Firstly, this isn't about SARS-COV-2. It is about the more broad concept of viral classification.
Secondly, journal articles, yes, I agree. And a lot of government funding should be pouring into research to be published and that needs to be available to help us fight this.
Journalism articles though are more tricky. Because they need to pay their employees, the journalists, and cover their costs. Given that 90% is all news now (my guess) is about covid-19, then there would be significantly less revenue for journalism if it said it couldn't paywall articles covid-19 articles. Additionally, advertising revenue is likely to collapse as a second order effect of the recession this crisis is bringing. Finally, there is a lot of competition for news, so any major news story has multiple free articles about it that will be accessible to all (with ads of course).
The highest quality journalism is currently coming from two places: paywalled websites and NPR. NPR is free and fulfills a comparable market position as BBC. That is your "public option". But not allowing paywalls would kill the quality reporting of the nytimes and Washington Post and turn them into CNN / Fox / MSNBC.
Along these lines, I wonder if we will eventually see charts like this for ALL human viruses with a person by person trace: https://nextstrain.org/ncov
Why so confident? We have the technical skills, but this also takes institutional cooperation we suck at. We don't even have a standard format for conventional medical records in the US!
I expect legislation that will require CDC and DHHS to establish surveillance programs. We will be sequencing. This will be academic labs and clinic labs most likely. There might be a national sequencing center established.
If we work together with China we might leverage their massive sequencing capacity.
That chart is fascinating - especially the extent of which some countries apparently have virus strains from every branch, while others have 1 or 2 distinct lineages (Washington State being the biggest one).
That does imply that the UK and Netherlands have seen the virus introduced from many sources, which suggests much more widespread transmission than eg New Zealand, which appears to have one lineage.
However, there's probably a huge sampling bias present. Hopefully we can keep doing this sort of genetic lineage testing at greater rates - it's incredibly informative on how it spreads.
I don't think the existing viruses that infect humans are so important. The problem is rather mutation - or evolution - any virus that at the moment does not affect humans can suddenly develop into one that infects humans, and this is how COVID-19 started. Land living animals are the greatest risk here because their bodies essentially work the same as humans and farming them increases the amount of viruses and thus the potential for a mutation to spread fast.
There are plenty of viruses that still do something, but we don't know what it is, because the something is not immediately threatening to public health.
For instance, there is a chicken virus (SMAM-1) that unconditionally increases adiposity in the infected bird, even when the chicken is fed the same amount as inunfected chickens. SMAM-1 is zoonotic to humans. It also makes them fat. Several human adenoviruses are suspected of doing similar things. But they have not been studied extensively, because the general prejudice is that people become morbidly obese due to their own lifestyle choices, and therefore excessive adiposity is a condition that should be first-treated with lifestyle intervention, rather than applying evidence-based medicine.
There are still a lot of nonscientific prejudices in general medicine. "Let's sequence all viruses in our patients," sounds a whole lot like "let's wash our hands before touching a new patient, so we don't spread diseases between them," which was once rejected by the experts as implausible hogwash.
Will the media ever understand the difference between "we underestimate tail risks all the time" and "we have been underestimating this specific tail risk"?
It generally seems like evolution is better described by continuums, not discrete entities: if one gene is changed among thousands, is the result worthy of a new name? Just like with languages vs dialects—those are the same thing, but on different scale.
Edit: to clarify, I'm aware of the criterion of sexual incompatibility, and that genes don't usually work one-by-one, but still—slapping an arbitrary Latin-ish name on each of the millions of, say, fly species seems of dubious use, at least to an outsider.
First, it's important to distinguish between genotype and phenotype. Most genetic mutations don't cause any change in behavior or appearance, so the two individuals are phenotypically equal.
With sexual reproduction, individuals can differ genetically but still be compatible, so there is some notion of a pool with a clear boundary. For viruses, this is of course a bit trickier because they "reproduce asexually"[0] and quite rapidly, so mutations happen at a high rate. But one useful property to distinguish them is which receptors (and thus which cells) they bind to, generally affecting what symptoms and diseases they cause.
[0]: Viruses are not considered living things, so the concept of reproduction is already quite a stretch.
> so there is some notion of a pool with a clear boundary.
That's a model that kind of works most of the times, but not always: the most known example are Bisons and Cows which can breed together and the offsprings are fertile : https://en.m.wikipedia.org/wiki/Beefalo
In fact, most of today's bisons have cows' genes in their genome.
A can breed with B, B can breed with C, C can breed with D, and D can breed with A.
But A cannot breed with C.
Are A and C part of the same species, or not? These "ring species" occur around geographic rings, such as the Arctic Circle, so each population remains genetically compatible with its neighbors... but not "across the ring".
Yeah. Basically the concept of species is bust taxonomically and largely a social construct at this point. (That is to say, what is a species is what the community agrees to be a species for the sake of convenience)
Well, genomic data is objectively discrete rather than continuous. And even if you really wanted to approach it as "continuums", what dimensions could you possibly use?
Perhaps you mean to say that strains should be defined in a fuzzy manner? If so, from my very limited knowledge of systematics, they already are.
It's discrete just like info that one has 19001.18 bucks in their account rather than 19000. Precise yes, useful not very.
I guess ‘behavior and appearance’, mentioned in another comment, are the more practical dimensions, but I still wonder how useful the distinctions are.
Current scientific literature suggests that viruses change by small amounts all the time, and every now again (3-5 years for influenza) there is big 'jump' in which a significantly novel strain is identified and characterised. See this excellent review for further explanation:
The evolution of seasonal influenza viruses - Velislava N. Petrova & Colin A. Russell
I think usually the gene name isn't changed. For example, I've noticed that bacterial genomes tend to start with the dnaA gene (many different sequences).
I like to think of genes as their amino acid or dna sequence only, and internally whenever I need to manage a ton of sequences their names are just hashes of those sequences.
I studied viruses for a job a few years ago. I looked at RNA viruses mostly and specifically influenza. The way they work is truly astonishing but you quickly realise it's an unfortunate inevitability given the way our genetics works.
One interesting thing I remember is that virtually every human over a year old or so is "infected" with at least a handful of viruses for life. The scare quotes are because we really don't know what effect these viruses have on us. They could be beneficial for all we know.
To add further complexity consider that bacteria get infected by viruses (called bacteriophages). All those bacteria inside you are in turn "infected" by viruses. Phages are so numerous that a drop of seawater contains about ten million of them. Also they are literally like microscopic genome injection machines. Look up some pictures and electron microscope images.
> virtually every human over a year old or so is "infected" with at least a handful of viruses for life
That sounds like a very interesting concept, and it's one that I haven't heard of before. If you don't want to write yourself, linking me to some reputable sources would be awesome too.
Not entirely sure what GP is talking about, but just off the top of my head, this is the situation for anyone who's ever had chickenpox: you get chickenpox, the sores appear and then go away, but the virus stays in you. If you become immunocompromised/stressed later on in life it can re-emerge as shingles (decades later even).
I simple example of this is chicken pox (Varicella Zoster).
A large proportion of adults have had it as kids. The immune system fights it off but virus particles can still 'hide' from it and lay dormant inside pheripheral nerve tissue.
A proof of this is 'shingles' in adults. i.e. a virus which probably infected the host +50 years ago and went dormant in their nerves finds the host immune system weak enough to come out again and start replicating.
I wonder if that statement was talking about endogenous viruses:
> Approximately 8% of the human genome is made up of endogenous retroviruses (ERVs), which are viral gene sequences that have become a permanent part of the human lineage after they infected our ancient ancestors.
> ..their expression has been implicated in diseases like autoimmune disorders and breast cancer.
> they can also be extremely useful for human survival. For example, they play a very important role as an interface between a pregnant mother and her fetus by regulating placental development and function.
> It has been suggested that viruses are not only necessary for the existence of placental mammals, but also for the existence of life in general.
> viruses were involved in most all major transitions of host biology in evolution
I'm learning as I read it, but quoting some passages that seem relevant:
> viruses are fully competent agents and editors of all host systems of instruction (DNA, RNA, epigenetic, translational etc.). Thus, they provide the host with new sources of instruction systems (not errors).
> In addition, they promote network formation by providing coherent societies (quasispecies populations) of agents able to edit host code content (and add new identity) in a diffuse, distributed manner, which promotes the creation of and editing of host regulatory networks.
> Thus, a viral role in the origin of the placental regulatory network can be expected. Viruses possess all the advantages of evolution relative to host: extreme genetic adaptability, extreme diversity, extreme numbers, extreme rates of genetic exchange, tolerance for ‘unfit’ variation, and the ability to reassemble from cryptic or ‘dead’ parts. They can transition between the chemical and living world.
> ..most initial genetic and selective events that transform host regulatory complexity are usually ‘pushed’ by virus action in a general direction of increasing complexity.
> Hence, we must always consider how any virus action on host will affect virus–host survival in their respective virosphere or virus habitat (e.g., reproductive tissue).
> A most significant development would be the emergence of a stable persistent relationship between virus and host as this represents a virus–host symbiosis that now protects the host form the same and often other lytic (disease causing) viruses.
I read something recently which was something of an epiphany. (Can't seem to find it, unfortunately).
The idea was that humans and other animals incorporate some viral genes and produce the protein (and/or RNA I guess), and it's adaptive to do so because it gives something useful to develop antibodies against. Elegant, and kind of suggestive for all those retrovirus residues lying around in our genomes, among other things.
I can't think of anything that is not a textbook. That said, I would recommend[0]. You will encounter a lot of vocabulary, just use Wikipedia and look on YouTube for animations/explanations etc. I think this will give you the most bang for your buck.
Bacteriophages are so cool. They look so futuristic yet they are incredibly ancient. Some researchers are also starting to look into bacteriophages as a potential treatment for antibiotic-resistant infections
Sure would be convenient if we had a predator for out most recent emerging predator. Big ask when putative prey has only been in existence for about three months in its current form though..
How is a virus species defined ? As I understand it a species is a group of organisms that can reproduce viably with each other. But a virus doesn't reproduce like that, they clone themselves by hijacking a cell's machinery, so there is no notion of compatibility between viruses. The article says that Covid-19 is "similar" to SARS so it was put in the same species, but that seems a rather soft definition. Especially if there are trillions of different viruses like the article says, some objective criterion is needed. Not to mention viruses mutate all the time, at what point does it become a new species?
Many human concepts only approximate the underlying physical reality, and the concept of "species" is a great example of that, especially when applied to a population of viruses. It's unclear whether having a truly accurate concept of species is even an achievable or desirable goal.
The International Committee on Taxonomy of Viruses (ICTV) is responsible for classifying viruses and they use a bunch of different criteria, such as chemical characteristics, structure (e.g. look at Covid-19 vs a bacteriophage), type of nucleic acid, mode of replication, host organisms, and the types of diseases they cause. They also group them based on common ancestors.
In other words, it becomes a new species when there's a change to the phenotypic traits above.
Yeah species is exta. hard for asexually reproducing species.
Sometimes two different viruses infect the same cell and we get a hybrid. Doing that in a lab and looking at the offspring vitality rate would be interesting, and mathematically coherent.
50 comments
[ 0.19 ms ] story [ 96.7 ms ] threadSecondly, journal articles, yes, I agree. And a lot of government funding should be pouring into research to be published and that needs to be available to help us fight this.
Journalism articles though are more tricky. Because they need to pay their employees, the journalists, and cover their costs. Given that 90% is all news now (my guess) is about covid-19, then there would be significantly less revenue for journalism if it said it couldn't paywall articles covid-19 articles. Additionally, advertising revenue is likely to collapse as a second order effect of the recession this crisis is bringing. Finally, there is a lot of competition for news, so any major news story has multiple free articles about it that will be accessible to all (with ads of course).
The highest quality journalism is currently coming from two places: paywalled websites and NPR. NPR is free and fulfills a comparable market position as BBC. That is your "public option". But not allowing paywalls would kill the quality reporting of the nytimes and Washington Post and turn them into CNN / Fox / MSNBC.
In an ideal world, we should be sequencing viruses for each single patient, just like we measure blood pressure.
That does imply that the UK and Netherlands have seen the virus introduced from many sources, which suggests much more widespread transmission than eg New Zealand, which appears to have one lineage.
However, there's probably a huge sampling bias present. Hopefully we can keep doing this sort of genetic lineage testing at greater rates - it's incredibly informative on how it spreads.
For instance, there is a chicken virus (SMAM-1) that unconditionally increases adiposity in the infected bird, even when the chicken is fed the same amount as inunfected chickens. SMAM-1 is zoonotic to humans. It also makes them fat. Several human adenoviruses are suspected of doing similar things. But they have not been studied extensively, because the general prejudice is that people become morbidly obese due to their own lifestyle choices, and therefore excessive adiposity is a condition that should be first-treated with lifestyle intervention, rather than applying evidence-based medicine.
There are still a lot of nonscientific prejudices in general medicine. "Let's sequence all viruses in our patients," sounds a whole lot like "let's wash our hands before touching a new patient, so we don't spread diseases between them," which was once rejected by the experts as implausible hogwash.
Edit: to clarify, I'm aware of the criterion of sexual incompatibility, and that genes don't usually work one-by-one, but still—slapping an arbitrary Latin-ish name on each of the millions of, say, fly species seems of dubious use, at least to an outsider.
With sexual reproduction, individuals can differ genetically but still be compatible, so there is some notion of a pool with a clear boundary. For viruses, this is of course a bit trickier because they "reproduce asexually"[0] and quite rapidly, so mutations happen at a high rate. But one useful property to distinguish them is which receptors (and thus which cells) they bind to, generally affecting what symptoms and diseases they cause.
[0]: Viruses are not considered living things, so the concept of reproduction is already quite a stretch.
That's a model that kind of works most of the times, but not always: the most known example are Bisons and Cows which can breed together and the offsprings are fertile : https://en.m.wikipedia.org/wiki/Beefalo
In fact, most of today's bisons have cows' genes in their genome.
The boundary isn't very clear.
https://en.wikipedia.org/wiki/Ring_species
A can breed with B, B can breed with C, C can breed with D, and D can breed with A.
But A cannot breed with C.
Are A and C part of the same species, or not? These "ring species" occur around geographic rings, such as the Arctic Circle, so each population remains genetically compatible with its neighbors... but not "across the ring".
https://upload.wikimedia.org/wikipedia/commons/thumb/8/8d/Ri...
Perhaps you mean to say that strains should be defined in a fuzzy manner? If so, from my very limited knowledge of systematics, they already are.
I guess ‘behavior and appearance’, mentioned in another comment, are the more practical dimensions, but I still wonder how useful the distinctions are.
The evolution of seasonal influenza viruses - Velislava N. Petrova & Colin A. Russell
https://www.nature.com/articles/nrmicro.2017.118
I like to think of genes as their amino acid or dna sequence only, and internally whenever I need to manage a ton of sequences their names are just hashes of those sequences.
One interesting thing I remember is that virtually every human over a year old or so is "infected" with at least a handful of viruses for life. The scare quotes are because we really don't know what effect these viruses have on us. They could be beneficial for all we know.
To add further complexity consider that bacteria get infected by viruses (called bacteriophages). All those bacteria inside you are in turn "infected" by viruses. Phages are so numerous that a drop of seawater contains about ten million of them. Also they are literally like microscopic genome injection machines. Look up some pictures and electron microscope images.
> virtually every human over a year old or so is "infected" with at least a handful of viruses for life
That sounds like a very interesting concept, and it's one that I haven't heard of before. If you don't want to write yourself, linking me to some reputable sources would be awesome too.
A large proportion of adults have had it as kids. The immune system fights it off but virus particles can still 'hide' from it and lay dormant inside pheripheral nerve tissue.
A proof of this is 'shingles' in adults. i.e. a virus which probably infected the host +50 years ago and went dormant in their nerves finds the host immune system weak enough to come out again and start replicating.
> Approximately 8% of the human genome is made up of endogenous retroviruses (ERVs), which are viral gene sequences that have become a permanent part of the human lineage after they infected our ancient ancestors.
> ..their expression has been implicated in diseases like autoimmune disorders and breast cancer.
> they can also be extremely useful for human survival. For example, they play a very important role as an interface between a pregnant mother and her fetus by regulating placental development and function.
> It has been suggested that viruses are not only necessary for the existence of placental mammals, but also for the existence of life in general.
The above is from a Medium article by a non-specialist: https://medium.com/medical-myths-and-models/the-human-genome...
---
It cites a paper presenting a "virus-first" perspective on the evolution of life:
Viruses and the placenta: the essential virus first view - https://onlinelibrary.wiley.com/doi/full/10.1111/apm.12485
> viruses were involved in most all major transitions of host biology in evolution
I'm learning as I read it, but quoting some passages that seem relevant:
> viruses are fully competent agents and editors of all host systems of instruction (DNA, RNA, epigenetic, translational etc.). Thus, they provide the host with new sources of instruction systems (not errors).
> In addition, they promote network formation by providing coherent societies (quasispecies populations) of agents able to edit host code content (and add new identity) in a diffuse, distributed manner, which promotes the creation of and editing of host regulatory networks.
> Thus, a viral role in the origin of the placental regulatory network can be expected. Viruses possess all the advantages of evolution relative to host: extreme genetic adaptability, extreme diversity, extreme numbers, extreme rates of genetic exchange, tolerance for ‘unfit’ variation, and the ability to reassemble from cryptic or ‘dead’ parts. They can transition between the chemical and living world.
> ..most initial genetic and selective events that transform host regulatory complexity are usually ‘pushed’ by virus action in a general direction of increasing complexity.
> Hence, we must always consider how any virus action on host will affect virus–host survival in their respective virosphere or virus habitat (e.g., reproductive tissue).
> A most significant development would be the emergence of a stable persistent relationship between virus and host as this represents a virus–host symbiosis that now protects the host form the same and often other lytic (disease causing) viruses.
[0] https://www.sciencedirect.com/book/9780123737410/viruses-and...
Edit: https://www.amazon.com/Planet-Viruses-Second-Carl-Zimmer/dp/... might be good, haven't read it though
I've read it and (excuse me) it's fucking fanstastic!
Short and sweet, and mind-blowing on every page.
https://en.wikipedia.org/wiki/Virophage
Sure would be convenient if we had a predator for out most recent emerging predator. Big ask when putative prey has only been in existence for about three months in its current form though..
In other words, it becomes a new species when there's a change to the phenotypic traits above.
Sometimes two different viruses infect the same cell and we get a hybrid. Doing that in a lab and looking at the offspring vitality rate would be interesting, and mathematically coherent.