SARS-CoV-2 spike D614G variant confers enhanced replication and transmissibility
biorxiv.org
biorxiv.org
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.
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.
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.
”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.”
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...
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.
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?
Didn't pneumonia, influenza (among small pox and others) have terrible consequences on American native Indians ?
> 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...
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.
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.
But it does seem very likely the vaccine will not be a one time shot and you’re good forever.
And the opposite, /could/ happen, too. The virus could mutate to have a longer incubation period, or be more deadly, or both.
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).
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.
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.
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.
Influenza refers to a class of viruses, not a single virus.
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.
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.
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.
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.
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...
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.
Do we really know that yet?
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.
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...
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.
> ... 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!
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.
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.
> 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...
Not, "hey, lets live with this guy until we can make a vaccine that works"...
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?
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?
I doubt they will let it go much further than Xinjiang.
It sounds like the former, but since it wasn't explicitly addressed in the abstract, I thought I'd ask.
https://medium.com/swlh/variants-lineages-and-strains-of-cor...
“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.”
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.
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:
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.