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].
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.
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.
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.
>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?
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.
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.
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.
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.
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)
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.
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.
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!
> 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.
> 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
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.
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.
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 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".
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).
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.
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.
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.
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.
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.
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...
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.
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]
[+] [-] gewa|5 years ago|reply
[1] https://onlinelibrary.wiley.com/doi/abs/10.1002/jmv.25902
[2] https://en.wikipedia.org/wiki/Clade
[3] https://nextstrain.org/ncov/global
[+] [-] kurthr|5 years ago|reply
https://blogs.sciencemag.org/pipeline/archives/2020/05/07/mu...
[+] [-] oehtXRwMkIs|5 years ago|reply
[+] [-] koheripbal|5 years ago|reply
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.
[+] [-] coldtea|5 years ago|reply
What about the reports of different strains that focus on having found them having different properties (such as "much more infective")? Are they bogus?
[+] [-] sradman|5 years ago|reply
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.
[+] [-] pbhjpbhj|5 years ago|reply
[+] [-] kerkeslager|5 years ago|reply
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.
[+] [-] micburks|5 years ago|reply
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/
[+] [-] escape_goat|5 years ago|reply
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.
[+] [-] kelnos|5 years ago|reply
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.
[+] [-] godelski|5 years ago|reply
> 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)
[+] [-] lmilcin|5 years ago|reply
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.
[+] [-] jobigoud|5 years ago|reply
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.
[+] [-] standardUser|5 years ago|reply
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.
[+] [-] chpmrc|5 years ago|reply
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!
[+] [-] ekianjo|5 years ago|reply
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.
[+] [-] acqq|5 years ago|reply
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.
[+] [-] ghaff|5 years ago|reply
-- 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
[+] [-] jepcommenter|5 years ago|reply
I absolutely recommend his virology lectures https://youtu.be/lj3NhPgOoX4
[+] [-] micburks|5 years ago|reply
https://www.microbe.tv/
[+] [-] brigandish|5 years ago|reply
> 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
[+] [-] skybrian|5 years ago|reply
Why the impulse to round off uncertainty to certainty? Ed Yong explained it better:
https://www.theatlantic.com/health/archive/2020/05/coronavir...
[+] [-] colmvp|5 years ago|reply
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.
[+] [-] ilitirit|5 years ago|reply
[+] [-] zbjornson|5 years ago|reply
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).
[+] [-] teh_klev|5 years ago|reply
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/
[+] [-] CapriciousCptl|5 years ago|reply
[+] [-] darkerside|5 years ago|reply
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
[+] [-] godelski|5 years ago|reply
So not all arguments need a burden of proof. It is the one that is making the claim that has the burden.
[+] [-] argwal|5 years ago|reply
[+] [-] unknown|5 years ago|reply
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[+] [-] eru|5 years ago|reply
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.
[+] [-] userbinator|5 years ago|reply
[+] [-] everybodyknows|5 years ago|reply
https://www.samoanic.ws/
[+] [-] Jaruzel|5 years ago|reply
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 ?
[+] [-] FriendlyNormie|5 years ago|reply
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[+] [-] Scarblac|5 years ago|reply
[+] [-] gregwebs|5 years ago|reply
[+] [-] xutopia|5 years ago|reply
[+] [-] drdec|5 years ago|reply
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.
[+] [-] downerending|5 years ago|reply
[+] [-] jcranmer|5 years ago|reply
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.
[+] [-] Gibbon1|5 years ago|reply
Virus fail that test.
Consider that a jet airliner passes more of the is it alive tests than a virus does.
[+] [-] CamperBob2|5 years ago|reply
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.
[+] [-] devy|5 years ago|reply
[1]: https://peterkolchinsky.com/bio
[2]: https://news.ycombinator.com/item?id=22900397
[+] [-] Oricle|5 years ago|reply
[deleted]
[+] [-] FriendlyNormie|5 years ago|reply
[deleted]
[+] [-] ianai|5 years ago|reply
Source: https://www.santafenewmexican.com/news/coronavirus/lanl-find...
[+] [-] narrator|5 years ago|reply