SARS-CoV-2 spike D614G variant confers enhanced replication and transmissibility(biorxiv.org)
biorxiv.org
SARS-CoV-2 spike D614G variant confers enhanced replication and transmissibility
https://www.biorxiv.org/content/10.1101/2020.10.27.357558v1
101 comments
Is a shit thing when a virus got a firmware update in 2020, but not my android phone.
And the virus updates make it more effective but every update makes my iPhone worse. Random freezes if you touch the screen at the wrong time, double-tap to zoom barely working...
Thanks for the laugh. So needed for this crappy year of hell.
for me it helps to know that this pandemic (including all the lockdowns) would be way worse without all of the digital innovations from the last 10-20 years.
Honestly, imagine how much worse the world would be (at least in 1st world countries) if we did not have the tech tools available to us.
I legitimately do not know what would have happened, but I feel like it would be much more violent and much deeper despair.
For all the headaches constant connection has brought, it has also alleviated an unknown number of them as well.
I legitimately do not know what would have happened, but I feel like it would be much more violent and much deeper despair.
For all the headaches constant connection has brought, it has also alleviated an unknown number of them as well.
I'm getting old. Last 20 years maybe, but I can't name a technology advancement that happened in the last 10 years that I would really miss. To me it seems like most technology is now done for the sake of doing it and solutions are looking for problems. Not to mention all the dystopian surveillance we have now.
Rose tinted glasses and all that, the start of the millennium was a much happier time period imo.
How does your age map to this Douglas Adams quote:
”I've come up with a set of rules that describe our reactions to technologies: 1. Anything that is in the world when you’re born is normal and ordinary and is just a natural part of the way the world works. 2. Anything that's invented between when you’re fifteen and thirty-five is new and exciting and revolutionary and you can probably get a career in it. 3. Anything invented after you're thirty-five is against the natural order of things.”
”I've come up with a set of rules that describe our reactions to technologies: 1. Anything that is in the world when you’re born is normal and ordinary and is just a natural part of the way the world works. 2. Anything that's invented between when you’re fifteen and thirty-five is new and exciting and revolutionary and you can probably get a career in it. 3. Anything invented after you're thirty-five is against the natural order of things.”
Have you used a 10 year old phone lately?
This is what I imaging would be a perfect set of devices:
1) a smart watch can read notification, messages, listen to music, podcasts, audio books, receive and make phone calls, voice chat, group chats;
2) a eink device to read books, browse internet for news (hackernews for example), emails;
3) game consoles or pc + project + vr for entertainment;
4) a tablet with keyboard for work (with access to servers in cloud) and netflix, youtube.
Yes, I use an old feature phone for voice calls. I'm fully aware I'm in a very small minority.
Indeed smart devices are the epitome of useless tech. In fact, I would argue they make life worse if one is conscious about their privacy and computing.
Indeed smart devices are the epitome of useless tech. In fact, I would argue they make life worse if one is conscious about their privacy and computing.
Just hope this over dependency on technology doesn't come to haunt us later: https://youtu.be/hESunUuFrzk
Something I have been wondering about, wouldn't a virus naturally evolve to be less deadly and more contagious over time? I.e. virus's tend to achieve a steady state like the cold and flu in the long run. If you are too deadly it hinders spread so I would expect Covid to get less deadly and more contagious over time, which kind of fits the data?
If you look at the death rate compared to March, it is dramatically lower, even though we're having 2x the cases. This could be because of better treatment, or because the virus itself is getting milder.
Or because more people (with mild symptoms) get traced and tested. We had a shortage of tests and masks on start of pandemic.
There are a lot of factors contributing, in particular the age distribution of those people getting infected.
One thing is "viral load", which has to do with how much of the virus is present at initial infection. Because immune system response takes time to ramp up, e.g. 10x more virus in the beginning means that it can do much more damage before the immune response. It's likely that social distancing and masks have reduced the average viral load at infection time.
One thing is "viral load", which has to do with how much of the virus is present at initial infection. Because immune system response takes time to ramp up, e.g. 10x more virus in the beginning means that it can do much more damage before the immune response. It's likely that social distancing and masks have reduced the average viral load at infection time.
In purely theoretical models virulence naturally evolved to a smaller value.
Influenza isn't in a steady state, there are hundreds of strains[0] that compete with each other and recombine to form novel versions. Each year's flu vaccine targets four of them based on modeling as to which will be most prevalent in the upcoming flu season[1/2].
0: https://www.cdc.gov/flu/about/viruses/types.htm
1: https://www.cdc.gov/flu/prevent/quadrivalent.htm
2: https://www.fda.gov/vaccines-blood-biologics/lot-release/inf...
0: https://www.cdc.gov/flu/about/viruses/types.htm
1: https://www.cdc.gov/flu/prevent/quadrivalent.htm
2: https://www.fda.gov/vaccines-blood-biologics/lot-release/inf...
Evolution is a random and long-term process. What you're thinking of is natural selection. Even that does not guarantee things will get better. For example, there was a worse second wave of Spanish Flu. Natural selection only implies there's less chance these terrible things will last. And, to adapt an economic adage, "The disease can remain deadly longer than you can remain alive."
Natural selection is the basic mechanism that enables evolution, the one is part of the other.
Generally, yes. But also we’re a bit unlucky that it isn’t very deadly: SARS was way deadlier To start with but as a result spread several orders of magnitude less (both naturally and because humans had a stronger reaction to “shut it down at all costs“).
The H1N1 virus from the 1918 pandemic grew less deadly over time, and essentially evolved into a seasonal flu that is still affecting people around the world today. Personally, I expect COVID19 to go the same way.
The H1N1 virus from the 1918 pandemic grew less deadly over time, and essentially evolved into a seasonal flu that is still affecting people around the world today. Personally, I expect COVID19 to go the same way.
The h1n1 is a bit of a strange case though because it jumps species boundary very often and mutates very quickly. COVID-19 appears to evolve much, much slower. Based on my limited understanding of virology, I think this means it's unlikely to become a seasonal problem unless the general populations immune system does not retain immunity to the same strain for a significant period of time.
We already know CoV2 rarely causes any symptoms in children. I wonder if there was a time in prehistory where common Rhinoviruses and Coronaviruses wiped out larger populations of elderly.
Even if our immune system memory doesn't last very long for these types of viruses, wouldn't young people getting exposed to it now likely reduce its impact long term?
It also seems like >95% of people who die from this are over 55 years old. When you get into your 70s~80s, aren't common colds one of the things that result in natural deaths, due to an aging immune system allowing pneumonia to set in where it wouldn't in a younger person?
Even if our immune system memory doesn't last very long for these types of viruses, wouldn't young people getting exposed to it now likely reduce its impact long term?
It also seems like >95% of people who die from this are over 55 years old. When you get into your 70s~80s, aren't common colds one of the things that result in natural deaths, due to an aging immune system allowing pneumonia to set in where it wouldn't in a younger person?
Yes that probably happened several times in human history. There are four other endemic coronaviruses. Most people catch them as children and build up some immunity, so even if they're reinfected later the symptoms are usually less severe. But they can be deadly to immunocompromised patients.
There is some strong circumstantial evidence that the 1889 "Russian flu" pandemic wasn't caused by influenza at all but rather by the emergence of HCoV-OC43. It killed about a million people worldwide.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7252012/
There is some strong circumstantial evidence that the 1889 "Russian flu" pandemic wasn't caused by influenza at all but rather by the emergence of HCoV-OC43. It killed about a million people worldwide.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7252012/
> We already know CoV2 rarely causes any symptoms in children. I wonder if there was a time in prehistory where common Rhinoviruses and Coronaviruses wiped out larger populations of elderly.
Didn't pneumonia, influenza (among small pox and others) have terrible consequences on American native Indians ?
Didn't pneumonia, influenza (among small pox and others) have terrible consequences on American native Indians ?
I believe small pox was the major one, I've heard among the Incas for example, it wiped out between 60 and 90 percent of the population. The main reason the colonists were able to spread so easily in the two continents is because disease wiped out huge swaths of the native population before many settlers even arrived. It's not like muskets are all that superior to bow and arrow (if at all, due to reload speed). Much of the land was just left vacant and unoccupied, and former cities abandoned.
And then came Colt's Revolver.
> A Texas Ranger, Captain Samuel Walker, wrote Colt a testimonial that read, in part:"Your pistols...[are] the most perfect weapon in the World... to keep the various warlike tribes of Indians and marauding Mexicans in subjection."
https://www.pbs.org/wgbh/theymadeamerica/whomade/colt_hi.htm...
> A Texas Ranger, Captain Samuel Walker, wrote Colt a testimonial that read, in part:"Your pistols...[are] the most perfect weapon in the World... to keep the various warlike tribes of Indians and marauding Mexicans in subjection."
https://www.pbs.org/wgbh/theymadeamerica/whomade/colt_hi.htm...
The 20th century decolonization wars showed that natives can adapt to modern weaponry fairly well.
But you need the numbers to pull this off. Sioux are not numerous enough to threaten American dominance of their territory. If they were as numerous as, say, Punjabis, that would be a different story.
But you need the numbers to pull this off. Sioux are not numerous enough to threaten American dominance of their territory. If they were as numerous as, say, Punjabis, that would be a different story.
Punjabis acquitted themselves fairly well in 1849.
It's already clear that the vaccine, when it gets released, won't be a one time thing and we'll need more in the future to counter the mutations. Unfortunately, just in anecdotally talking to friends about it, it doesn't seem that this is widely known. It will be interesting to see how things play out as more people start to realize this. I suspect a lot of anti-vaxxers will be even more emboldened by it.
I don’t think anything is “clear” - there are even indications that people exposed to the original SARS virus have their immune systems primed to more quickly respond to SARS-CoV-2.
I do not think mutations are the main problem, just the fading of immune system memory.
But it does seem very likely the vaccine will not be a one time shot and you’re good forever.
But it does seem very likely the vaccine will not be a one time shot and you’re good forever.
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Look for counter examples. Have we seen this in HIV? Smallpox? It's a plausibility. It's far from a guarantee.
And the opposite, /could/ happen, too. The virus could mutate to have a longer incubation period, or be more deadly, or both.
And the opposite, /could/ happen, too. The virus could mutate to have a longer incubation period, or be more deadly, or both.
I have seen a statemen somewhere tha for viruses it goes "transimissability, mortality, stealthiness: pick two". Not sure how true it is, but looks plausible.
At least for natural viruses. Engineered ones could be extremely terrifying.
Conventional wisdom often claims that virus evolve to become less fatal - but I don't think that matches the historical record.
There's evidence for influenza virus existing thousands of years before 1918. As such, it seems to have evolved into a much more deadly strain at that point.
Reproducing more efficiently is a win for natural selection and will normally result in a dominant strain: whether that strain is more deadly or not is going to be random.
We might optimistically anticipate some regression to the mean fatality rate (where the mean is close to 0).
There's evidence for influenza virus existing thousands of years before 1918. As such, it seems to have evolved into a much more deadly strain at that point.
Reproducing more efficiently is a win for natural selection and will normally result in a dominant strain: whether that strain is more deadly or not is going to be random.
We might optimistically anticipate some regression to the mean fatality rate (where the mean is close to 0).
> There's evidence for influenza virus existing thousands of years before 1918. As such, it seems to have evolved into a much more deadly strain at that point.
Influenza refers to a class of viruses, not a single virus.
Influenza refers to a class of viruses, not a single virus.
You seem to be suggesting that 1918 influenza occurred spontaneously and independently of other influenza? No.
"Occurred spontaneously" no. Independently, yes.
Just like SARS-CoV-2 wasn't a thing a year ago, but crossed over to humans late 2019, the 1918 Spanish flu virus did indeed only start infecting humans in 1918, independently of other viruses. 1918 just happens to be the year it (most likely) crossed over from an animal to a human.
Just like SARS-CoV-2 wasn't a thing a year ago, but crossed over to humans late 2019, the 1918 Spanish flu virus did indeed only start infecting humans in 1918, independently of other viruses. 1918 just happens to be the year it (most likely) crossed over from an animal to a human.
Independently, no.
Assuming generously that you are right about this, why (for example) are viruses crossing over in the other direction - from humans to animals - never considered important?
We might only care about the part of viral evolution and epidemiology that we closely observe or are immediately impacted by, but that does not mean the other aspects of evolution are independent.
Assuming generously that you are right about this, why (for example) are viruses crossing over in the other direction - from humans to animals - never considered important?
We might only care about the part of viral evolution and epidemiology that we closely observe or are immediately impacted by, but that does not mean the other aspects of evolution are independent.
> Reproducing more efficiently is a win for natural selection and will normally result in a dominant strain: whether that strain is more deadly or not is going to be random.
The conventional wisdom is such because a virus that is swiftly fatal and/or has more dramatic health consequences would have less chance to propagate to other hosts. For instance, because the original host will be unable to move or will look threatening to others so they will know not to reside close to them. This should make it less than random.
Unless of course some unforeseen factor makes this reasoning untrue.
The conventional wisdom is such because a virus that is swiftly fatal and/or has more dramatic health consequences would have less chance to propagate to other hosts. For instance, because the original host will be unable to move or will look threatening to others so they will know not to reside close to them. This should make it less than random.
Unless of course some unforeseen factor makes this reasoning untrue.
Taken to extremes, it's easy to see how a virus that is 50% fatal within 24 hours will not last long itself.
Is there really very much selection pressure between 1% and 2% fatality rates over 4 week timespans, though? Especially if immunity is conveyed by infection, I don't see any reason why a virus like that would evolve to be less fatal within the timescales that humans care about.
Is there really very much selection pressure between 1% and 2% fatality rates over 4 week timespans, though? Especially if immunity is conveyed by infection, I don't see any reason why a virus like that would evolve to be less fatal within the timescales that humans care about.
Generally if it's twice as fatal it'll probably makes people twice as sick so they're more likely to go out less, stay home more, and less likely to infect other people.
However if it did damage in a way that doesn't manifest for a long time this wouldn't necessarily be the case. But that would be the exception more than the rule.
However if it did damage in a way that doesn't manifest for a long time this wouldn't necessarily be the case. But that would be the exception more than the rule.
I think what happened with the 1918 pandemic (and the 2019 one for that matter) is a virus hopping between species can "reset the clock" on that trend and start as very fatal for humans.
I can imagine that a single nucleotide polymorphism doesn't care about what seems natural.
No, but its effect on the virus population kind of does.
Are you saying that a virus population has a conscience or morality ?
No the person is speaking about the evolutionary nature of the virus
But the way viruses evolve to be less deadly is that the deadlier strains kill a bunch of people quickly, before they can spread too much. So that's not exactly reassuring for any given mutation.
Only if they are so deadly that it's harming their transmissibility.
I keep wondering what unintended consequences our nearly-unprecedented efforts on non-pharmaceutical interventions ("lockdown", social distancing, masks, etc.) might end up having on the virus - for example, could all our isolation and distancing be accidentally selecting for strains of the virus that transmit more readily over further distances?
The mitigations are effective in slowing the spread (to varying degrees, due to a multitude of factors), which in turn slow down the rate of mutation. In any case, I would expect the dispersion of the virus to follow a pattern similar to https://www.youtube.com/watch?v=plVk4NVIUh8
Don't know about your country/region but here the mitigations are put in effect because hospitals can't handle the pressure anymore.
That will be a tough one to measure.
However measurement of the impact of lock-downs/social distancing upon existing known virus's like colds and flu's would give an insight into that whole area.
However measurement of the impact of lock-downs/social distancing upon existing known virus's like colds and flu's would give an insight into that whole area.
That is mostly due to the way they are spread as a less impacted infected person would be more outgoing and spread that virus more. When somebody more impacted by a virus would be more isolated due to the impact. So the less impacting one gets more exposure and spread.
So that in itself would be a factor, however virus can mutate in various ways and it is the mutations that effect the incubation period and that window of being infectious but not showing any symptoms - that is always going to impact things and certainly a large factor in why COVID managed to spread better than expected.
But much hindsight and data analysis will play out for years and years, after all - we are still looking at the Spanish flu data and seeing different aspects to this day.
So that in itself would be a factor, however virus can mutate in various ways and it is the mutations that effect the incubation period and that window of being infectious but not showing any symptoms - that is always going to impact things and certainly a large factor in why COVID managed to spread better than expected.
But much hindsight and data analysis will play out for years and years, after all - we are still looking at the Spanish flu data and seeing different aspects to this day.
You would think – but viruses don't necessarily become less deadly.
The virus wants to maximize transmissibility, and that might require trading off further against the host's health and increasing its death rate.
An example is Myxoma virus. It was intentionally introduced to pest Australian rabbit populations (to cull them) and studied.
After ~30 years of evolution, they found the dominant strain had a 70-95% death rate and left long-lasting lesions. Other strains with higher (~99%) and lower (~50%) death rates weren't as stable & prevalent.
Once a virus is transmitted (enough), what happens to the health of its host is irrelevant.
[1] https://www.sciencedirect.com/topics/immunology-and-microbio...
The virus wants to maximize transmissibility, and that might require trading off further against the host's health and increasing its death rate.
An example is Myxoma virus. It was intentionally introduced to pest Australian rabbit populations (to cull them) and studied.
After ~30 years of evolution, they found the dominant strain had a 70-95% death rate and left long-lasting lesions. Other strains with higher (~99%) and lower (~50%) death rates weren't as stable & prevalent.
Once a virus is transmitted (enough), what happens to the health of its host is irrelevant.
[1] https://www.sciencedirect.com/topics/immunology-and-microbio...
It basically needs to be extremely contagious without symptoms that stop the spread - like killing the host.
Which in part this virus has, asymptomatic and pre-symptomatic are as contagious as symptomatic. If it's enough to spread, doesn't matter much if the host dies after a few days or not.
Which in part this virus has, asymptomatic and pre-symptomatic are as contagious as symptomatic. If it's enough to spread, doesn't matter much if the host dies after a few days or not.
>Which in part this virus has, asymptomatic and pre-symptomatic are as contagious as symptomatic.
Do we really know that yet?
Do we really know that yet?
>Infectiousness may peak before symptom onset (7). Viral loads appear to be similar between asymptomatic and symptomatic patients (8), although the implications for infectiousness are unclear. People experiencing symptoms may self-isolate or seek medical care, but those with no or mild symptoms may continue to circulate in the community. Because of this, those without severe symptoms have the potential to be “superspreaders” and may have an outsized influence on maintaining the epidemic.
Source: https://science.sciencemag.org/content/370/6515/406
While it's not confirmed they are more infectious, they walk among the community without being aware, therefore more prone for spreading.
Source: https://science.sciencemag.org/content/370/6515/406
While it's not confirmed they are more infectious, they walk among the community without being aware, therefore more prone for spreading.
It's not like the virus has a brain. Statistically most could become less deadly, but it doesn't mean all will follow the same pattern. In this case, the virus becomes less deadly as we know how to treat it better and most infected and tested now are younger people.
We're unlucky in that Covid takes such a long time to kill. It's a little under a week until symptoms onset, another week until serious illness [1]. Hospital patients aren't dying of Covid until almost 2 weeks after admission [2]. So we're talking about victims dying maybe a month after exposure.
With other illnesses there's evolutionary pressure to be less deadly so that the host doesn't die before infecting others, but that's not a problem for Covid where people are most contagious before symptom onset.
[1] https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-guida...
[2] https://www.bmj.com/content/369/bmj.m1923.full
With other illnesses there's evolutionary pressure to be less deadly so that the host doesn't die before infecting others, but that's not a problem for Covid where people are most contagious before symptom onset.
[1] https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-guida...
[2] https://www.bmj.com/content/369/bmj.m1923.full
Could someone with some background ELI5 this for those of us who lack expertise?
AFAIK this is the variant that formed in northern Italy back in February and is since ruling the world
That's why it's not good to have a new virus going around in among us. That's why the whole response should have been - isolate and eliminate the virus.
Not, "hey, lets live with this guy until we can make a vaccine that works"...
Not, "hey, lets live with this guy until we can make a vaccine that works"...
The Asian vs. the Euro-American model.
Where has the virus been eliminated successfully in Asia by that model? New Zealand may be the only real success story, and it's a very tiny population island.
India has seen a likely tens of millions of cases.
Bangladesh, Indonesia and the Philippines have all seen bad outbreaks now.
Nepal is currently being buried in cases.
Case numbers are booming in Malaysia at present.
Japan has never managed to eliminate it and continues to see persistent cases, despite their relative success. The same with Singapore.
Did you mean to say that a few countries in Asia have managed to limit the virus, while the rest of Asia has entirely failed at doing so?
India has seen a likely tens of millions of cases.
Bangladesh, Indonesia and the Philippines have all seen bad outbreaks now.
Nepal is currently being buried in cases.
Case numbers are booming in Malaysia at present.
Japan has never managed to eliminate it and continues to see persistent cases, despite their relative success. The same with Singapore.
Did you mean to say that a few countries in Asia have managed to limit the virus, while the rest of Asia has entirely failed at doing so?
But that's the odd thing, isn't the procedure of the "asian model", which was used in NZ, on the "text manuals" of dealing with viruses?
Specially after a first wave, we know how the virus behaved, how we behaved with the virus, and what cost it had (not only deaths, but the stress on health systems that gradually lose the ability to cope with infections, and evolve to the colapse of general health services, other than covid-19). Basically, the virus infection fatality rate might not be as high as we thought, but it ends up collapsing health services, so more deaths direct and indirect are accounted for.
They were hammering us to live in the new normal, what kind of message is that for a population living in a pandemic?
Specially after a first wave, we know how the virus behaved, how we behaved with the virus, and what cost it had (not only deaths, but the stress on health systems that gradually lose the ability to cope with infections, and evolve to the colapse of general health services, other than covid-19). Basically, the virus infection fatality rate might not be as high as we thought, but it ends up collapsing health services, so more deaths direct and indirect are accounted for.
They were hammering us to live in the new normal, what kind of message is that for a population living in a pandemic?
There's a spike in Xinjiang, right now (but a blip by Western standards). It's _really_ hard to eliminate it. New Zealand is still seeing the odd case here and there.
But that could be related to international travelling, or simply community transmission of asymptomatic cases, and China protocol might be to test everyone from that city and apply localized quarantines.
I doubt they will let it go much further than Xinjiang.
I doubt they will let it go much further than Xinjiang.
This is what worries me a little about widespread mask use. It will start selecting strains that spread more through aerosols, touch, or are easier to contract.
Masks imposes such a hurdle on spreading that, even in the (incredible improbable) event that some virus strain gained a 20% more effectivity of transmission through masks, the mask itself would be restricting 99.99% of the spreading. Overall it means that in place of 1 transmission each 10,000 contacts with mask you'll have maybe 2-3 transmissions of this super-virus even with masks, but 5,000 transmissions without masks.
Off-topic:
> ... made available under a CC-BY-ND 4.0 International license.
I'm quite pleased to see more and more academic and scientific papers being licensed as such in recent times!
> ... made available under a CC-BY-ND 4.0 International license.
I'm quite pleased to see more and more academic and scientific papers being licensed as such in recent times!
Why ND and not BY-SA?
Derivative works from a biology paper can result in disinformation.
It should still be BY-SA. Ancillary and auxiliary sources are key to scientific criticism.
What form of criticisms are possible with BY-SA that aren't with BY-CC? Criticism would usually come in the form of new papers which merely reference the previous one.
Direct editing of offending paper while adding you to authors. (that derivative work should still be referenced to the same DOI et al.)
[deleted]
Use of the CC BY ND license is meant to reflect the common practice of sharing academic papers, which was often done informally, as opposed to a paywall. I can send you a copy of my paper; you can pass on copies to colleagues. But in doing so, you wouldn't edit it. That's not a freedom which is necessary for sharing a paper. The paper is a complete product. Moreover it would be a breech of the integrity of the work to edit it. If a correction is required, there is a proper route for that: erratum or corrigendum, published in the original venue.
The first catch of "ND" is that this excludes translation, but that really is not considered to be an issue for two reasons: (1) Scientists are generally expected to be proficient in English and able to read a paper in English - as once was the case for chemists being proficient in German. (2) For popularization and dissemination, media outlets are able to write summaries in other languages.
The second catch is that we really should have some kind of formal secondary license for images and figures within a paper (ideally CC-BY), to allow them to be used separately, since reuse of these should be as frictionless as possible. As a former grad student, it was a pain when writing the review section in a thesis! Though many journals & academic publishers achieve this through having blanket forms that an academic can download for permission to re-use images; for others one needs to consult with the authors of a paper which can be tricky.
And to counter your other comment:
> Ancillary and auxiliary sources are key to scientific criticism.
The licensing does nothing whatsoever to prevent scientific criticism. The Berne Convention [1] explicitly allows for quoting from other works, even if not licensed whatsoever:
> 10.1 It shall be permissible to make quotations from a work which has already been lawfully made available to the public, provided that their making is compatible with fair practice, and their extent does not exceed that justified by the purpose, including quotations from newspaper articles and periodicals in the form of press summaries.
Criticism is never a matter of editing someone else's work; it's commenting about the work. You don't need a license to do that. If one has free access to the full text, which CC BY ND provides, then one has everything necessary to understand the criticism.
[1] https://wipolex.wipo.int/en/text/283698
The first catch of "ND" is that this excludes translation, but that really is not considered to be an issue for two reasons: (1) Scientists are generally expected to be proficient in English and able to read a paper in English - as once was the case for chemists being proficient in German. (2) For popularization and dissemination, media outlets are able to write summaries in other languages.
The second catch is that we really should have some kind of formal secondary license for images and figures within a paper (ideally CC-BY), to allow them to be used separately, since reuse of these should be as frictionless as possible. As a former grad student, it was a pain when writing the review section in a thesis! Though many journals & academic publishers achieve this through having blanket forms that an academic can download for permission to re-use images; for others one needs to consult with the authors of a paper which can be tricky.
And to counter your other comment:
> Ancillary and auxiliary sources are key to scientific criticism.
The licensing does nothing whatsoever to prevent scientific criticism. The Berne Convention [1] explicitly allows for quoting from other works, even if not licensed whatsoever:
> 10.1 It shall be permissible to make quotations from a work which has already been lawfully made available to the public, provided that their making is compatible with fair practice, and their extent does not exceed that justified by the purpose, including quotations from newspaper articles and periodicals in the form of press summaries.
Criticism is never a matter of editing someone else's work; it's commenting about the work. You don't need a license to do that. If one has free access to the full text, which CC BY ND provides, then one has everything necessary to understand the criticism.
[1] https://wipolex.wipo.int/en/text/283698
I thought fair use was automatically disclaimed when you receive an explicit licence, reducing the baseline to taint=derivation (which is the main reason open source developers avoid looking at closed source software that performs similar function), unless your licence specifies otherwise.
And some countries are not signatory to Berne convention, instead to Buenos Aires convention, which is much stricter and does not have a common fair use stipulation.
> Criticism is never a matter of editing someone else's work; it's commenting about the work.
It is. Every consumption is an edit. You edit to remove everything not related to your criticism and add your opinion.
And some countries are not signatory to Berne convention, instead to Buenos Aires convention, which is much stricter and does not have a common fair use stipulation.
> Criticism is never a matter of editing someone else's work; it's commenting about the work.
It is. Every consumption is an edit. You edit to remove everything not related to your criticism and add your opinion.
Regarding this claim:
> fair use was automatically disclaimed
Here's what the organization behind the CC licenses explains:
> By design, CC licenses do not reduce, limit, or restrict any rights under exceptions and limitations to copyright, such as fair use or fair dealing. If your use of CC-licensed material would otherwise be allowed because of an applicable exception or limitation, you do not need to rely on the CC license or comply with its terms and conditions. This is a fundamental principle of CC licensing. [1]
Regarding this ridiculous assertion:
> And some countries are not signatory to Berne convention, instead to Buenos Aires convention, which is much stricter and does not have a common fair use stipulation.
Every country that is a signatory of the Buenos Aires Convention [2] is ALSO a signatory to the Berne Convention. [3]
Your last claim is not worth substantive reply.
[1] https://creativecommonsusa.org/index.php/ufaqs/what-is-the-d...
[2] https://en.wikipedia.org/wiki/File:Buenos_Aires_Convention_S...
[3] https://en.wikipedia.org/wiki/File:Berne_Convention_signator...
> fair use was automatically disclaimed
Here's what the organization behind the CC licenses explains:
> By design, CC licenses do not reduce, limit, or restrict any rights under exceptions and limitations to copyright, such as fair use or fair dealing. If your use of CC-licensed material would otherwise be allowed because of an applicable exception or limitation, you do not need to rely on the CC license or comply with its terms and conditions. This is a fundamental principle of CC licensing. [1]
Regarding this ridiculous assertion:
> And some countries are not signatory to Berne convention, instead to Buenos Aires convention, which is much stricter and does not have a common fair use stipulation.
Every country that is a signatory of the Buenos Aires Convention [2] is ALSO a signatory to the Berne Convention. [3]
Your last claim is not worth substantive reply.
[1] https://creativecommonsusa.org/index.php/ufaqs/what-is-the-d...
[2] https://en.wikipedia.org/wiki/File:Buenos_Aires_Convention_S...
[3] https://en.wikipedia.org/wiki/File:Berne_Convention_signator...
One thing isn't clear to me, for lack of background knowledge: have there been several strains since the beginning of the pandemic, or is this study based on evidence of mutation in the wild?
It sounds like the former, but since it wasn't explicitly addressed in the abstract, I thought I'd ask.
It sounds like the former, but since it wasn't explicitly addressed in the abstract, I thought I'd ask.
Doesn't the first phrase of the abstract state that the latter is the case: "During the evolution in humans ...."?
There have been variants but none so dissimilar that they are considered a new strain. The terminology is very precise here but the media have been mixing it up, causing confusion.
https://medium.com/swlh/variants-lineages-and-strains-of-cor...
https://medium.com/swlh/variants-lineages-and-strains-of-cor...
Thanks for this link. From the article she states:
“Mutations that alter any of the following can lead to a new strain:
pathogenicity virulence immunogenicity.”
And
“ Another way that the term strain is used is when a particular variant of the virus (the virus with a specific set of mutations) ”
This sounds like the mutation referenced in the paper could be considered a “new strain” given the above?
“ Until there is clear evidence supporting functional or immunogenic differences among the variants, it is appropriate to consider all of these lineages of the same virus.”
“Mutations that alter any of the following can lead to a new strain:
pathogenicity virulence immunogenicity.”
And
“ Another way that the term strain is used is when a particular variant of the virus (the virus with a specific set of mutations) ”
This sounds like the mutation referenced in the paper could be considered a “new strain” given the above?
“ Until there is clear evidence supporting functional or immunogenic differences among the variants, it is appropriate to consider all of these lineages of the same virus.”
This is not my area of expertise, but I think I can help answer the question. Everything mutates a lot, so there is a lot of genetic variability. These are usually pretty minor, but really help with tracing, as you can correlate "family trees" of mutations. The big one early in the pandemic was you could see the difference in the genome between the China/West Coast USA and Europe/East Coast USA infections.
I'm not sure of the strict scholastic definition of a strain, but I think they're derived from branches of that family tree. Most of those branches behave pretty similarly as they have mutations that aren't really impactful, but some of those behave differently, and those are the "strains/variants" we're talking about.
On an interesting note on how genetics are used to target therapies, what researchers can do is look at all the different mutations and they can find parts of the genome that change a lot, and parts that change very little. The parts that change very little are often critical for the function of the virus. Mutations to those still happen, but because of the critical nature of the part that mutated, the virus isn't able to reproduce as effectively and so doesn't show up as often. Researchers can use those as targets for treatments, as disrupting those can impact the effectiveness of the virus.
If I got any of that wrong (or I'm using the wrong vocabulary), I'd love to hear from someone with an actual background in this stuff.
I'm not sure of the strict scholastic definition of a strain, but I think they're derived from branches of that family tree. Most of those branches behave pretty similarly as they have mutations that aren't really impactful, but some of those behave differently, and those are the "strains/variants" we're talking about.
On an interesting note on how genetics are used to target therapies, what researchers can do is look at all the different mutations and they can find parts of the genome that change a lot, and parts that change very little. The parts that change very little are often critical for the function of the virus. Mutations to those still happen, but because of the critical nature of the part that mutated, the virus isn't able to reproduce as effectively and so doesn't show up as often. Researchers can use those as targets for treatments, as disrupting those can impact the effectiveness of the virus.
If I got any of that wrong (or I'm using the wrong vocabulary), I'd love to hear from someone with an actual background in this stuff.
There are thousands of mutations which have been observed. Some are consequential - changing the virus' behaviour - others are not. What constitutes a "strain" is fuzzy, since viruses are constantly evolving and it's an artificial category or human construct. To get away from that, it's often helpful to think in terms of phylogeny or genetic relationships.
You can see a phylogenetic tree of the clades (essentially a "family tree" determined through mutations of the virus) & a map showing the distribution of the different clades of the virus worldwide on GSAID platform:
https://www.gisaid.org/epiflu-applications/phylodynamics/
You can see a phylogenetic tree of the clades (essentially a "family tree" determined through mutations of the virus) & a map showing the distribution of the different clades of the virus worldwide on GSAID platform:
https://www.gisaid.org/epiflu-applications/phylodynamics/
With our current knowledge we can only say that there's only one strain, but they are accumulating changes randomly. Usually those changes are deletereous (bad for the virus), some are neutral and a very minor amount increase the fitness of the virus (good for the virus).
It has been proposed that one of those mutations (D614G) increases the fitness of the virus. If that was the case, viruses with D614G would slowly take over the population. The problem here is that if some "founder effect" [1] happens, it will appear exactly like some mutation gives an increased fitness but what happened in reality was that some guy travelled to a meeting and infected 100 people.
This mutation was first reported in january-2020 in Germany (AFAIK), so it's a very posible that it was just one of the very first viruses to arrive in Europe and "founded" a new population when the virus was spreading almost freely. Then some scientist noted that a lot of european sequences included the mutation and hipotesized that the change was behind the quick spreading of march and april.
Right now, about 80% of the sequences reported to Gisaid include that mutation, but that is about the same percentage than in april/may. I'm personally inclined to believe that D614G is close to have neutral effects, as other variants of the virus without the mutation are also being quite successful in spreading and keeping themselves in the population.
[1] https://en.wikipedia.org/wiki/Founder_effect
It has been proposed that one of those mutations (D614G) increases the fitness of the virus. If that was the case, viruses with D614G would slowly take over the population. The problem here is that if some "founder effect" [1] happens, it will appear exactly like some mutation gives an increased fitness but what happened in reality was that some guy travelled to a meeting and infected 100 people.
This mutation was first reported in january-2020 in Germany (AFAIK), so it's a very posible that it was just one of the very first viruses to arrive in Europe and "founded" a new population when the virus was spreading almost freely. Then some scientist noted that a lot of european sequences included the mutation and hipotesized that the change was behind the quick spreading of march and april.
Right now, about 80% of the sequences reported to Gisaid include that mutation, but that is about the same percentage than in april/may. I'm personally inclined to believe that D614G is close to have neutral effects, as other variants of the virus without the mutation are also being quite successful in spreading and keeping themselves in the population.
[1] https://en.wikipedia.org/wiki/Founder_effect