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Government Response To The Coronavirus (15 Viewers)
- Thread starter James Daulton
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Rich Conway
Footballguy
If you don't think I've earned a track record of fair, well-reasoned arguments (along with occasional, in the moment, possibly over-the-top snark) over the course of 20+ years here, that's fine. Personally, I do think you've earned that track record. It's why I engage with you and not with plenty of others.
As for Kung Flu and China virus, yes, that was problematic for a variety of reasons.
Let's also not pretend that when floated his lab theory, he was floating it in the deliberate bioweapon sense, rather than legit research (which the US helped fund) and accidental leak perhaps caused by poor safety protocols. That was what I objected to.
Ramblin Wreck
Footballguy
You need to force others to inject something into their body to think clearly? Feel sorry for you.
The Commish
Footballguy
The Z Machine
Footballguy
Not forcing anyone to do anything. But when we speak of thinking clearly, perhaps we should consider those that reject a vaccine with an excellent record of clinical data.
What we do know is that Dr. Shi (the bat lady at WIV) collaborated with US coronavirus researcher Ralph S Baric, and in November 2015 they created a novel virus by taking the backbone of the SARS1 virus and replacing its spike protein with one from a bat virus (known as SHC014-CoV). Shi then set out to create novel coronaviruses with the highest possible infectivity for human cells. That much is known.
Unfortunately we don't know if Shi did or did not generate SARS2 in her lab because her records have been sealed, but as wade's article says, "it seems she was certainly on the right track to have done so."
The Z Machine
Footballguy
Doug B
Footballguy
Why did you read "force others" into Z's comment? Is it all that different if it's spelled out explicitly as "... when conservatives start getting willfully vaccinated at levels that support herd immunity ..."?
See my prior response a few posts up. While we don't know if it was THE SARS2 virus, we do know that they were doing work on coronaviruses modified with the spike protein that is the signature of SARS2. All of that is in Wade's article, clearly spelled out - https://nicholaswade.medium.com/origin-of-covid-following-the-clues-6f03564c038
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quick-hands
Footballguy
I dont think you understand that excellent clinical data isnt recognized with about 7 or 8 months of clinical data. Id go with promising.
The Z Machine
Footballguy
So the rapid decreases in death due to COVID in Israel, UK, and USA are due to?
And the extremely low rates of serious side effects from the vaccines are just an anomaly? Or we just haven't seen the bad results yet, even from those in Phase 1 and Phase 2 trials that have had the vaccine for over a year.
Here is the genetic evidence portion of the Wade Article that strongly indicates that SARS2 was created (yes, I am using that word because it is the most accurate) in the lab.
Comparing the Rival Scenarios of SARS2 Origin
The evidence above adds up to a serious case that the SARS2 virus could have been created in a lab, from which it then escaped. But the case, however substantial, falls short of proof. Proof would consist of evidence from the Wuhan Institute of Virology, or related labs in Wuhan, that SARS2 or a predecessor virus was under development there. For lack of access to such records, another approach is to take certain salient facts about the SARS2 virus and ask how well each is explained by the two rival scenarios of origin, those of natural emergence and lab escape. Here are four tests of the two hypotheses. A couple have some technical detail, but these are among the most persuasive for those who may care to follow the argument.
1) The place of origin.
Start with geography. The two closest known relatives of the SARS2 virus were collected from bats living in caves in Yunnan, a province of southern China. If the SARS2 virus had first infected people living around the Yunnan caves, that would strongly support the idea that the virus had spilled over to people naturally. But this isn’t what happened. The pandemic broke out 1,500 kilometers away, in Wuhan.
Beta-coronaviruses, the family of bat viruses to which SARS2 belongs, infect the horseshoe bat Rhinolophus affinis, which ranges across southern China. The bats’ range is 50 kilometers, so it’s unlikely that any made it to Wuhan. In any case, the first cases of the Covid-19 pandemic probably occurred in September, when temperatures in Hubei province are already cold enough to send bats into hibernation.
What if the bat viruses infected some intermediate host first? You would need a longstanding population of bats in frequent proximity with an intermediate host, which in turn must often cross paths with people. All these exchanges of virus must take place somewhere outside Wuhan, a busy metropolis which so far as is known is not a natural habitat of Rhinolophusbat colonies. The infected person (or animal) carrying this highly transmissible virus must have traveled to Wuhan without infecting anyone else. No one in his or her family got sick. If the person jumped on a train to Wuhan, no fellow passengers fell ill.
It’s a stretch, in other words, to get the pandemic to break out naturally outside Wuhan and then, without leaving any trace, to make its first appearance there.
For the lab escape scenario, a Wuhan origin for the virus is a no-brainer. Wuhan is home to China’s leading center of coronavirus research where, as noted above, researchers were genetically engineering bat coronaviruses to attack human cells. They were doing so under the minimal safety conditions of a BSL2 lab. If a virus with the unexpected infectiousness of SARS2 had been generated there, its escape would be no surprise.
2) Natural history and evolution
The initial location of the pandemic is a small part of a larger problem, that of its natural history. Viruses don’t just make one time jumps from one species to another. The coronavirus spike protein, adapted to attack bat cells, needs repeated jumps to another species, most of which fail, before it gains a lucky mutation. Mutation — a change in one of its RNA units — causes a different amino acid unit to be incorporated into its spike protein and makes the spike protein better able to attack the cells of some other species.
Through several more such mutation-driven adjustments, the virus adapts to its new host, say some animal with which bats are in frequent contact. The whole process then resumes as the virus moves from this intermediate host to people.
In the case of SARS1, researchers have documented the successive changes in its spike protein as the virus evolved step by step into a dangerous pathogen. After it had gotten from bats into civets, there were six further changes in its spike protein before it became a mild pathogen in people. After a further 14 changes, the virus was much better adapted to humans, and with a further 4 the epidemic took off.
But when you look for the fingerprints of a similar transition in SARS2, a strange surprise awaits. The virus has changed hardly at all, at least until recently. From its very first appearance, it was well adapted to human cells. Researchers led by Alina Chan of the Broad Institute compared SARS2 with late stage SARS1, which by then was well adapted to human cells, and found that the two viruses were similarly well adapted. “By the time SARS-CoV-2 was first detected in late 2019, it was already pre-adapted to human transmission to an extent similar to late epidemic SARS-CoV,” they wrote.
Even those who think lab origin unlikely agree that SARS2 genomes are remarkably uniform. Dr. Baric writes that “early strains identified in Wuhan, China, showed limited genetic diversity, which suggests that the virus may have been introduced from a single source.”
A single source would of course be compatible with lab escape, less so with the massive variation and selection which is evolution’s hallmark way of doing business.
The uniform structure of SARS2 genomes gives no hint of any passage through an intermediate animal host, and no such host has been identified in nature.
Proponents of natural emergence suggest that SARS2 incubated in a yet-to-be found human population before gaining its special properties. Or that it jumped to a host animal outside China.
All these conjectures are possible, but strained. Proponents of lab leak have a simpler explanation. SARS2 was adapted to human cells from the start because it was grown in humanized mice or in lab cultures of human cells, just as described in Dr. Daszak’s grant proposal. Its genome shows little diversity because the hallmark of lab cultures is uniformity.
Proponents of laboratory escape joke that of course the SARS2 virus infected an intermediary host species before spreading to people, and that they have identified it — a humanized mouse from the Wuhan Institute of Virology.
3) The furin cleavage site.
The furin cleavage site is a minute part of the virus’s anatomy but one that exerts great influence on its infectivity. It sits in the middle of the SARS2 spike protein. It also lies at the heart of the puzzle of where the virus came from.
The spike protein has two sub-units with different roles. The first, called S1, recognizes the virus’s target, a protein called angiotensin converting enzyme-2 (or ACE2) which studs the surface of cells lining the human airways. The second, S2, helps the virus, once anchored to the cell, to fuse with the cell’s membrane. After the virus’s outer membrane has coalesced with that of the stricken cell, the viral genome is injected into the cell, hijacks its protein-making machinery and forces it to generate new viruses.
But this invasion cannot begin until the S1 and S2 subunits have been cut apart. And there, right at the S1/S2 junction, is the furin cleavage site that ensures the spike protein will be cleaved in exactly the right place.
The virus, a model of economic design, does not carry its own cleaver. It relies on the cell to do the cleaving for it. Human cells have a protein cutting tool on their surface known as furin. Furin will cut any protein chain that carries its signature target cutting site. This is the sequence of amino acid units proline-arginine-arginine-alanine, or PRRA in the code that refers to each amino acid by a letter of the alphabet. PRRA is the amino acid sequence at the core of SARS2’s furin cleavage site.
Viruses have all kinds of clever tricks, so why does the furin cleavage site stand out? Because of all known SARS-related beta-coronaviruses, only SARS2 possesses a furin cleavage site. All the other viruses have their S2 unit cleaved at a different site and by a different mechanism.
How then did SARS2 acquire its furin cleavage site? Either the site evolved naturally, or it was inserted by researchers at the S1/S2 junction in a gain-of-function experiment.
Consider natural origin first. Two ways viruses evolve are by mutation and by recombination. Mutation is the process of random change in DNA (or RNA for coronaviruses) that usually results in one amino acid in a protein chain being switched for another. Many of these changes harm the virus but natural selection retains the few that do something useful. Mutation is the process by which the SARS1 spike protein gradually switched its preferred target cells from those of bats to civets, and then to humans.
Mutation seems a less likely way for SARS2’s furin cleavage site to be generated, even though it can’t completely be ruled out. The site’s four amino acid units are all together, and all at just the right place in the S1/S2 junction. Mutation is a random process triggered by copying errors (when new viral genomes are being generated) or by chemical decay of genomic units. So it typically affects single amino acids at different spots in a protein chain. A string of amino acids like that of the furin cleavage site is much more likely to be acquired all together through a quite different process known as recombination.
Recombination is an inadvertent swapping of genomic material that occurs when two viruses happen to invade the same cell, and their progeny are assembled with bits and pieces of RNA belonging to the other. Beta-coronaviruses will only combine with other beta-coronaviruses but can acquire, by recombination, almost any genetic element present in the collective genomic pool. What they cannot acquire is an element the pool does not possess. And no known SARS-related beta-coronavirus, the class to which SARS2 belongs, possesses a furin cleavage site.
Proponents of natural emergence say SARS2 could have picked up the site from some as yet unknown beta-coronavirus. But bat SARS-related beta-coronaviruses evidently don’t need a furin cleavage site to infect bat cells, so there’s no great likelihood that any in fact possesses one, and indeed none has been found so far.
The proponents’ next argument is that SARS2 acquired its furin cleavage site from people. A predecessor of SARS2 could have been circulating in the human population for months or years until at some point it acquired a furin cleavage site from human cells. It would then have been ready to break out as a pandemic.
If this is what happened, there should be traces in hospital surveillance records of the people infected by the slowly evolving virus. But none has so far come to light. According to the WHO report on the origins of the virus, the sentinel hospitals in Hubei province, home of Wuhan, routinely monitor influenza-like illnesses and “no evidence to suggest substantial SARSCoV-2 transmission in the months preceding the outbreak in December was observed.”
So it’s hard to explain how the SARS2 virus picked up its furin cleavage site naturally, whether by mutation or recombination.
That leaves a gain-of-function experiment. For those who think SARS2 may have escaped from a lab, explaining the furin cleavage site is no problem at all. “Since 1992 the virology community has known that the one sure way to make a virus deadlier is to give it a furin cleavage site at the S1/S2 junction in the laboratory,” writes Dr. Steven Quay, a biotech entrepreneur interested in the origins of SARS2. “At least eleven gain-of-function experiments, adding a furin site to make a virus more infective, are published in the open literature, including [by] Dr. Zhengli Shi, head of coronavirus research at the Wuhan Institute of Virology.”
4) A Question of Codons
There’s another aspect of the furin cleavage site that narrows the path for a natural emergence origin even further.
As everyone knows (or may at least recall from high school), the genetic code uses three units of DNA to specify each amino acid unit of a protein chain. When read in groups of 3, the 4 different kinds of DNA unit can specify 4 x 4 x 4 or 64 different triplets, or codons as they are called. Since there are only 20 kinds of amino acid, there are more than enough codons to go around, allowing some amino acids to be specified by more than one codon. The amino acid arginine, for instance, can be designated by any of the six codons CGU, CGC, CGA, CGG, AGA or AGG, where A, U, G and C stand for the four different kinds of unit in RNA.
Here’s where it gets interesting. Different organisms have different codon preferences. Human cells like to designate arginine with the codons CGT, CGC or CGG. But CGG is coronavirus’s least popular codon for arginine. Keep that in mind when looking at how the amino acids in the furin cleavage site are encoded in the SARS2 genome.
Now the functional reason why SARS2 has a furin cleavage site, and its cousin viruses don’t, can be seen by lining up (in a computer) the string of nearly 30,000 nucleotides in its genome with those of its cousin coronaviruses, of which the closest so far known is one called RaTG13. Compared with RaTG13, SARS2 has a 12-nucleotide insert right at the S1/S2 junction. The insert is the sequence T-CCT-CGG-CGG-GC. The CCT codes for proline, the two CGG’s for two arginines, and the GC is the beginning of a GCA codon that codes for alanine.
There are several curious features about this insert but the oddest is that of the two side-by-side CGG codons. Only 5% of SARS2’s arginine codons are CGG, and the double codon CGG-CGG has not been found in any other beta-coronavirus. So how did SARS2 acquire a pair of arginine codons that are favored by human cells but not by coronaviruses?
Proponents of natural emergence have an up-hill task to explain all the features of SARS2’s furin cleavage site. They have to postulate a recombination event at a site on the virus’s genome where recombinations are rare, and the insertion of a 12-nucleotide sequence with a double arginine codon unknown in the beta-coronavirus repertoire, at the only site in the genome that would significantly expand the virus’s infectivity.
“Yes, but your wording makes this sound unlikely — viruses are specialists at unusual events,” is the riposte of David L. Robertson, a virologist at the University of Glasgow who regards lab escape as a conspiracy theory. “Recombination is naturally very, very frequent in these viruses, there are recombination breakpoints in the spike protein and these codons appear unusual exactly because we’ve not sampled enough.”
Dr. Robertson is correct that evolution is always producing results that may seem unlikely but in fact are not. Viruses can generate untold numbers of variants but we see only the one-in-a-billion that natural selection picks for survival. But this argument could be pushed too far. For instance any result of a gain-of-function experiment could be explained as one that evolution would have arrived at in time. And the numbers game can be played the other way. For the furin cleavage site to arise naturally in SARS2, a chain of events has to happen, each of which is quite unlikely for the reasons given above. A long chain with several improbable steps is unlikely to ever be completed.
For the lab escape scenario, the double CGG codon is no surprise. The human-preferred codon is routinely used in labs. So anyone who wanted to insert a furin cleavage site into the virus’s genome would synthesize the PRRA-making sequence in the lab and would be likely to use CGG codons to do so.
“When I first saw the furin cleavage site in the viral sequence, with its arginine codons, I said to my wife it was the smoking gun for the origin of the virus,” said David Baltimore, an eminent virologist and former president of CalTech. “These features make a powerful challenge to the idea of a natural origin for SARS2,” he said.
Comparing the Rival Scenarios of SARS2 Origin
The evidence above adds up to a serious case that the SARS2 virus could have been created in a lab, from which it then escaped. But the case, however substantial, falls short of proof. Proof would consist of evidence from the Wuhan Institute of Virology, or related labs in Wuhan, that SARS2 or a predecessor virus was under development there. For lack of access to such records, another approach is to take certain salient facts about the SARS2 virus and ask how well each is explained by the two rival scenarios of origin, those of natural emergence and lab escape. Here are four tests of the two hypotheses. A couple have some technical detail, but these are among the most persuasive for those who may care to follow the argument.
1) The place of origin.
Start with geography. The two closest known relatives of the SARS2 virus were collected from bats living in caves in Yunnan, a province of southern China. If the SARS2 virus had first infected people living around the Yunnan caves, that would strongly support the idea that the virus had spilled over to people naturally. But this isn’t what happened. The pandemic broke out 1,500 kilometers away, in Wuhan.
Beta-coronaviruses, the family of bat viruses to which SARS2 belongs, infect the horseshoe bat Rhinolophus affinis, which ranges across southern China. The bats’ range is 50 kilometers, so it’s unlikely that any made it to Wuhan. In any case, the first cases of the Covid-19 pandemic probably occurred in September, when temperatures in Hubei province are already cold enough to send bats into hibernation.
What if the bat viruses infected some intermediate host first? You would need a longstanding population of bats in frequent proximity with an intermediate host, which in turn must often cross paths with people. All these exchanges of virus must take place somewhere outside Wuhan, a busy metropolis which so far as is known is not a natural habitat of Rhinolophusbat colonies. The infected person (or animal) carrying this highly transmissible virus must have traveled to Wuhan without infecting anyone else. No one in his or her family got sick. If the person jumped on a train to Wuhan, no fellow passengers fell ill.
It’s a stretch, in other words, to get the pandemic to break out naturally outside Wuhan and then, without leaving any trace, to make its first appearance there.
For the lab escape scenario, a Wuhan origin for the virus is a no-brainer. Wuhan is home to China’s leading center of coronavirus research where, as noted above, researchers were genetically engineering bat coronaviruses to attack human cells. They were doing so under the minimal safety conditions of a BSL2 lab. If a virus with the unexpected infectiousness of SARS2 had been generated there, its escape would be no surprise.
2) Natural history and evolution
The initial location of the pandemic is a small part of a larger problem, that of its natural history. Viruses don’t just make one time jumps from one species to another. The coronavirus spike protein, adapted to attack bat cells, needs repeated jumps to another species, most of which fail, before it gains a lucky mutation. Mutation — a change in one of its RNA units — causes a different amino acid unit to be incorporated into its spike protein and makes the spike protein better able to attack the cells of some other species.
Through several more such mutation-driven adjustments, the virus adapts to its new host, say some animal with which bats are in frequent contact. The whole process then resumes as the virus moves from this intermediate host to people.
In the case of SARS1, researchers have documented the successive changes in its spike protein as the virus evolved step by step into a dangerous pathogen. After it had gotten from bats into civets, there were six further changes in its spike protein before it became a mild pathogen in people. After a further 14 changes, the virus was much better adapted to humans, and with a further 4 the epidemic took off.
But when you look for the fingerprints of a similar transition in SARS2, a strange surprise awaits. The virus has changed hardly at all, at least until recently. From its very first appearance, it was well adapted to human cells. Researchers led by Alina Chan of the Broad Institute compared SARS2 with late stage SARS1, which by then was well adapted to human cells, and found that the two viruses were similarly well adapted. “By the time SARS-CoV-2 was first detected in late 2019, it was already pre-adapted to human transmission to an extent similar to late epidemic SARS-CoV,” they wrote.
Even those who think lab origin unlikely agree that SARS2 genomes are remarkably uniform. Dr. Baric writes that “early strains identified in Wuhan, China, showed limited genetic diversity, which suggests that the virus may have been introduced from a single source.”
A single source would of course be compatible with lab escape, less so with the massive variation and selection which is evolution’s hallmark way of doing business.
The uniform structure of SARS2 genomes gives no hint of any passage through an intermediate animal host, and no such host has been identified in nature.
Proponents of natural emergence suggest that SARS2 incubated in a yet-to-be found human population before gaining its special properties. Or that it jumped to a host animal outside China.
All these conjectures are possible, but strained. Proponents of lab leak have a simpler explanation. SARS2 was adapted to human cells from the start because it was grown in humanized mice or in lab cultures of human cells, just as described in Dr. Daszak’s grant proposal. Its genome shows little diversity because the hallmark of lab cultures is uniformity.
Proponents of laboratory escape joke that of course the SARS2 virus infected an intermediary host species before spreading to people, and that they have identified it — a humanized mouse from the Wuhan Institute of Virology.
3) The furin cleavage site.
The furin cleavage site is a minute part of the virus’s anatomy but one that exerts great influence on its infectivity. It sits in the middle of the SARS2 spike protein. It also lies at the heart of the puzzle of where the virus came from.
The spike protein has two sub-units with different roles. The first, called S1, recognizes the virus’s target, a protein called angiotensin converting enzyme-2 (or ACE2) which studs the surface of cells lining the human airways. The second, S2, helps the virus, once anchored to the cell, to fuse with the cell’s membrane. After the virus’s outer membrane has coalesced with that of the stricken cell, the viral genome is injected into the cell, hijacks its protein-making machinery and forces it to generate new viruses.
But this invasion cannot begin until the S1 and S2 subunits have been cut apart. And there, right at the S1/S2 junction, is the furin cleavage site that ensures the spike protein will be cleaved in exactly the right place.
The virus, a model of economic design, does not carry its own cleaver. It relies on the cell to do the cleaving for it. Human cells have a protein cutting tool on their surface known as furin. Furin will cut any protein chain that carries its signature target cutting site. This is the sequence of amino acid units proline-arginine-arginine-alanine, or PRRA in the code that refers to each amino acid by a letter of the alphabet. PRRA is the amino acid sequence at the core of SARS2’s furin cleavage site.
Viruses have all kinds of clever tricks, so why does the furin cleavage site stand out? Because of all known SARS-related beta-coronaviruses, only SARS2 possesses a furin cleavage site. All the other viruses have their S2 unit cleaved at a different site and by a different mechanism.
How then did SARS2 acquire its furin cleavage site? Either the site evolved naturally, or it was inserted by researchers at the S1/S2 junction in a gain-of-function experiment.
Consider natural origin first. Two ways viruses evolve are by mutation and by recombination. Mutation is the process of random change in DNA (or RNA for coronaviruses) that usually results in one amino acid in a protein chain being switched for another. Many of these changes harm the virus but natural selection retains the few that do something useful. Mutation is the process by which the SARS1 spike protein gradually switched its preferred target cells from those of bats to civets, and then to humans.
Mutation seems a less likely way for SARS2’s furin cleavage site to be generated, even though it can’t completely be ruled out. The site’s four amino acid units are all together, and all at just the right place in the S1/S2 junction. Mutation is a random process triggered by copying errors (when new viral genomes are being generated) or by chemical decay of genomic units. So it typically affects single amino acids at different spots in a protein chain. A string of amino acids like that of the furin cleavage site is much more likely to be acquired all together through a quite different process known as recombination.
Recombination is an inadvertent swapping of genomic material that occurs when two viruses happen to invade the same cell, and their progeny are assembled with bits and pieces of RNA belonging to the other. Beta-coronaviruses will only combine with other beta-coronaviruses but can acquire, by recombination, almost any genetic element present in the collective genomic pool. What they cannot acquire is an element the pool does not possess. And no known SARS-related beta-coronavirus, the class to which SARS2 belongs, possesses a furin cleavage site.
Proponents of natural emergence say SARS2 could have picked up the site from some as yet unknown beta-coronavirus. But bat SARS-related beta-coronaviruses evidently don’t need a furin cleavage site to infect bat cells, so there’s no great likelihood that any in fact possesses one, and indeed none has been found so far.
The proponents’ next argument is that SARS2 acquired its furin cleavage site from people. A predecessor of SARS2 could have been circulating in the human population for months or years until at some point it acquired a furin cleavage site from human cells. It would then have been ready to break out as a pandemic.
If this is what happened, there should be traces in hospital surveillance records of the people infected by the slowly evolving virus. But none has so far come to light. According to the WHO report on the origins of the virus, the sentinel hospitals in Hubei province, home of Wuhan, routinely monitor influenza-like illnesses and “no evidence to suggest substantial SARSCoV-2 transmission in the months preceding the outbreak in December was observed.”
So it’s hard to explain how the SARS2 virus picked up its furin cleavage site naturally, whether by mutation or recombination.
That leaves a gain-of-function experiment. For those who think SARS2 may have escaped from a lab, explaining the furin cleavage site is no problem at all. “Since 1992 the virology community has known that the one sure way to make a virus deadlier is to give it a furin cleavage site at the S1/S2 junction in the laboratory,” writes Dr. Steven Quay, a biotech entrepreneur interested in the origins of SARS2. “At least eleven gain-of-function experiments, adding a furin site to make a virus more infective, are published in the open literature, including [by] Dr. Zhengli Shi, head of coronavirus research at the Wuhan Institute of Virology.”
4) A Question of Codons
There’s another aspect of the furin cleavage site that narrows the path for a natural emergence origin even further.
As everyone knows (or may at least recall from high school), the genetic code uses three units of DNA to specify each amino acid unit of a protein chain. When read in groups of 3, the 4 different kinds of DNA unit can specify 4 x 4 x 4 or 64 different triplets, or codons as they are called. Since there are only 20 kinds of amino acid, there are more than enough codons to go around, allowing some amino acids to be specified by more than one codon. The amino acid arginine, for instance, can be designated by any of the six codons CGU, CGC, CGA, CGG, AGA or AGG, where A, U, G and C stand for the four different kinds of unit in RNA.
Here’s where it gets interesting. Different organisms have different codon preferences. Human cells like to designate arginine with the codons CGT, CGC or CGG. But CGG is coronavirus’s least popular codon for arginine. Keep that in mind when looking at how the amino acids in the furin cleavage site are encoded in the SARS2 genome.
Now the functional reason why SARS2 has a furin cleavage site, and its cousin viruses don’t, can be seen by lining up (in a computer) the string of nearly 30,000 nucleotides in its genome with those of its cousin coronaviruses, of which the closest so far known is one called RaTG13. Compared with RaTG13, SARS2 has a 12-nucleotide insert right at the S1/S2 junction. The insert is the sequence T-CCT-CGG-CGG-GC. The CCT codes for proline, the two CGG’s for two arginines, and the GC is the beginning of a GCA codon that codes for alanine.
There are several curious features about this insert but the oddest is that of the two side-by-side CGG codons. Only 5% of SARS2’s arginine codons are CGG, and the double codon CGG-CGG has not been found in any other beta-coronavirus. So how did SARS2 acquire a pair of arginine codons that are favored by human cells but not by coronaviruses?
Proponents of natural emergence have an up-hill task to explain all the features of SARS2’s furin cleavage site. They have to postulate a recombination event at a site on the virus’s genome where recombinations are rare, and the insertion of a 12-nucleotide sequence with a double arginine codon unknown in the beta-coronavirus repertoire, at the only site in the genome that would significantly expand the virus’s infectivity.
“Yes, but your wording makes this sound unlikely — viruses are specialists at unusual events,” is the riposte of David L. Robertson, a virologist at the University of Glasgow who regards lab escape as a conspiracy theory. “Recombination is naturally very, very frequent in these viruses, there are recombination breakpoints in the spike protein and these codons appear unusual exactly because we’ve not sampled enough.”
Dr. Robertson is correct that evolution is always producing results that may seem unlikely but in fact are not. Viruses can generate untold numbers of variants but we see only the one-in-a-billion that natural selection picks for survival. But this argument could be pushed too far. For instance any result of a gain-of-function experiment could be explained as one that evolution would have arrived at in time. And the numbers game can be played the other way. For the furin cleavage site to arise naturally in SARS2, a chain of events has to happen, each of which is quite unlikely for the reasons given above. A long chain with several improbable steps is unlikely to ever be completed.
For the lab escape scenario, the double CGG codon is no surprise. The human-preferred codon is routinely used in labs. So anyone who wanted to insert a furin cleavage site into the virus’s genome would synthesize the PRRA-making sequence in the lab and would be likely to use CGG codons to do so.
“When I first saw the furin cleavage site in the viral sequence, with its arginine codons, I said to my wife it was the smoking gun for the origin of the virus,” said David Baltimore, an eminent virologist and former president of CalTech. “These features make a powerful challenge to the idea of a natural origin for SARS2,” he said.
quick-hands
Footballguy
The Commish
Footballguy
Thanks....this article is littered with a bunch of qualifications "if, then, or, maybe, potentially" and on and on. Don't get me wrong. I tend to appreciate all that more than the nonsense we normally get, but at the end of the day it's speculation (theorizing might be the better word here). And that's perfectly fine too. Any dots connected at this point based on this are speculation though. Yes, it's true that they were studying how to make corona virus jump at the facility and yes they were studying what came to be COVID-19 at the facility. This article does nothing to link them together in a meaningful way. As more info comes out, that might happen, but it hasn't yet.
This is why I asked the question I did about the specific virus....thanks for the article
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One of the things that has made Wade's article so compelling for so many people is the even-handedness with which he approaches it. He lays out all the evidence and lets the reader decide.Thanks....this article is littered with a bunch of qualifications "if, then, or, maybe, potentially" and on and on. Don't get me wrong. I tend to appreciate all that more than the nonsense we normally get, but at the end of the day it's speculation (theorizing might be the better word here). And that's perfectly fine too. Any dots connected at this point based on this are speculation though. Yes, it's true that they were studying how to make corona virus jump at the facility and yes they were studying what came to be COVID-19 at the facility. This article does nothing to link them together in a meaningful way. As more info comes out, that might happen, but it hasn't yet.
This is why I asked the question I did about the specific virus....thanks for the article
The Z Machine
Footballguy
Shula-holic
Footballguy
What an incredible coincidence it would take that the epicenter of this outbreak occurred in the entire world just where that lab happens to be. When I first heard Tom Cotton float this idea out there I thought it was a political talking point/theory. Now that I'm seeing all the backtracking from the people who said that it had to be naturally occurring it's appearing this is more than likely true. Of course the Chinese are doing all they can to cover this up and nobody seems to be making a huge effort to get to the bottom of it.
What about it isn’t even handed? He presents all the available evidence from both arguments. He doesn’t even come out and say which argument he supports. Just because the preponderance of evidence points to one side doesn’t mean it wasn’t handled fairly.
Terminalxylem
Footballguy
Although I think all the talk of Fauci’s culpability is overblown, that article is pretty persuasive and a good read. Thanks for posting.
I read it. I'd say it's very even handed. Just because much of the circumstantial evidence, which is all we have due to China not being forthcoming, points to a lab release doesn't mean it wasn't even handed.
Thunderlips
Footballguy
Kung Flu was just cheap heat for the slack jawed yokels in the bleacher section. China Virus sounded silly. I just think he liked saying "China". He sure did overpronounce it.
If he pushed the narrative the whole time of calling it the Wuhan Strain or something to that affect.....there would have been way less blowback and painting him as a racist.
The Commish
Footballguy
I think this is my issue.....there isn't enough information to decide even though he leads the reader to believe there is enough information to decide. I don't consider that "even handed" personally.ekbeats said:
Grace Under Pressure
Footballguy
China has wet markets everywhere, but the virology lab is in Wuhan. That plus the lab staff positives in November, Ozcam's Razor points to the lab.
The origin should be pursued to the fullest degree, can't have this happening again.
In any case the Chinese government is culpable and owes the world a complete explanation.
The origin should be pursued to the fullest degree, can't have this happening again.
In any case the Chinese government is culpable and owes the world a complete explanation.
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IvanKaramazov
Footballguy
The covid-19 pandemic was the biggest news story since 9/11 and one of two or three defining events of our lifetimes. It would be nice to know stuff about it.
It's weird to me that wanting to know stuff requires some kind of pragmatic justification.
Grace Under Pressure
Footballguy
To me, it's getting that 100% explanation. I think absolutely knowing the origin vs. it being up in the air leads to more and better placed precautions so this doesn't happen again.
The Wade article suggests that the lab was using level 2 protocols when they should have been using level 4. That's a problem if true. Personally, my biggest issue RIGHT NOW if that the Chinese government is not being forthcoming with the evidence and data to show whether this did or did not happen in their lab. On top of that, the WHO has basically just done and said whatever China told them to. This is not how the international community is supposed to act, and it prevents us from knowing whether we should care and, if so, to what extent.
Terminalxylem
Footballguy
I think you’re conflating the mainstream media with “the left”. While the MSM is certainly guilty of liberal bias, that doesn’t mean all, or even most liberals buy what they’re selling.IvanKaramazov said:
People on all parts of the political spectrum have questioned the proximity of the WIV to the birthplace of the pandemic. But “the left” has been more willing to accept the expert opinion offered on what is a pretty esoteric topic. This probably reflects greater distrust of the scientific “establishment” amongst conservatives, not greater understanding of the evidence supporting a bioengineered virus. But if you want claim the right had furin cleavage on their minds the whole time, have at it.
And the only people being accused of nuttiness were those who suggested the virus was an intentionally released bioweapon, or similar nefarious claims.
moleculo
Footballguy
from a curiosity stand point, I get it. What happens next? sanctions? restitution? China isn't going to want to play ball, so is it worth risking WWIII over it?
moleculo
Footballguy
I think it's absolutely fair that the WHO should use the virus as leverage to force their way into inspecting Chinese labs and ensuring safety protocols are appropriate and followed. That should happen regardless of cause.
Terminalxylem
Footballguy
The Z Machine said:
It’s a great article, but he clearly is steering his readers in one direction.
moleculo
Footballguy
The Z Machine
Footballguy
If the Chinese government is covering things up, there's really very little anyone can do to "get to the bottom of it". Short of espionage and a whistleblower that is willing to put their life and their family's life on the line, then the Chinese government can shut the lid on any investigation.Shula-holic said:
Terminalxylem
Footballguy
It would certainly warrant some review and revision of lab protocols, if not wholesale scrapping of gain-of-function research. And I suspect some of their funding might not be renewed.
ETA Depending on how egregious the evidence is China covered up, international sanctions are probably warranted. Don’t want a war, but it’s hard to overlook three and a half million people killed by the virus, and counting.
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The Z Machine
Footballguy
Or maybe there should be a ban on gain of function research for deadly viruses. Just like there's a ban on chemical weapons development.
The Z Machine
Footballguy
GordonGekko
Footballguy
ekbeats said:
Very good article, thank you for bringing it to our attention.
But I think it raises an even more troubling issue.
Direct Headline: The Thucydides Trap
When one great power threatens to displace another, war is almost always the result -- but it doesn’t have to be.
By Graham Allison June 9, 2017, 10:21 AM
https://foreignpolicy.com/2017/06/09/the-thucydides-trap/
******
If you look back on all recorded human history, war between the United States and China appears inevitable.
There is a natural pathway of attack against the United States by China
1) Wipe out all orbital platforms with kinetic energy weapon capability ( i.e. the basis of all the Space X secret missions)
2) Wipe out America's carrier groups, then use their own KEW platforms to track and bombard US submarine groups.
3) Use and activate sleeper cells to wipe out the major ports, major trucking hubs, airports, food distribution centers, electrical grids, water & sewage treatment, and the financial districts. Roving sniper teams will create chaos in urban centers.
4) Use chemical warfare/biological warfare to cripple the United States role as "The World's Bread Basket" America's leverage is not just military and financial, it's the ability to help feed the entire world. You wipe that out, you wipe out many natural allies and alliances and leverage. A starving population cannot hold up the resource/logistical chain to support a world war. This type of attack naturally takes out first responders in it's first wave, which has a devastating impact on maintaining civil order.
If there is clear indications that COVID19 was a preplanned and structured/layered attack, then America's best defense is to immediately go on the offensive. That means staging fabricated attacks on Russian soil that implicate China. China is more than happy to go to war with America, but no one on the face of the planet wants to go to war with Russia.
Some people are still parsing this into a political tribalism talking point. No, it's about inevitable war. And unlike many other wars before it, this one is going to have parts of it fought on American soil. China cannot invade our nation in a formal military manner, it doesn't have the resource chain to do it, it can however hone decades of tactical knowledge and strategy gleaned from asymmetrical warfare to establish widespread terrorism all across the country.
China isn't looking to negotiate. This is part of America's arrogance that refuses to fully understand China's arrogance. China isn't look for a solution. They aren't looking for peace. They aren't looking for compromise. They can't be bought nor extorted nor blackmailed nor any manner of "diplomacy" that involves sitting at a table and parsing human lives like cattle politely.
They want a fight. Give them one. If punches have to be thrown, always be the guy who hits first.
Everyone wants to believe you can solve any problem with a conversation. Without understanding if the other person isn't willing to talk, he'll certainly listen when you punch him in the mouth.
-fish-
Footballguy
For one, if the three lab workers that got sick did have Covid-19 and it was reported to WHO, that would have moved the date it was known from December 31 to November 29. The gene map was leaked on January 11 and then officially provided a couple days later. Since Moderna and Pfizer only needed a weekend to put together their vaccines, it is possible we would have had a vaccine a month earlier (assuming that the gene map would have been released earlier). We also would have known that it was a novel coronavirus and not a viral pneumonia, which is what WHO first thought it was. Containment and the response from the international community and the US may have been different.
IvanKaramazov
Footballguy
I misunderstood where you were going with this -- fair question.
For the record, I'm not interested in "punishing" China over an accidental lab release. China behaved badly in the early stages of the pandemic, and they're not exactly forthcoming with reliable information, but that's just China being China. I would oppose sanctions, and restitution just isn't going to happen even if we demanded them.
the moops
Footballguy
I find it fascinating that so many people just throw up their arms and say "what difference does it make?" If this was indeed a man-made disaster, which it appears now it was, why wouldn't we want to know everything possible if for no other reason to prevent it from happening again? Gain-of-function research has always been controversial, and for good reason. Perhaps we might want to consider worldwide protocols with UN inspections? Are you comfortable that the WIV is doing this type of research in BSL 2 which is the equivalent of a Dentist's office? And if China was indeed culpable then yes, sanctions and restitution should very much be on the table.
There have been a few whistleblowers already. One had to leave the country and now lives in the US in fear for her life. She was also ridiculed by the press for her claims.
Shula-holic
Footballguy
I’d be willing to bet espionage wise there are already foreign governments who do know. There’s been some statements made from other governments who aren’t exactly known for conspiracy theories that seem to indicate this.
One of the possibilities is that they did this on purpose. They may have literally fired the first shot.
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