us having way more advanced biotechnology than exists anywhere today.
Of course, that also means that detecting different strains is dependent on understanding those interactions and where they differ. If the post-infection cluster of pediatric multisystem inflammatory syndrome in NYC isn't just NYC being better at identifying that effect, it could well be a sign of a different strain with meaningfully different interactions with hosts. (It could still be a variety of other things, too.)
Doctors in the UK were seeing this throughout April, and issued an alert in late April: https://twitter.com/PICSociety/status/1254508725227982848
https://www.santafenewmexican.com/news/coronavirus/lanl-find...
What is the biological process that does this? I'd love to learn more.
Influenza is smaller about 13K nucleotides vs 30K for corona, it mutates about 4 times faster. It can maintain its larger genome basically because it has better tech. (It seems to better integrate with what it can find in host cells.)
"We demonstrate here, at the molecular level, that CoVs have indeed acquired an enzyme able to enhance the overall fidelity, and that this event might have directly promoted the jump in size of CoV genomes"
"Well before the discovery of nsp14-ExoN in the large Nidovirales genomes (22), this observation led to Drake’s visionary proposition that “RNA viruses would have to acquire several host genes and adapt them to RNA substrates to achieve a major reduction in spontaneous mutation rate. The result would be a substantial increase in genome size” "
https://www.pnas.org/content/115/2/E162
https://www.ncbi.nlm.nih.gov/genomes/GenomesGroup.cgi?taxid=...
https://www.ncbi.nlm.nih.gov/nuccore/1798174254
"Specifically, SARS-CoV-2 seems to have a mutation rate of less than 25 mutations per year, whereas the seasonal flu has a mutation rate of almost 50 mutations per year."
https://www.livescience.com/coronavirus-mutation-rate.html
Someone reading this might be wondering how speciation can be measured with viruses, since viruses don't reproduce sexually. Well, we don't test whether different species of animals can reproduce with each other. There's no way to conduct such experiments at any meaningful scale. The vast majority of defined species are educated guesses, and in reality has very little to do with whether two groups of organisms can reproduce with each other. In a lot of cases, species are simply determined by the appearance or behavior of one group of organisms over another group of closely related organisms. The term "species" didn't even originally have anything specifically to do with reproduction; the word effectively meant "looks like", which is why the words "species" and "spectacle" share the first 4 letters.
"They've been in the room an hour, sir. Nothing's happening."
"Hmmm... Ok, looks like polar bears and flamingoes are different species. Mark that down. Next on the list... swap out the flamingo for the barnacle. Be sure to keep watching closely."
Viruses clearly reproduce with humans. By a strict "reproduction / species" definition, Viruses are human.
The species definition you brought up does not apply to asexual organisms, for them it's a matter of genomic analysis. As for sexual organisms, it is still a good definition because it is stricter and more "correct" than genomic analysis, although bioinformatics has been getting pretty good with the addition of more sophisticated statistical techniques that go past simple DNA-DNA hybridization.
https://blogs.sciencemag.org/pipeline/archives/2020/05/07/mu...
> So far no one has shown that any of these virus isolates differ in any fundamental property.
A different sequence is prevalent elsewhere. Not proof, but suggestive of a property difference.
Also, the virus originated from one point (Wuhan) and was spread more or less simultaneously across the world. It would be quite odd if one strain hopped on all the west/east-bound planes, while another strain found its way only to the south-bound planes. Not to mention that the 'second wave' of infections in APAC originated largely from Europe.
> sunlight (UV-B), heat/humidity
Much of Asia is in the northern hemisphere (e.g. China and Japan); same season as Europe and USA.
Australia is in Asia too, close to China with much travel between.
I agree there are many factors and it's early. But the low cases and deaths over all countries in Asia has a peculiar uniformity - in contrast to elsewhere.
Most geographers would disagree. It's a 12-hour flight from Beijing to Sydney, no closer than Beijing to San Francisco.
Referring to Australia as being "close to China" is like saying Russia is close to England. It's its own continent.
To put it in more concrete terms, any (direct) flight you look up from Wuhan to any city in Australia is 12+ hours. That's a much longer flight than New York to London.
I'm just pointing out something interesting in the data I was curious about. It's a pity HN picks out one detail and ignores the interesting thing... but upon reflection, pedantry is typical of today's HN, and partly why pg withdrew.
Regarding Australia, it's often said we are in the Asia region. And for the specific purposes here, of initial transmission, we have much contact with China, through tourism, education, primary produce and trade in general. It's expected we'd get initial infection direct from China (which trwcing shows we did), rather than via Europe.
https://www.virology.ws/2020/05/07/there-is-one-and-only-one...
A series of similar events in similar circumstances can be explained by a series of different causes, but it seems worth looking at a similar cause, no? This is at the stage of initial hypothesis.
Gosh, maybe people thought I was saying it was the absolute truth.
I absolutely recommend his virology lectures https://youtu.be/lj3NhPgOoX4
https://www.microbe.tv/
If there's only one 'strain' then that means one 'vaccine' will work on all patients, correct?
So it's unlike the Flu where the vaccine only works half the time and they keep having to update it ?
https://www.samoanic.ws/
Source: https://www.santafenewmexican.com/news/coronavirus/lanl-find...
The other big factor is the different government responses, but these are all over the map. Specifically, the lack of a lockdown does not always equal a high rate of transmission, and the presence of a lockdown does not always result in a low enough rate of transmission to avoid a crisis. This is something we should all be curious about.
On that topic, Cuomo just declared that among the last batch of infected people in NY, more than 80% were apparently respecting the lockdown and staying at home and we have no idea how they were even contaminated. Puzzling.
I also think there is a likelihood that between presymptomatic/asymptomatic transmission, and the possibility of 2 week incubation this seems like a nightmare to track transmission.
A friend who had SARS-cov2 was sick for 30+ days. So it’s not clear to me that a mild infection would be over in 14 days.
I'd like to see the same study done outside of NY, because the NY lockdown was one of the most stringent in the country, from what I've read.
Edit: okay, okay, I didn't specify "a mild infection that stays mild and goes away". We know complications can arise and the infection can progress into severe symptoms. Plenty of examples.
Please don't spread misinformation.
Kinda like when you don't take a full course of antibiotics, the latent infection grows again to problem levels.
You indicate this is wrong thinking (not a suprise as it's just a null hypothesis from someone without biology training): so what is going on when you have a cough/blocked nose for weeks on end?
{# I'm very curious to find if the virus I had was Covid19; it sent me to bed with mild flu-like symptoms, gave a tight chest, had me occasionally [not persistently] coughing for weeks. No noticeable anosmia. Very little phlegm; no snot (nasal/sinus mucus).}
I think it would be worth a test, at least.
Here is a pretty approachable summary of how transmission happens that contains a review of some specific cases where airflow was critical to transmitting the infection: https://erinbromage.wixsite.com/covid19/post/the-risks-know-.... None of these occurred in isolated spaces connected by shared ventilation but I would be cautious about saying flatly that it can't happen.
I'd be interested in any references you can point to that explain why that doesn't happen. A priori I would expect virus particles to be able to remain airborne indefinitely. Viruses are very small, much smaller than pollen grains that I believe are well known to remain airborne over long distances so I would think Brownian motion from collisions with air molecules would suffice to keep them aloft.
Also, please be aware that a name is often not enough to show that a source is relatively trustworthy, some credentials can help; this is a worldwide forum.
Can you share what degree of certainty you ascribe to that claim?
Edit: Also, does this change it? https://erinbromage.wixsite.com/covid19/post/the-risks-know-...
I don't think we've actually had any fecal transmission with SARS-2 either, or even had someone successfully culture live virus from a stool sample. We've seen a lot of virus RNA show up in stool from infected patients but that might be due to swallowed saliva. I'd try to avoid contact with other people's feces in any event but the danger here really does seem to be mostly droplets.
Of the new New York City hospitalizations, 90 percent have not been traveling by car service, personal automobile, mass transit or even walking around. If they've been working, they've been doing it from home and apparently weren't going out much, the governor said."
https://www.nbcnewyork.com/news/coronavirus/subway-shutdown-...
This points out that perhaps transmission across apartment building is significant.
* Hospitalizations, not cases and not infections. That skews old/out of the workforce.
* The stat is that 66% live at home and 84% not working.
* That doesn't mean they are 100% to the letter respecting social distancing. Nor does it mean they don't have housemates that aren't working. (That could be the case, but there's no data).
https://i.imgur.com/b9RAr8g.jpg
Cuomo:
> 66% of the people were at home, which is shocking to us...This is a surprise: Overwhelmingly, the people were at home...We thought maybe they were taking public transportation, and we’ve taken special precautions on public transportation, but actually no, because these people were literally at home.
That chart is titled "Source of Admission," not "Was supposed to be staying home." Someone providing critical services who woke up with a fever and got tested would fall under "home."
There's also nothing to compare it to. What percent of people are in those circumstances?
To what I think he misread and was surprised by, the idea that most people getting hospitalized were sheltering in-place (a stat I haven't seen), with how many New Yorkers who have been exposed to SARS-CoV2, you'd expect essential workers who are going out every day to be more likely to be immune at this point, those sheltering in place aren't. More people are sheltering in-place than out working, they're less likely to have been exposed, so I wouldn't be surprised to see more of them infected. But again, that's not the data Cuomo was talking about with "66%."
I'm writing this because I think HN is one of the very few communities able to properly discuss ideas with hard science and facts. So any observation, correction, criticism etc. is more than welcome!
I propose that if you pay very close attention to the nature of discussions, over a long period of time, across a broad spectrum of differing topics, you may notice that the ability to "discuss ideas with hard science and facts" varies greatly according to the topic.
Or to be more specific...when the topic involves issues that are "political or values oriented", as this one does, the discussion and thinking styles exhibited in the comments much more resembles that which you would find within less "logically capable" communities.
The COVID discussions have been the single most frustrating experience for me on HN since I joined. Ever single comment I’ve made downvoted, even accused of contributing to millions of deaths (an account which was thankfully banned for making the remark).
It’s only in the last week or two that it’s started to become remotely possible to have intellectual discussions on COVID, but it’s still overwhelmingly politicized and unscientific.
For a non-critical issue this would lower the quality of discourse slightly, but it's not an exceptional problem. In the case of critical major issues involving active disinformation this is highly irresponsible behavior.
Assuming your description of "the" problem is accurate (I suspect it isn't - and it's "a" problem, not "the" problem, pardon the nitpicking), what do you propose should be done about it? On an individual basis, a community basis, a governmental basis, etc - what should be do? Because as far as I can tell, we (the citizens of planet Earth) seem to be stuck in this recursive loop of anger, finger pointing, and general failure. And it doesn't seem like anyone else notices.
Well, mostly no one.
https://i.imgur.com/QA6vSzC.png
I don't necessarily think that's what should be done in practice, but it seems consistent with how western society responds to this behavior in other settings.
I don't necessarily think there is a good solution, either - I just mean to say that people who do that, even if they are well-meaning, are behaving unethically. That's because they believe in their own perspective with 100% probability, but that's obviously unreasonable from a Bayesian perspective. If they accounted for even a small probability that they are wrong then their behavior would change dramatically.
Completely agree, but I believe this behaviour applies to 90%+ of those who express confident opinions on the matters of the day, and downvote anyone who dares question those opinions when they can't put together a convincing argument for their strong assertions.
Some evidence for the frequency of this behaviour exists, we could have insight into it, but I suspect we shall choose to not discuss such things. Only downvote them.
https://en.wikipedia.org/wiki/Epistemic_humility
https://behavioralscientist.org/epistemic-humility-coronavir...
https://plato.stanford.edu/entries/wisdom/
(These links are not directed at you personally, just to be clear).
Let's see how this one fares.
If a politician stands between the scientific advisors and the people then when they make pronouncements saying "this is for medical reasons" when in fact the reasons are primarily financial, or tempered by the interests of other parties (their personal backers), that needs to be made clear.
When the UK said "we're using different models" they should have been publishing those models, among with the facts they were relying on, published a list of all people who had input to that decision and the context.
A rolling diary of all people any senior politician had contact with; a list of every shareholding by any member of a politician's family; and such information need to be openly accessible in real time.
Basically we need to treat them as an obsessive helicopter-parent would treat their teenage children, they need to have tracking devices, they need to have "friends" (employees of opposition parties) that attend every meeting they go to, they've down they simply can't be trusted.
But of course you can't do any of those things because corrupt politicians won't vote for it. We're stuck at a local minima of democraacy, IMO.
How to progress? I don't see a way, politicians have enough of the population in their thrall (eg using media manipulation) to sustain the current system. Two things that may help are to have bodies parallel to government adopted ones, like UK's SAGE but excluding the politicians, and have media that will report direct from those bodies to the people rather than via a filter of politicisation. Maybe then enough people can get onboard to bit-by-bit elect trustworthy officials interested in government for the good of the people.
Everything should be published (it isn't), and nothing should be censored, without good reason (not the case today). That so few people seem to realize this is mind boggling to me. But then, it's human nature, so it shouldn't be surprising.
> How to progress? I don't see a way, politicians have enough of the population in their thrall (eg using media manipulation) to sustain the current system. Two things that may help are to have bodies parallel to government adopted ones, like UK's SAGE but excluding the politicians, and have media that will report direct from those bodies to the people rather than via a filter of politicisation. Maybe then enough people can get onboard to bit-by-bit elect trustworthy officials interested in government for the good of the people.
This idea, and others like it, seem like a very plausible way out of this mess. I really see no other way.
But how much effort, in man-hours, is being expended in this direction, as compared to, oh I don't know, people having the same arguments year after year, in thread after thread?
HN as a community places value on interesting, well informed debates, but that value isn't universally shared outside of HN. It takes regular exposure to build that value in new members but over time they'll either embrace it or wash out of the community as long as we do our best to consistently embrace it positively.
Keep debating and pushing forward on interesting conversations, keep doing it politely and in the interest of meaningful debate.
Yes indeed. Reddit is famous for this, and getting worse by the day. But how might we know, for sure, the degree to which that also happens here? And I don't mean that rhetorically. We can all instantaneously generate "an" answer to that question, based on heuristics, but how accurate is that answer? To gain some certainty, it would require looking at actual data, which is firstly dependent on a willingness to look at the data, which is firstly dependent on a willingness to consider the idea that there may be a problem. This last point seems like a rather touchy subject.
"building values in new members" also seems like a well-accepted but heuristically-based idea. Is it, in fact, only new members who lack these values? Luckily, HN profiles contain an "accounted_created" attribute...with a little effort writing some scraping code (something I don't presently know how to do), I suspect some more precise, evidence-based answers would quickly reveal themselves.
What would be even more revealing would be if one had access to voting history. This way, we could get a decent feel for how certain individuals feel about this general topic. But alas, you and I don't have access to that data. But someone does (see: willingness to look at the data). Shall we truly pursue righteousness, or should we just declare ourselves to be, by fiat, as seems to be the most popular approach in broad society?
> HN as a community places value on interesting, well informed debates...
In the abstract, principled[1] sense, sure. But, how well do we "walk the talk"? Once again: what does the data say?
> as long as we do our best to consistently embrace it positively
And consistently. But now we're back to where we started.
> Keep debating and pushing forward on interesting conversations, keep doing it politely and in the interest of meaningful debate.
Despite the obvious unpopularity, and repeatedly inconsistent (again, based on topic) evaluation of "meaningful debate", as well as the HN Guidelines in general, I seem unable to stop lol
[1] "Lord, I promise not to sin!" Inconsistent adherence to an ideology, however strongly held in theory or principle, is not a problem only within the domain of religion, I suspect. Rather, it seems more like something inherent in human beings. Failure rates may vary fairly significantly across domains (or may not!), but this is a difference in degree, not a difference in kind.
The other issue is that communities are dynamic, and behaviors trend. You're probably not going to see a flat correlation, you're going to see something that resembles a wave function.
True. But not impossible.
And I would recommend comparing effort to potential reward. Imagine, just for fun, the possibility that HN could find a way to discuss climate change[1] in a disciplined, truthful, and non-heuristic manner. What might the value of that discovery be? And if we could find a way do it, perhaps others could as well?
> and only as accurate as the person making the judgement call
How deeply have you thought about that? Like, say it was an engineering problem you've been asked to solve - have you put as much effort into thinking about it as you would if it was a paid assignment?
https://en.wikipedia.org/wiki/Clarke%27s_three_laws
> In other words, we'd just be making ad hoc judgements again, but calling them something else because we made those ad hoc judgements in a csv instead of a comment.
Do you realize you are:
a) predicting the future
b) making several assumptions
c) utilizing loaded terms (which is harmful not only to others, but sometimes also to oneself)
https://en.wikipedia.org/wiki/Loaded_language
> The other issue is that communities are dynamic, and behaviors trend.
This is true.
> You're probably not going to see a flat correlation, you're going to see something that resembles a wave function.
Your prediction may be correct. But it also may be incorrect.
[1] A topic we seem to loooooove to talk about as if it only involves climate science, and has no psychological aspect whatsoever.
> Loaded words and phrases have significant emotional implications and involve strongly positive or negative reactions beyond their literal meaning.
I hope 'ad hoc', 'judgements', 'csv' and 'comment' don't carry any strongly positive or negative reactions, nor stereotypes or implications. (Though I have known a few people to have negative reactions to the idea of csv files...)
I would very much like for us to have a written language that has the same bandwidth as a long form, in-person discussion. But we have to play the hand we've been dealt, not the hand we wish we'd been dealt.
And to be clear, I don't object to your complaint, or consider it unreasonable - quite the contrary: this is the type of conversation I think we need more of. My comment above could have been improved by adding some disclaimers to make it explicit that I am not intending to speak in an "accusatory" manner, but I reckon the vast majority of people would have read it that way, and for good reason. So, apologies for that.
The ideas I had in mind are somewhat (again, limited by the fundamental shortcomings in our written language) captured in here:
> Loaded language (also known as loaded terms, emotive language, high-inference language and language-persuasive techniques) is rhetoric used to influence an audience by using words and phrases with strong connotations associated with them in order to invoke an emotional response and/or exploit stereotypes.[1][2][3] Loaded words and phrases have significant emotional implications and involve strongly positive or negative reactions beyond their literal meaning.
(The intent, emotional, and exploit parts I do not consider at all relevant to this discussion).
The larger, more abstract point that I'd like to make is: reality is infinitely complex, and we as individuals reason upon it with far from infinitely powerful minds. Now, start layering on all the other complexities, like collective reasoning (hampered by language and a variety of other things), necessities of being forced to make incredibly imprecise/coarse group decisions on a strict timeline (our political systems), complex and imperfect incentive systems, asymmetry and inaccuracy of information, advances in some domains (science, technology, industrialization) without corresponding advances in complementary domains (psychology, consciousness, etc), and so forth...and before too long you've got a bit of a mess on your hands.
[1] https://www.timesofisrael.com/the-end-of-exponential-growth-...
1) Testing is all over the place and mostly done only on people that are hospitalized. This creates a huge selection bias in official numbers, especially when we're talking about a disease where we're seeing claims from 25-80% of carriers being asymptomatic. There's plenty of evidence to show that many people that suspect themselves (i.e. they show symptoms) are not getting tested because they aren't "sick enough". So all we can do is guess that official numbers are on the low side. This is part of why we see wildly different CFR numbers (as opposed to IFR) in different countries. (Obviously there are other factors as well, but this one captures effects like living conditions)
2) Deaths are being attributed in different ways. In some areas any pneumonia death is being counted while in others the person must have tested positive for covid. In America the attribution even varies by state. What makes this more complicated is that when the metric changes these tend to be deaths added on a single day (creating spikes). This makes it difficult to do 1 to 1 comparisons.
3) The disease's fatality rate drastically changes with the victim's age. There's strong evidence to show that if you're healthy and young that you have little to worry. But if you're relatively healthy and old you should be concerned. There are drastic differences in country's age, and thus this makes a big difference in comparisons.
4) The number of cases isn't exactly a bad thing. Let's take Sweden for example. If their method for containment (develop herd immunity in the general population, isolate the elderly and immunocompromised, and social distance strictly to not overwhelm hospitals) is effective you'd expect a faster rate of new cases AND deaths. But if their method is the better solution they will have less total deaths by the end. But are they right? No one knows yet because we need time. Time is a difficult factor to work into these comparisons, which are often single snapshots rather than growth rates and inflections.
Deaths, on the other hand, are easier (but not perfectly) to count because it is much more clear that someone has died. The symptoms are trivially obvious. The difficulty here is that there is no universal attribution (even within the US) as to what constitutes a covid death. Let's show a tricky example. Let's say an elderly patient had a stroke and are in the hospital. You THEN get infected and die. Did you die from the stroke or covid? Is this as deadly as a disease that kills a healthy 60 year old? How do we distinguish this?
I'm just trying to say that without context these simple comparisons can miss a lot of nuance of the reality of the situation. The thing here is that there are a significant number of variables at play and without discussing those variables you can get inaccurate results.
The problem is in the question itself. Behind it is an expectation that there is just a tiny number of "magic spells" or "a trick" that would "solve" the problem, and that anything else is unnecessary.
The reality is the opposite: all the countries, and where the regulation was weaker, the people on their own, with the time attempted with different levels of success to protect themselves. They all did many things, many real people on many different levels, and with many not identical results. But it's much more complex than the assumption behind the question.
For example, people like to quote Sweden as some "magical other way country" whereas the universities and upper schools were shut down there too, it still has more deaths per capita than the US, the rate of new confirmed cases is not sinking etc.
Also, those who claim that there is an "impact" which "is different" typically don't try to fairly compare the actual impacts which are eventually much more similar when compared properly than implied in such a claim with no correct comparison done.
That is, a lot of such "arguments" are frauds which depend on those hearing it not willing or being able to look at the data properly.
I worked in finance for years, and I can tell you: if those who promote various claims in the news, media and social media would trade while ignoring so much data which is here so obviously available to find and compare, like they do in their claims, they would lose all their money in a blink of an eye.
I don't know how it would be possible to organize that, but if people who claim bullsh.t would have to invest some money behind their claims, and lose it if their claims would be proven wrong, we'd have much less insane conversations.
Just looking at the raw data and comparing can show you that a lot of claims floating around are plainly and completely false.
One page that allows magnificently easy comparison is
https://www.worldometers.info/coronavirus/
Additionally, one should search for the original sources of the information for different countries, and compare the numbers based on that additional information.
I can especially recommend translate.google.com for an amazingly efficient way to read some information from the original sources.
-- We will probably be able to make some statements about what practices seem to have various effects for better or worse and what environmental factors (like density and isolation) tilt the results in one direction or another
-- There will remain debate over what we should have done given the benefit of perfect hindsight
-- However, we're also going to conclude that some of the wide variation in outcomes can best be described as luck of the draw
The question is when as any government (puppet shows for the "chosen ones") ever told the truth? Not when has it told a lie?!
What do people with power and control want? Always more!
To differentiate between founder effects and a selective advantage driving the increasing frequency of the G clade in the GISAID data, we applied the suite of tools that we had been developing for the SARS-CoV-2 analysis pipeline (Fig. 2, Fig. 3, Fig. S2 and Fig. S3). A clear and consistent pattern was observed in almost every place where adequate sampling was available. In most countries and states where the COVID-19 epidemic was initiated and where sequences were sampled prior to March 1, the D614 form was the dominant local form early in the epidemic (orange in Figs. 2 and 3). Wherever G614 entered a population, a rapid rise in its frequency followed, and in many cases G614 became the dominant local form in a matter of only a few weeks (Fig. 3 and S3).
The world is not easily classified. But people persist. So we end up with situations like "is Pluto a planet?" and "is a virus alive?" Then people start focusing on their classifications and definitions when in fact they don't actually matter to the reality of the situation.
I need to dumb this down more if the audience is a 5 year old.
People like to give things names. Like the colors: red, orange, yellow, green, blue and purple. But sometimes a color can't be easily named.
For example the shirt I'm wearing might look blue to me and green to you. Then we start arguing about what color the shirt is when what we really should talk about is if it matches my pants.
Viruses lack several things that are often deemed necessary for life. The most important (in descending order):
* They lack the internal structure all other life has [this is the cell].
* They lack the ability to "eat" to "live" [metabolism].
* They lack the ability to make more of themselves without "borrowing" others' abilities.
Because the scientific community carefully picked certain completely-arbitrary attributes with the intent of drawing a bright line of division between viruses and cell-based organisms. This doesn't make the slightest bit of sense to Mother Nature, of course, but it makes sense to the scientists.
A much better definition of "Alive" would simply be, "Subject to the rules of evolution by natural selection." Viruses certainly quality under that rubric.
Virus fail that test.
Consider that a jet airliner passes more of the is it alive tests than a virus does.
There are some more nuanced claims which are made or hinted at:
1. There's not adequate evidence to prove a difference in mortality between the L and S variations of the virus.
2. There's not adequate evidence to prove increased viral transmission over time of the virus.
And if your definition of the word "strain" is "reserved only for special changes that confer a new property to the virus", then both of those would be arguments that there's not adequate evidence to prove the existence of different strains of the virus.
However, is the definition of the word "strain" really the important point you want to communicate? Either point 1 or 2 could have been made without talking about the word "strain" (note how I sidestepped the whole strain/isolate issue by using the word "variation"). I would argue that either of those two points are much more important than the meaning of the word "strain".
Sure, using the proper jargon is a strong indicator of expertise in a field. But jargon arises from expertise, not the other way around. Correcting people's jargon before they have the adequate mental framework to differentiate between the terms just creates conflict and is counterproductive.
What this pandemic has taught me over anything else is that wielding scientific terms without proper understanding is damaging to progress of science itself. It becomes difficult to tease apart legend from fact, especially for those not trained to do so. I go crazy every day listening to half-baked hypotheses and conspiracies that don't understand the foundations for the things they're claiming.
All this said, Dr. Racaniello is very gracious and humble. He has dedicated his life to teaching, both in the classroom and through his podcasts. I highly suggest sending him your concerns about his discourse and subscribing to his podacast TWIV [0]. He and his colleagues respond to every email at the end of each podcast.
[0] http://www.microbe.tv/twiv/
Yes, it's necessary to describe terms, but there's a big difference between giving a definition of "strain" at the beginning of your talk, and explicitly correcting everyone who has misused the term. One is necessary for clarity, the other is unnecessary and combative.
> What this pandemic has taught me over anything else is that wielding scientific terms without proper understanding is damaging to progress of science itself. It becomes difficult to tease apart legend from fact, especially for those not trained to do so. I go crazy every day listening to half-baked hypotheses and conspiracies that don't understand the foundations for the things they're claiming.
I don't think that's true. It's not the terms being misused. You can still say the wrong thing with the right terms.
Let's take a summary of the story that was going around for a bit, "There are two strains of coronavirus, the S strain and the L strain. The L strain is more deadly but it isn't spreading as quickly because sufferers are more likely to be identified and treated/quarantined."
That statement is wrong, because there isn't enough scientific evidence to declare any of that. But is the problem the misuse of the word "strain"? I don't think so. Consider the following: "There are two variants of coronavirus, the S variant and the L variant. The L variant is more deadly but it isn't spreading as quickly because sufferers are more likely to be identified and treated/quarantined."
I'm not an expert in the field, but as far as I know, the word "variant" doesn't have any specific meaning that would say it's being misused here. But nothing has changed: the summary is still 100%, completely wrong, because there still isn't adequate scientific evidence to say there are different variants with different mortality rates.
And, critically, even knowing the definition of the word strain, I can still say the first version of this incorrect statement and be wrong, not because I'm misusing the word, but because there isn't adequate scientific evidence for what I'm saying.
> All this said, Dr. Racaniello is very gracious and humble. He has dedicated his life to teaching, both in the classroom and through his podcasts. I highly suggest sending him your concerns about his discourse and subscribing to his podacast TWIV [0]. He and his colleagues respond to every email at the end of each podcast.
I'll do that.
Completely ignoring what "strain" means to a virologist, when you tell a layperson that there is a new strain of something, they generally will worry, and think one (or more) of the following: a) the existing vaccine or vaccine in development won't cover the new strain, b) existing treatments for people who are sick won't be effective, c) it's easier to catch, d) they're more likely to die of it. The fact that a new strain is related to a distinct biological difference doesn't matter; what people care about is what a strain means for their health.
So even if you ignore the scientific-jargon meaning, it's important to recognize the layperson meaning, and ensure that you stamp out inaccuracies based on that meaning as well. As much as you'd like to educate everyone as to the true meaning of some terms, it's a losing battle, so you might as well just recognize how people use a term and speak to that usage. In this particular case, the scientific and layperson meanings aren't exactly the same, but it's just as important in both arenas to clear up misinformation.
For example, if the narrative were, "The S strain and the L strain aren't meaningfully different", would that be a concern? Sure, but not a big one. Sure, it makes no sense to call them "strains" if they aren't meaningfully different--that's a misuse of the word "strain". But the layperson would have the correct impression of the situation from that statement.
The layperson would have the correct impression of "The S strain and the L strain aren't meaningfully different", but the wrong impression of nearly every other sentence starting with "The S strain and the L strain..."
There are two critical weaknesses in what has been written, taken as technical communication rather than blowing off steam.
Firstly, it does not do a good job of providing the reader with an alternate word that expresses the relationship for which 'strain' is being misused (in the author's opinion).
I believe that he himself would describe identical genome sequences as being the same virus 'isolate', but he doesn't explain that well, and the practical etymology of the term — the notion that the same virus isolate could be isolated in two different instances — makes adoption difficult. If this is indeed how 'isolate' would be routinely used (I am not even sure, as he doesn't establish this clearly) then it would be an instance of something that we might call 'deep jargon' or 'cryptic jargon', when normal words have specific meanings in a professional context that require a mental compartmentalization.
Secondly, it does not establish why it is important for a less-informed reader to draw the distinction between a _____ of the virus and a new strain of the virus. We can imagine that there are differences in importance between a mere genetic difference, a genetic difference with functional biological consequences, and a genetic difference with epidemiological consequences. It is probably our expectations for the last of these, based on prior experience, which makes the distinction important; a very critical difference would be if the immune response to one strain was ineffectual against the other. However, this is muddled in an attempt to instead explain why it is difficult to distinguish the founder effect from biological selection.
That's an interesting hypothesis and you're making me think that maybe I was wrong. It certainly was effective in getting me to stop misusing the word "strain".
My argument was based on the idea that they were trying to communicate the fact that there are no meaningful differences between different genetic sequences of SARS-CoV-2, and got bogged down in the semantics of the words "strain" and "isolate".
> is the definition of the word "strain" really the important point you want to communicate?
I think in the author's case, yes. If you are unfamiliar with the subject you learn some nuance about the subject and the terminology used. A basic understanding of the science should have already clued you into that viruses don't replicate perfectly, so the reader should question at what point a change constitutes a new strain. The author answers this question in the beginning.
> A virus strain is an isolate with a different biological property, such as binding to a different receptor, or having a distinctly different stability at higher temperatures, to give just two of many possible examples.
So we learn simply that the different isolate has to have a new biological property. More akin to having a third arm rather than a difference in skin color.
The author circles back to this with a clear example:
> The most recent offender is a preprint claiming that SARS-CoV-2 with an amino acid change in the spike glycoprotein (D614G) increases the transmissibility of the virus.
> Until proven otherwise, their emergence is likely due to the founder effect. Let’s say a virus with D614G emerges during replication in a person’s respiratory tract. If viruses with that change infect the next person, and the next, and so on, then the D614G change will predominate. The change is simply __a single nucleotide polymorphism of little consequence.__
I do think here the author could have strengthened their argument by noting what the founder's effect is.
> (via wiki) the loss of genetic variation that occurs when a new population is established by a very small number of individuals from a larger population.
So the author gives a reasonable assertion for this observation. We then apply Occam's razor and we have the author's thesis. (He should have stated this explicitly)
Yeah. My concern isn't that the meaning wasn't clear. My concern was that by focusing on the semantics of the jargon, it comes across as combative and alienates readers over something which is ultimately not important.
I think you and I are at a point of understanding where we're able to receive this feedback on the terminology and correct our own usage very quickly. I've certainly taken note.
Viruses get small mutations as they multiply. By now, there is likely huge amount if unique viruses, not a single one. But, most mutations don't actually change anything because they might hit non coding part or maybe she mething unimportant so for the purpose of our communication we lump them together and call them strain.
Most of the time we only start discerning differences when they change the virus behaviour in an interesting way, and most of interesting stuff is around how it propagates, what it does to us and what it is susceptible to.
The final thesis thus should be that there's no adequate evidence that there are two strains. Not an affirmation that there is only one strain. Absence of proof vs proof of absence.
[1]: https://peterkolchinsky.com/bio
[2]: https://news.ycombinator.com/item?id=22900397
His website Microbe.tv[2] also hosts various regular podcasts (which are also published as audio to YouTube) about virology and microbiology, they're very interesting.
I can thoroughly recommend.
[0]: https://en.wikipedia.org/wiki/Vincent_Racaniello
[1]: https://www.youtube.com/user/profvrr/videos
[2]: https://www.microbe.tv/
Anyway, this was the money line to me: "For an amino acid change such as D614S to be positively selected, as opposed to being maintained as a consequence of the founder effect, requires selective pressure. For such an already highly transmissible virus, the nature of such selection pressure is difficult to discern."
QED
So not all arguments need a burden of proof. It is the one that is making the claim that has the burden.
What this piece should be titled is "We don't have any evidence yet of multiple strains."
This would be akin to one person making the claim: "Unicorns are not only real, but are causing a global pandemic" and then someone writing an article titled "Unicorns aren't real, STFU". The second title doesn't have the burden of proof and we wouldn't be having this conversation if these were the titles of the respective articles.
Why is the unicorns title an accurate analogy? Because the science doesn't expect there to be multiple strains in the same way the science doesn't expect unicorns to exist. I'm using the same vernacular here that we use in science. I didn't say "unicorns don't exist" but "we don't expect unicorns to exist". This is how we say things.
It's speaking different languages that have a high overlap, but key words may have completely different meanings.
And, when you're talking to a regular person, being able to speak English will help you convey your point.
> Well we're chimps that can barely communicate with one another even when we speak the same language.
Doesn't matter, the author still made an unsubstantiated claim, and hence is unscientific. He should change the title.