Meet the Coronavirus Family: Viruses, Virus Groups, and SARS-CoV-2 in Context · 5:30pm Mar 27th, 2020
Blog Number 72: "Where Did That Coronavirus Come From?" Edition
Did you know, for instance, that "coronavirus" in scientific terms describes a family of viruses? The current strain is known as SARS-CoV-2, but what does that jumble of letters mean, and why "2"? And why's "COVID-19" tossed into the mix as well?
Well, here's a handy breakdown, starting with the broadest basics on viruses and their families, and zooming in, like an electron microscope, to our current specific miniature menace.
Contents below, then the meat of the blog post itself.
CONTENTS SECTION
VIRUS
What IS a Virus?
The Parts of a Virus
The Ongoing War Between a Virus and its Host
BALTIMORE CLASSIFICATION GROUP IV
(+)ssRNA viruses
(+)
ss
RNA
CORONAVIRUS
Peplomers: the Coronavirus's Key to Success
Typical Coronavirus Targets
Bats and Coronaviruses
The Four Houses of Coronavirus: Meet the Family
BETACORONAVIRUS
The Distant Cousins of SARS-CoV-2
SEVERE ACUTE RESPIRATORY SYNDROME-RELATED CORONAVIRUSES
The Brothers and Sisters of SARS-CoV-2
SARS-CoV: The First-Born
SARS-CoV: The Death Count
SARS-CoV-2
A Ray of Hope?
VIRUS
What IS a Virus?
At its most basic, a virus is a borderline living thing, probably better thought of as a tiny molecular hijacker.
Most living things are far more complicated than a virus. Living things are made of at least one cell (a single bacterium is as small as this gets), which itself is a complex capsule of molecules that can do all kinds of things. It can:
- break down and build up chemicals to gain energy (metabolism);
- regulate itself to keep internal conditions in a particular state (homeostasis);
- split off from a parent cell to make more cells (reproduction);
- change over time in response to conditions (adaptation);
- and grow bigger (erm... growth).
Cells contain cytoplasm, which broadly speaking is water plus the organelles (organ-like molecular structures that do all the work, a.k.a. the machinery) and basic molecules (a.k.a. the stock).
The DNA in a living cell gets special quarters in all this, kept in a nucleus with its own nucleoplasm. Think of it as the government district, carrying the base instructions that the rest of the cell then acts upon.
Compared to a virus, a cell is a large city full of hustle and bustle. By contrast, a virus would be like a dilapidated house lost in the countryside; impressive in its own design, but minuscule, inert, near-empty, and nothing like the rich variety and activity of a city in full swing.
Viruses are shadow life forms. They do some of the things listed above, which is why some biologists consider them as life forms at all, but even then not in a typical way. They can reproduce, but only by hijacking the machinery in a cell. They adapt, but mostly by becoming more adept at hijacking a cell. And while I suppose they "use" the energy in their host cell to replicate, on their own they don't really practise homeostasis or growth, which is why they can die off if left on a surface with no cell to steal from.
The Parts of a Virus
At bottom, a virus mainly has two parts. Think of it as a cargo container. The replicating molecule (usually RNA, but DNA viruses exist too) is the precious cargo inside. This is protected and transported by the capsid, which is a shell of proteins that acts as the container.
The job of the capsid is to infiltrate the cell's membrane and thus carry the precious cargo as close to the cell's replicating machinery as possible.
The job of the replicating molecule is to hijack this machinery, either in the cytoplasm itself or in the nucleus, and replicate like crazy once it gets inside, overwhelming the cell to breaking point and then bursting out to infect more cells.
Stealth, subversion, a complete revolution of the cell's policy, mass conversion, followed by spreading the word to other areas: well, since we compared the nucleus to the government district, you can make you own comparison at this point. 
The Ongoing War Between a Virus and its Host
Of course, cells don't take this lying down, and their design will generally improve the defences as they adapt, such as using proteins to make "border checks" on the cell membrane before anything's allowed in. To counter that, the capsid design of a virus over generations will change to better get around these improving defences of the host cell, e.g. by faking passes so that border control positively lets them in.
This is also why viruses don't, Resident Evil notwithstanding, cross over into lots of other species. Once you become an adept lockpick of one particular lock, you're not necessarily designed to take advantage of other locks. They tend to be specific to, at best, a handful of target species, which are usually closely related; this is why humans more often get viral diseases from fellow mammals than from, say, reptiles.
What makes viruses particularly dangerous compared with, say, disease-causing bacteria is how rapidly they can adapt to new situations, which is one reason why the common cold is so hard to cure. The best conditions for breeding new forms of life involve fecundity (when viruses replicate, they replicate a lot), volatility (virus RNA in particular can mutate much faster than the more traditional DNA, meaning their "government policy" can leap over new obstacles rather than get stuck in the discussion stage), and strong selective pressure (ironically, the constant barrage of defences stacked against them; this really is a case of "what doesn't kill you makes you stronger").
Got that? Now we know what a virus is, how do we sort out all the various types of virus? Enter the next section.
BALTIMORE CLASSIFICATION GROUP IV
(+)ssRNA viruses
Now let's start zeroing in on our current coronavirus strain. Viruses can be classified according to the Baltimore Classification, developed by David Baltimore (who, funnily enough, was actually born in New York City). There are seven groups, and the one we want is...
Group IV: (+)ssRNA viruses.
Don't worry: it's not as intimidating as it looks. That classification can be broken down to make sense of it.
(+)
This refers to how the virus's replicating molecule "translates" its instructions into protein manufacture, ultimately to make more viruses. It only applies to single-stranded viruses (see the next part for what that means).
A bit of background first: in a normal, healthy cell, the DNA carries the original instructions simply because it has a particular sequence of molecules in a string (which can be represented as A, C, G, and T, after the names of the particular molecules used). But it's not meaningful if it sits in the nucleus doing nothing. Normally, the cell's own RNA molecules attach to the DNA in a particular way (they "read" the code) and then they take this to yet more RNA to convert the code, bit-by-bit, into a string of peptides which make up a full protein. The proteins ultimately are the taskmasters that do important jobs around the cell and, in complex life forms, also do jobs in various parts of an organism's body.
There's more to it than the brief summary here, but basically: DNA holds the book of instructions, RNA reads the book and follows it, and proteins are the result.
Now, back to viruses. A virus has to insert itself into this system in order to get its own instructions read and followed. It has to make "sense". A single-stranded virus has an advantage in that respect, because it's already in a form that's easy to read. It's like an open book. But how that book's read is what makes the difference between a positive (+) sense and a negative (-) sense virus.
See, when an RNA molecule reads the DNA molecule, it actually makes a mirror image of the sequence. This gets flipped back again (naturally) when the next RNA molecule reads it in turn, so you end up with the original message.
A negative (-) sense virus starts with the inverted message, and ends up needing it read (and hence mirrored) by another RNA molecule before the "actual" message is ready for making proteins.
A positive (+) sense virus has it easy by comparison. It starts with the "actual message" already, so it's immediately ready for making proteins itself.
This positive and negative distinction is called "sense" or "strand", and the distinction between positive and negative "sense" can be called "sense" and "antisense", or "positive strand" and "negative strand". If they're the negative, they belong in Group V. If they're the positive, they belong in Group IV. Our coronavirus is one of these positive types.
Note that this only applies to a single-stranded RNA virus. (Obviously, a DNA virus needs an RNA reader regardless, as it's just holding the instructions, not acting on them). What does that mean? Well...
ss
Basically, "single-stranded", as opposed to "double-stranded", which would be ds.
This one's easy enough to understand. DNA in a cell usually comes in what's called a "base pair". If you could take the double helix of one of your DNA molecules and straighten it so that it looked like a ladder, the two rails would each be (don't worry about remembering this name) the phosphate-deoxyribose support, or "backbone", and the rungs between them would be the nucleobases, which carry the "letters" of the DNA message (A, C, G, and T, remember) and hence its instructions. Each rung is made of two nucleobases, the right half and the left half, joined together in the middle.
RNA has a similar structure, but with small differences in the backbone and the nucleobases (for instance, they have a phosphate-ribose support, or "backbone", instead of a phosphate-deoxyribose one).
Cells aren't alone here: some viruses, DNA or RNA, obey this traditional layout too. Those in Groups I, III, and VII are of this kind.
The rest of the viruses don't.
Whether they have DNA or RNA, they basically have a ladder chopped in half vertically, with one backbone (the rail of the ladder) and one nucleobase (half of the rung). Since this is the form needed to "read" the replicating molecule, they can in theory be read quicker. The book's basically lying wide open; you don't need to peel the closed pages apart first to open it.
RNA
The "RNA" part should be obvious enough by now - this is a virus whose replicating molecule is RNA. Groups III, IV, V, and VI fit into that category. The rest use DNA.
Put it together, and you've got (deep breath) a positive-sense single-stranded RNA virus...
...or (+)ssRNA virus, which is what Group IV consists of.
On a minor note, you might be wondering how we've got seven groups, in that case. After all, we've got single-stranded and double-stranded, DNA and RNA, which gives four possibilities. The positive-sense and negative-sense thing only applies to one of those four possibilities anyway, so that gives us five groups. What are the other two?
Well, they're a couple of odd cases where the virus's replicating molecules don't translate directly, but use an intermediate, from RNA to DNA (Group VI) and from DNA to RNA (Group VII). Kind of like an ambassador, I suppose. It's complicated. The whole thing can be summed up in our classification system as RT (which I like to think of as Really Tortuous).
For a grand finale, all seven groups of the Baltimore Classification can be represented thus. Hopefully, you know enough by now to translate the seemingly intimidating jumble:
- Group I: dsDNA viruses
- Group II: ssDNA viruses
- Group III: dsRNA viruses
- Group IV: (+)ssRNA viruses
- Group V: (−)ssRNA viruses
- Group VI: ssRNA-RT viruses
- Group VII: dsDNA-RT viruses
Anyway I've gone on long enough. Time to move on!
Now we know our coronavirus is part of Group IV, the (+)ssRNA virus group, where next?
I'm going to be a bit cheeky and skip over the next few checkpoints in our viral family tree, simply because it gets a bit technical there and I don't want to get carried away. If you're interested, the next levels down in our hierarchy (from "virus" at the top to "SARS-CoV-2" at the bottom) are called Nidovirales, then Cornidovirineae, then Coronaviridae, and finally Orthocoronavirinae. Only then do we come to our next stop... the coronavirus!
CORONAVIRUS
What we call the "coronavirus" at the moment is actually one member of the much larger coronavirus family. The name "coronavirus" derives from the characteristic shape of their capsid: it looks a bit like a crown seen from the top, or like the corona of the sun (specifically when it's obvious to the naked eye during a solar eclipse, though for goodness' sake don't look at a solar eclipse with a naked eye). This is caused by projections radiating off the capsid, like spikes on a ball.
Those "spikes" are actually the virus's secret weapon.
Peplomers: the Coronavirus's Key to Success
Each spike of the coronavirus is called a peplomer. The peplomer is made of a special kind of protein called a glycoprotein, which in other forms are also used in the human body to carry out a range of functions. Collagen, for instance, is a glycoprotein, and one of the most abundant proteins in the human body, found especially in the tendons, ligaments, and skin. One of its major functions is to act as a structural support.
The peplomer of a coronavirus, though, has a very different purpose. It is specifically designed to bind to particular target cells, so these are basically the passes which fool the border control of the cell membrane (which I mentioned earlier).
This so-called border control is actually a type of receptor, a protein embedded in the cell membrane, called a specific transmembrane carrier protein. These proteins bind to a particular molecule and, like all receptors, respond appropriately; in this case, it actively carries the particular molecule through the membrane wall.
This only works if the molecule in question is the right shape, like a key in a lock, though the comparison isn't perfect as some carrier proteins can be more generous (allowing something in if it's iffy but broadly the right shape) or more stringent (allowing only a particular shape in a very particular orientation, say, and saying NO if it's the tiniest bit misaligned).
This is how the coronavirus infiltrates a cell. In fact, one of the reasons coronaviruses are covered with peplomers (the spikes) is because it increases the chance that one of them will hit the target carrier protein in just the right way to fool it.
Typical Coronavirus Targets
What cell, though, would be of interest? Would any cell do, so long as it belonged to the same animal, for instance?
Well, no, because even within a single body, different cell types have different carrier proteins. This makes sense: a neural cell in the brain specializes in ferrying charged particles through its membrane, along its length in a continuous wave, in order to carry a signal, so it doesn't need the same kind of carrier protein as a stomach cell, which needs to release particular digestive enzymes and tackle all kinds of chemicals in the food we eat. So a virus will, like a specialist locksmith, likely target cells in particular body systems.
Usually, coronaviruses target mammalian lung cells.
Coronaviruses as a family usually target mammals, in any case, though some have birds among their list of casualties (the Bulbul coronavirus HKU11, for instance, favours the Chinese bubul bird). In particular, they specialize in attacking the cells in the respiratory system (namely the lungs), as you doubtless can figure out by this point from all the news over how the SARS-CoV-2 virus has affected people. This makes sense: if you enter the body via the mouth and nose, the lungs are a likely destination, and a much safer bet than the acid-and-enzyme-ridden stomach. The respiratory tract is a common target for pathogens of all kinds.
The favoured cells in this case are located in the alveolar sacs, which are the berry-like collections at the end of bronchioles, which in turn are the smallest branches coming off the larger branches of the bronchus tubes, which in turn branch off from the two main bronchi (right and left, one for each lung), which in turn branch off from the main windpipe (the trachea). The whole set of branching types looks a bit like an upside-down tree.
This is the route taken by the oxygen we breathe in and the carbon dioxide we breathe out (and many other gases besides, in either direction, as well as whatever else happens to be mixed in with them).
The alveolar sacs are especially important because they are where the gas in the lungs is exchanged with the gas in the body's blood vessels. Unfortunately, this also requires them to be thin-walled and to allow molecules to cross their borders often, making them easy targets for a penetrating virus.
Bats and Coronaviruses
It's also well-known that a bat species is considered a likely culprit for the origin of this current pandemic.
What's less well-known is the fact that a lot of these coronaviruses target bats as a matter of course; the current SARS-CoV-2 virus is actually pretty typical, in that respect. There's also:
- Miniopterus bat coronavirus 1 (Mi-BatCoV 1A)
- Miniopterus bat coronavirus HKU8 (Mi-BatCoV HKU8)
- Rhinolophus bat coronavirus HKU2 (Rh-BatCoV HKU2)
- Scotophilus bat coronavirus 512 (Sc-BatCoV 512)
- Pipistrellus bat coronavirus HKU5 (Pi-BatCoV HKU5)
- Rousettus bat coronavirus HKU9 (Ro-BatCoV HKU9)
- Tylonycteris bat coronavirus HKU4 (Ty-BatCoV HKU4)
Incidentally, it's not only coronaviruses that like bat victims: bats just seem especially susceptible to viruses in general, as they are also host to the rabies virus, Australian bat lyssavirus, Nipah virus, Hendra virus, Lassa virus, Ebola virus, the Marburg virus, and various hantaviruses. In fact, bats as a whole - oddly enough - seem unusually tolerant of such viruses too, meaning that they won't necessarily have the averse reactions that, say, humans would when exposed to them. I'm not sure why that is, but (speculating here) it might simply be that some viruses work so hard to penetrate the defences of a particular bat species that it makes them, in a sense, "overqualified" to tackle the defences of other species.
Of course, to be fair, this bat bias might be a result of bats simply getting more attention, science-wise, than most other species. Still, it's remarkable at least how often they come up as host species in the coronavirus family, in particular.
The Four Houses of Coronavirus: Meet the Family
Speaking of which, there are four major genera (kinds) of coronavirus: Alphacoronavirus, Betacoronavirus, Gammacoronavirus, and Deltacoronavirus (notice a pattern here?). The distinction is mostly one of family resemblance and origin: the Alpha- and Beta- genera are closely related and likely originated from a bat-infecting common ancestor, whereas the Gamma- and Delta- genera are more likely to have originated from an ancestral strain that terrorized pigs or birds in the past.
Our SARS-CoV-2 virus belongs in the Betacoronavirus genus, along with some darkly familiar cousins that you might be familiar with, considering two of them were severe enough to be responsible for two notable 21st-century epidemics.
BETACORONAVIRUS
The Distant Cousins of SARS-CoV-2
Within the Betacoronavirus genus, we find further subgroups. One of these has a member, interestingly enough, called by the more straightforward name of Human coronavirus HKU1 (HCoV-HKU1). It was a nasty enough coronavirus strain that resembled the common cold but could, in a few cases, lead to more severe illnesses like bronchiolitis (inflammation of the bronchioles) and the ever-dreaded pneumonia.
As a side note: inflammation is not just caused by the disease-carrying agent, be it a virus, a bacterium, or anything bigger. It's also a result of the body's natural immune response to the same. The body swarms the site with everything from white blood cells (leukocytes), which are basically the armed response unit cordoning off the area, to phagocytes, which are basically the cleanup crew who "eat" and destroy affected matter, all the way to various cell-derived mediators, which are basically the people in the midst of the crisis pointing out the worst fires.
That Human coronavirus HKU1 was first noticed in Hong Kong back in 2005, though that's not considered the same as where it originated. The original carrier was probably a species of mouse, based on its genetic similarity to the Murine coronavirus (MCoV).
Another "human coronavirus", Human coronavirus OC43 (HCoV-OC43), is more readily associated with Bovine coronavirus (BCoV), which infects cattle, as well as with various equine and porcine coronaviruses.
The odds are you haven't heard much about any of these relatives. Understandable enough: in the grand scheme of things, they're certainly not as dangerous as SARS-CoV-2, though you wouldn't necessarily want to catch them.
All these Betacoronavirus strains so far mentioned are members of the Embecovirus subspecies, and more closely related to each other than to the SARS-CoV-2 strain.
Betacoronavirus has a few more subspecies like that, two of which have far more familiar members to us humans.
One, the Merbecovirus subspecies, contains the MERS-CoV virus, responsible for an outbreak of MERS (Middle-Eastern Respiratory Syndrome) especially during 2012-2015 (the outbreak is still technically ongoing, as of 2019). Thankfully (thankful in relative terms), and despite cases appearing across the Northern Hemisphere and Africa, this failed to become a pandemic, with most of the victims concentrated on the Middle East (hence the name). And as if determined to be as stereotypical of the Middle East as possible, it's a disease transmissible via camels too.
The subspecies of greatest interest to us is the Serbecovirus subspecies, because that contains all the SARS-related coronaviruses, including the one responsible for the pandemic. In fact, it's more commonly known as that, and since it's a more indicative name, I'll use the latter name instead of the former for the next section.
SEVERE ACUTE RESPIRATORY SYNDROME-RELATED CORONAVIRUSES
The Brothers and Sisters of SARS-CoV-2
SARS-CoV-2 belongs to a notorious bunch called the severe acute respiratory syndrome-related coronaviruses, or SARSr-CoV for short. What unites them (apart from being related, of course) is their method of infiltration: their peplomers are specifically designed to attach to the ACE2 carrier protein in a lung cell.
ACE2 stands for angiotensin-converting enzyme 2. (Enzymes are proteins which serve as catalysts; they help in speeding up chemical reactions without actually being affected by them).
In case you're wondering why it's got a "2" on it and what the first one was, the original ACE is a separate protein which has a similar function. Their name comes from one of their most important functions: they convert a hormone called angiotensin into its various forms in order to control blood pressure in capillaries, for instance in the alveolar sacs of the lungs. ACE2 counters the activity of the original ACE, thus helping to maintain a balanced blood pressure (this is an example of homeostasis, one of the things viruses can't do).
Since this involves a transfer of molecules through the cell membrane, this is exactly the kind of thing that a virus would exploit. So naturally, SARSr-CoV viruses aren't the only ones who can do this. Yet another "human coronavirus", Human coronavirus NL63 (HCoV-NL63), uses the same ACE2 point of entry, though it's not closely related to the SARSr-CoV viruses; it's a member of the neighbouring Alphacoronavirus genus we met further back. It's just a distant cousin that developed the same good trick independently.
When a SARSr-CoV virus breaks in, however, the "Severe Acute Respiratory Syndrome" coronavirus certainly lives up to its name.
SARS-CoV: The First-Born
The original SARS-CoV was the one responsible for the 2002-2004 SARS outbreak (technically two distinct outbreaks within a 2-year timeframe, but that's nitpicking).
Like the current strain, bats are suspected to have been the original carriers (with, oddly, civets as an intermediary host in that case, as opposed to pangolins in the case of SARS-CoV-2). It also spread using the same medium: water droplets from people's noses and mouths carrying through the air, and indirectly by contact between a surface and unwashed hands.
Furthermore, the symptoms for the two diseases overlap (fever, persistent coughing, difficulty breathing). On top of that, the virus, in addition, tended to be more dangerous for older people, and resulted in severe damage to the lungs (for instance, by causing pneumonia).
It was even dealt with in a similar fashion, by isolating suspected carriers and erecting limitations on where and when people could travel, though obviously not to the same drastic degree as our SARS-CoV-2 pandemic.
SARS-CoV: The Death Count
All the same, the fatality rate of SARS-CoV was shockingly high, as high as 1 in 10 infectees.
Compared with the current pandemic, the result was not globally serious: over 8,000 infectees were reported, and of those, 774 died. The vast majority of those deaths occurred in China and Hong Kong. But if the current SARS-CoV-2 virus had the same fatal-versus-non-fatal ratio (and thus was just as deadly as its predecessor), then the current death count would be at least twice as severe. (Worryingly, we still don't have a stable idea of what the ratio of fatal-versus-non-fatal cases is for SARS-CoV-2, and likely won't have a consistent figure for a while yet).
Still, 774 deaths from the original SARS, most of them in two countries, seems downright merciful now. To put that into perspective, the global death count for COVID-19 surpassed that total on February 9th this year, back when COVID-19 fatalities were still largely confined to China.
The original SARS outbreak originated in China too, specifically the Guangdong Province near Hong Kong. In less than two years, it was over. No new cases have been reported since.
Rather worryingly, no anti-viral drug was ever successfully developed for the original SARS virus, and no vaccine has yet been researched for it either. It simply came and went of its own accord.
SARS-CoV-2
There's plenty to worry about, regarding the current pandemic of COVID-19. Or Coronavirus Disease 2019, in its full form: the viruses and their resultant diseases traditionally get different names, and while it's usually obvious what you mean if you use them interchangeably, it isn't technically right, akin to talking about a crime and a criminal as if they were the same thing.
Most obviously, a pandemic of this scale and speed is rare. Just sticking to this century alone, we find the Swine Flu outbreak of 2009-2010 and, technically since it's still ongoing, the HIV/AIDS pandemic.
There have, of course, been lots of serious and lethal diseases throughout history (not even ancient history: many of these diseases were monstrous problems during the 20th and 21st centuries) that make COVID-19 look like a young upstart: tuberculosis, malaria, measles, smallpox prior to its eradication, cholera, and various forms of influenza such as swine flu.
What makes COVID-19 so dangerous, apart from the fact that it's happening everywhere right now, is how much of it remains unknown, even compared with the original SARS outbreak. No one knows how far it'll go, how many people in total have been infected (keep in mind the official tallies, for various reasons, are all-but-guaranteed to be underestimates), who'll recover versus who'll suffer and who'll perish if they get it, and how persistent and ineradicable it'll prove.
Unlike many of those historical diseases, which are often confined to developing countries by now, this thing has hit rich nations good and hard, and is still hitting them good and hard, and getting better and harder at it. We have no idea if this might prove to be a short-term blip that vanishes as quickly as it arrived (not considered likely), or will become one of the worst diseases in human history. We don't even know what the total economic fallout will look like.
If the original SARS-CoV virus had gotten over its own self-limiting problems and figured out how to spread effectively, so that it could infect virtually every corner of the globe, then it would probably have looked something like this.
A Ray of Hope?
Let's not be too gloomy, however. On the other hand, the original SARS wasn't getting nearly as much attention as the current pandemic, and since the original SARS largely cleared itself up on its own anyway (possibly because having such a high fatality rate tended to work against it as an infectious disease), it was considerably less urgent, only qualifying as a two-year epidemic with few global repercussions (hence not as much incentive to prioritize research on it).
Plus, we know a lot more about viruses and disease today, in 2020, than we did back then, during 2002-2004. In fact, our collectively knowing so much about this SARS-CoV-2 virus, its relatives, and viruses in general, has helped me to compile so much information about it for this very blog post, and in a remarkably short amount of time! All the information here is accessible through the public domain, mostly via Wikipedia but also using the World Health Organization and the NHS websites.
Still, viruses are tricky customers, and this is the trickiest yet. All we can do at present is wait, hope, and in the meantime do what we can to make the virus harder to catch.
I hope this has been, if not necessarily useful, at least educational and entertaining for a few passing readers. For now, Impossible Numbers out.
Well, it was extremely educational to me! Thanks for putting this together; it filled in a lot of whats and hows that I didn't even know I didn't know.
Another thing that wasn't the same during the SARS-CoV outbreak was the level of globalization. As stated, the infections were largely confined to just mainland China and Hong Kong; the level of international travel and even travel within the country wasn't high enough to really give the virus a boost.
The much higher level of international travel for business and tourism is what really gave SARS-CoV-2 the kick it needed to go global. I've been telling people that this is the end of the world, but not in the sense that we're all going to die and civilization will collapse. But the world we've gotten used to is over; from here forward, we're going to have to do things differently than we were, and that's not that bad.
5229831
Music to my ears indeed. Although I have to admit a lot of this is more of academic than practical interest: it won't protect you against the virus, but at least you'll have an excruciatingly detailed idea of what the virus will do to you if you get it!
5229840
Yeah, I dread to think... To be honest, it feels like it's radically changing the world right now. I myself went from an ignorant "never heard of it" to a mildly annoyed "silly people are going on about it" to a nervous "aren't we overreacting a bit?" to a total realization shock of "oh my god what the hell is this thing!?" in the span of less than two weeks. I still feel like I'm struggling to process just how big a deal this is.
Phew, this is a lot of hard science you dropped here and I have to admit that I didn't read it all..... In my thoughts, I am more busy with what comes after the apocalypse.
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That sounds a lot like humanity, to me. It isn't hard to see parallels.
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Um-hm, although the virus in "Resident Evil" was artificially created and designed to befall many different creatures and to cause heavy mutations that essentially created entirely new lifeforms that you probably haven't even seen in your worst nightmares before.
The new coronavirus is lab-created, too, despite the infos they try to feed us with. But it looks like it isn't nearly as exciting as the T- or G-Virus, pity.
I am surprised you write so much about the virus and that you are so interested in it. Although, I would have expected to see an essay on the importance of authors in a post-apocalyptic world. Hope that comes next.
5230002
Sorry if it was a bit tricky to read, though if it helps, I did at one point consider chopping it up into different blog posts and posting each one as a more manageable chunk. So it's probably better thought of as something to nibble at and come back to later, like a fridge snack.
Plus, I wasn't sure how technical to get, at times. I can get a bit carried away!
Still, I like to think of it as a different, subtler way of dealing with the current crisis. Know thy enemy, familiarize oneself with the strange and new, and all that.
To be fair, RE can get away with that sort of thing, being fictional; artistic license has been excusing good stories for centuries. Trying to make a multi-species virus in real life, though, would be incredibly difficult, considering how hard it really is to penetrate even one body's natural defences. Almost as hard as developing a virus that made your muscles swell to monstrous size and sprout fully functional eyes at random, all in a matter of seconds.
Interesting. I haven't yet come across a source that says as much. Do you have a lead I could follow?
Frankly, I'm thankful. One of the few good points about the current coronavirus is that it's very easy to sit back and say, "Well, at least it's not the T-virus."
When your entire daily work schedule is turned upside-down overnight, naturally you'd be a bit curious about the agent responsible, surely? Besides, I'm a great fan of science. It's a reliable source of education and entertainment for me personally (I'm not unconvinced that this might all turn out to be some kind of "knowledge therapy" I'm putting myself through). All I know is that I'm suddenly incredibly fascinated by it.
Alas, well beyond my talents and know-how. I couldn't begin to explain the importance of authors in a normal world, much less in a world all still new to me. I daresay someone might consider it. How the creative arts will respond to the crisis in the coming months: now, that would be a topic worthy of discussion.
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As far as I know, the only evidence we have that it was lab-created is a scientist or doctor in China asserting that someone was "involved with the evolution" of the virus, which is not really a smoking gun. It's possible additional evidence has surfaced since then and I just haven't seen it.
However, there is a level 4 biolab in Wuhan, less than a mile from the market where the virus is speculated to have originated, so the possibility that it was lab-engineered or even just escaped due to a security breach are not wholly improbable (especially after concern was previously expressed over the safety of this lab). They also don't matter right now. All that matters right now is getting the spread contained, and outside of a lab, the virus will mutate unpredictably; even if there is a lab with the exact sequencing of the original virus, it'll be next to worthless by now.
Very thorough and well-researched! SciShow recently released a video about why bats harbor so many dangerous diseases and yet seem to be unaffected by most of them. Like most facets of virology, it's a complex and fascinating topic.
Not looking to start a fight, but as far as research published in technical journals is concerned, the latest consensus I've seen is that a lab-based origin of SARS-CoV-2 is unlikely (here is a press release about that study).
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Thanks for the comment! And thanks for the video link, of course. I was wondering about those super-immune bats myself...
Too true. Honestly, I feel like we could insert a lot of -ologies and -ographies and -onomies in there, and the statement would still stand. The world can be such a mind-bogglingly complex place. But that's what makes learning so fun!
EDIT, 31/03/2020:
Should point out that I've since added all seven groups of the Baltimore Classification to the original post. This comment here is in case anyone saw the original post, when it wasn't up yet.
More significantly, I've corrected an error in the original post. It originally said:
The bold section was incorrect - at that point, the W.H.O. were counting China's deaths separately and I only noticed the table with the death count for countries outside of China at the time. Once you count up both China's deaths and everyone else's, the actual total for March 10th is far, far greater than I originally stated.
The death count of 774 was actually surpassed much earlier, during February 9th this year. I've since corrected the original post. It now reads:
My mistake!