For context, I have a background in evolutionary theory (though nothing specific to viruses or pathogens) and have recently transitioned from part time to full time research in the longtermist biosecurity space.
When investigating this question, I found researcher’s arguments pretty easy to follow, but found some of the claims about ease of engineering to be hard to follow because they often relied on tacit knowledge like “how hard / expensive is it make an infectious clone of a new coronavirus”. And some the more technical molecular phylogenetics were difficult as well (what can we infer from dN/dS of various parts of the SARS-CoV-2 vs. RATG13 genomes, and how does selection for codon preference influence this analysis). I’d love to talk with someone who feels like they have a good grasp of either of these areas.
There are a group of researchers concerned with CoV19 origins who frequent Twitter and use the moniker #DRASTIC. They count a number of geneticists / microbiologists in their number. See this list:
Ok, so here is what I read (my knowledge may be out of date):
There is a way to set up a chain of animals in a “gain of function” experiment. You start with the wild-type virus, and infect the first animal. You put a gap to the next animal where the viral particles able to bridge that gap (out of the very large number of copies some mutated in the infected animal) are more probable to be capable of bridging gaps.
Eventually in the last animal, the gap is a large air gap, and the virus is now airborne in lab animals. All it takes for a leak after that is a single mistake by a laboratory employee—such as a faulty seal or air filter or procedure error—and they become infected. They then spread it to someone in Wuhan and that’s your outbreak.
This same ‘gap bridging’ is what is creating these mutant variants of Covid that are more infectious.
Anyways this chain of events can occur ‘naturally’, in the same way that enough U-235 can concentrate itself naturally to form a nuclear reactor, it just isn’t very likely.
Part of this is the exactness of the setup. In a laboratory gain of function experiment, you carefully control each gap to force the virus to evolve to bridge it. (each gap is a little bit more difficult in a smooth progression) In some random cave or mineshaft, conditions are chaotic and the virus is not under as much pressure. Sort of like the difference between using pure neutron reflectors and pure uranium ore to make a nuclear pile and relying on nature to make one by accident.
Why do people do this sort of experiment? Why do they deliberately try to create infectious plagues? Is there some real, useful knowledge that comes out of such experiments, or do they just want to see the world burn?
GoF research assists with vaccine development. Apparently that was the reasoning behind GoF research conducted on bat CoVs at the Wuhan Inst. of Virology.
And the results of all these experiments were lots of novel contagions and no vaccines. Complete and utter madness.
Well it’s hard to study something in theory. Making a plague—and using a procedure that could happen in nature it’s just improbable—allows for these scientists to play around with it and see how it works.
I think it’s research that should be done...in teleoperated labs in the middle of a hot desert or other wasteland free of hosts to spread it...
Viruses are known to sometimes jump from one species to another, so what is different about how they are encouraged to do so in a lab? Are they doing anything but forcing it to happen faster?
I am not a biologist and this is wild speculation, but I wonder if, when you force pathogens to pass from one host species to another to another to another, are you selecting them not just for making each individual jump, but for being able to jump from any species to any other more easily? You would then end up with a meta-infective virus able to mutate fast enough to spread through the whole animal kingdom and outpace any attempts at vaccination.
Fortunately such a meta virus that can kill everything is probably difficult to produce from the set of amino acids shared in common to life on earth.
(This is essentially what a gray goo scenario is—life on earth is probably not maximally efficient and it is probably possible to build full synthetic organisms on the scale of cells that self replicate with optimized internal components)
For context, I have a background in evolutionary theory (though nothing specific to viruses or pathogens) and have recently transitioned from part time to full time research in the longtermist biosecurity space.
When investigating this question, I found researcher’s arguments pretty easy to follow, but found some of the claims about ease of engineering to be hard to follow because they often relied on tacit knowledge like “how hard / expensive is it make an infectious clone of a new coronavirus”. And some the more technical molecular phylogenetics were difficult as well (what can we infer from dN/dS of various parts of the SARS-CoV-2 vs. RATG13 genomes, and how does selection for codon preference influence this analysis). I’d love to talk with someone who feels like they have a good grasp of either of these areas.
There are a group of researchers concerned with CoV19 origins who frequent Twitter and use the moniker #DRASTIC. They count a number of geneticists / microbiologists in their number. See this list:
https://twitter.com/i/lists/1344953249334513666
@ydeigin, @__ice9, @MonaRahalkar, @Rossana38510044, @Ayjchan and @AntGDuarte may be good candidates for your questions.
Note that they consider RATG13 to be a chimera designed to obfuscate research.
Ok, so here is what I read (my knowledge may be out of date):
There is a way to set up a chain of animals in a “gain of function” experiment. You start with the wild-type virus, and infect the first animal. You put a gap to the next animal where the viral particles able to bridge that gap (out of the very large number of copies some mutated in the infected animal) are more probable to be capable of bridging gaps.
Eventually in the last animal, the gap is a large air gap, and the virus is now airborne in lab animals. All it takes for a leak after that is a single mistake by a laboratory employee—such as a faulty seal or air filter or procedure error—and they become infected. They then spread it to someone in Wuhan and that’s your outbreak.
This same ‘gap bridging’ is what is creating these mutant variants of Covid that are more infectious.
Anyways this chain of events can occur ‘naturally’, in the same way that enough U-235 can concentrate itself naturally to form a nuclear reactor, it just isn’t very likely.
Part of this is the exactness of the setup. In a laboratory gain of function experiment, you carefully control each gap to force the virus to evolve to bridge it. (each gap is a little bit more difficult in a smooth progression) In some random cave or mineshaft, conditions are chaotic and the virus is not under as much pressure. Sort of like the difference between using pure neutron reflectors and pure uranium ore to make a nuclear pile and relying on nature to make one by accident.
Why do people do this sort of experiment? Why do they deliberately try to create infectious plagues? Is there some real, useful knowledge that comes out of such experiments, or do they just want to see the world burn?
GoF research assists with vaccine development. Apparently that was the reasoning behind GoF research conducted on bat CoVs at the Wuhan Inst. of Virology.
And the results of all these experiments were lots of novel contagions and no vaccines. Complete and utter madness.
https://www.nature.com/news/engineered-bat-virus-stirs-debate-over-risky-research-%201.18787#/b1
Well it’s hard to study something in theory. Making a plague—and using a procedure that could happen in nature it’s just improbable—allows for these scientists to play around with it and see how it works.
I think it’s research that should be done...in teleoperated labs in the middle of a hot desert or other wasteland free of hosts to spread it...
Viruses are known to sometimes jump from one species to another, so what is different about how they are encouraged to do so in a lab? Are they doing anything but forcing it to happen faster?
I am not a biologist and this is wild speculation, but I wonder if, when you force pathogens to pass from one host species to another to another to another, are you selecting them not just for making each individual jump, but for being able to jump from any species to any other more easily? You would then end up with a meta-infective virus able to mutate fast enough to spread through the whole animal kingdom and outpace any attempts at vaccination.
They are forcing it to happen a lot faster, yes.
Fortunately such a meta virus that can kill everything is probably difficult to produce from the set of amino acids shared in common to life on earth. (This is essentially what a gray goo scenario is—life on earth is probably not maximally efficient and it is probably possible to build full synthetic organisms on the scale of cells that self replicate with optimized internal components)