I haven't written a description yet. Here's a diagram I just made (I'm on my phone rn, please forgive any spelling issues) https://owo.whats-th.is/56opvAS.html
Minimum I've seen was 1.5g. Usually between 2 and 3.5.
The issue with psychedelics is not that their ingestion might kill you, but rather what you will do to yourself or others while on them. No amount of reading and Youtube videos can prepare you for a strong psychedelic experience. Once in it, you have to go through it, and accidents do happen.
I've found that people who do psychedelics in repetition usually _think_ they are some sort of key to their problems, they'll help them fix themselves, yada yada yada. One trip is enough for people for whom that is true. If you have to do them repeatedly, the issue is elsewhere. I am against full-on prohibition, but also skeptical about the "pro-psychedelic" sentiment in vogue.
1. Write _anything_ that works. Dependencies, code quality don't matter. Code is idiosyncratic but can be understood by a reviewer.
2. Apply abstractions _everywhere_. Re-implement data structures and algorithms (maybe unknowingly). Code is now very hard to understand.
3. Figure out one is completely unable to update or even maintain code written 6 months ago. Rewritten code suddenly becomes clearer, one begins to think about programming as an craft and not just hacking things on a keyboard until you get the desired result. Dependencies, judicious comments, code quality and a sane terseness become important. The journey starts here.
Personally, step 1 was very short as I learned to program on the job. I was responsible for code, and so I needed to get it together quick. A language like Python makes 2 very easy, and 3 came very quickly too since, as I mentioned, I was responsible for the code (one man team).
I have met people who work at large institutions who are stuck at 1. Others with degrees in CS who are stuck at 2. Some just "get it" and go straight to 3. But typically, the real journey starts when you need to go on with work but your prior self is preventing you from being efficient. You need to get rid of that prior self's work to move on.
Try the Canadian Multilingual French layout on a standard QWERTY keyboard.
à is \
è is '
é is /
ç is ]
accent grave is right-alt+[+letter
and
"specials" are right-alt+num (±@£¢¤¬{}[]) but for any glyph used in programming, I usually switch back to US keyboard using alt+caps-lock. Ça fonctionne très bien pour moi!
On a ISO layout (with the inverted-L "enter" key), you also get ù between left shift and z.
Accolades ({}) and brackets ([]) are on alt-7-8 and alt-9-0. A bit annoying to type, but manageable. At least it's somewhat logical (pairs are next to one another).
The CSA layout is pretty nice, I use it everywhere (writing French and writing code) and don't have problems with {}[]() because these characters are juxtaposed (unlike the french AZERTY).
I see this is a WIP without support for the Scheme numerical tower, tail calls, continuations, etc. If you're looking for such features, Gambit Scheme can compile to JS with those features working and comes at ~600kb gzipped (for the _whole_ system). You can see it in action at https://try.gambitscheme.org but I don't know if it's the latest version.
Yep, basically. I looked into Racketscript a while ago, seems like it was a graduate thesis project that heavily built off of a similar python project iirc. It's based on a very old version of rkt, pre-chez, and probably would need a huge investment just to work with the newer ecosystem.
Iirc, an interesting bullet-point in their backend rework to make the move to chez meant that doing things like targeting js might be easier now than ever. I would absolutely love a js backend for rkt, it seems like it would be a huge boon to the ecosystem.
The transition to the Chez Scheme back end is almost bug compatible [1], so if it worked in the old version, it should work in the new one.
One advantage or migrating it to the Chez Scheme version is that some tricky functions (like print or display that have like a million of corner cases) are implemented in Racket or in Chez Scheme, so it's not necessary to write them again in JavaScript.
[1] For example in the old version, only the small chars were interned and in the new version all are interned, so code like (eq? #\λ (integer->char (char->integer #\λ))) may have a different result. It's true in the new version, but in the old version it may be false if the optimizer is not aggressive enough with the constant folding.
Sadly "I didn't know Gambit could do X" seems to be a frequent sentiment considering the project's documentation. The configure script hints at many a feature that isn't described anywhere.
Gambit has some syntax to call functions in the host language (C/Python/Ruby/etc). That syntax is what is used to call Javascript functions that exist in the context where the compiled script is executed (window/node). As far as using stuff like ES6 style imports and the like, there is a project on Github called gambscript but it isn't complete as far as I can see. Someone out there can get closer but I know it isn't me.
Implementing the numerical tower is not too difficult. There may be some problems to ensure fixnums are singletons and bignums are efficient, but it looks possible.
Tail calls and continuations are more difficult if you want them to be efficient.
For some folks who'd like me to trust their web knowledge, having an expired certificate certainly doesn't give me any more trust than I already had.
More on topic: I wonder how the REPL story is with Racketscript? Nothing seems to be mentioned in the README nor in the repository which would make this project a non-starter for the people who got used to ClojureScript and similar efforts.
That is a bummer about the expired certificate. You can access the site using http instead of https if you are comfortable doing so. I have never seen this live REPL before and have just used their Github repo to get the latest: https://github.com/gambit/gambit
I think it is great someone is trying to get Racket compiling to Javascript again. I also agree with you about the REPL; while it is interesting to compile Racket to JS, having a REPL, a live environment and all the features of something like ClojureScript has much more utility.
Sorry about the certificate... I hadn't noticed it had expired. That is fixed now and you can visit https://try.gambitscheme.org/ to try it out (don't type anything in the REPL and you will get an automatic demo).
The last part of the demo shows how to use threads in the browser and also the JavaScript FFI. The FFI based on an infix syntax is explained in greater detail in this ELS'21 paper: http://www.iro.umontreal.ca/~feeley/papers/BelangerFeeleyELS... . The paper contains several examples. Here's a simple one you can type at the REPL:
Basically a backslash switches to JavaScript (with infix syntax) and a backquote switches back to Scheme (with prefix syntax).
The whole Gambit system fits in a 640KB gzipped JavaScript file, so it is reasonably fast to load.
If you are interested in a really tiny Scheme implementation in JavaScript that supports tail-calls and call/cc and an incremental Scheme compiler and a REPL and most of the R4RS procedures, you might want to try out the Ribbit Scheme implementation which is just under 6 KB of (non-gzipped) JavaScript: https://udem-dlteam.github.io/ribbit/repl-max.html . That implementation is described in a paper at the VMIL'21 workshop (presentation on October 19).
Fails in Brave (Chromium 91) with shields up, here's the stack:
three.module.js:21344 Uncaught (in promise) TypeError:
Cannot read property 'indexOf' of null
at new ch (three.module.js:21344)
at ht (three.module.js:24988)
at new gh (three.module.js:25021)
at m (CanvasSystem.js:30)
at S.addSystem (World.js:379)
at be (initialize.js:112)
at async onCreate (index.js:47)
The calculation is simple and could have been made in early 2020. What's the joint probability of occurrence given everything you know about the origins of SARS-CoV-2?
There is _very_ high probability that this is just a human error.
I don’t dispute it is one point of suspicion, but Wuhan is also one of the 10 biggest cities in China. It isn’t a surprise the first US outbreak was in the biggest city. The first cases could have been anywhere.
If there were more evidence that it was lab made then the location would be another point, not to me without further evidence it doesn’t mean all that much.
And there have been 2 emerging coronavirus outbreaks in the last 20 years due to natural origin. Why is it so hard to believe there would be another one.
> I don’t dispute it is one point of suspicion, but Wuhan is also one of the 10 biggest cities in China. It isn’t a surprise the first US outbreak was in the biggest city. The first cases could have been anywhere.
Is that really so for animal-borne viruses though? I thought they came from place with lots of animals, hence the focus on the market. If it just showed up on some random high-rise employee downtown that would be hard to believe.
And after it starts, of course a highly-infectious virus shows up at densely populated places quickly. But for the same reason, I would also think it's hard for the first cases to travel to dense areas and spread the disease there without leaving a trail of cases along the trip. Ultimately they should point back to the animals they came from and testing can confirm it. Or at least rule various places out, if the govt was accommodating.
Plus wasn't the first US case somewhere in Washington state.
The first death in the U.S. was only discovered at least a month later, and this is long after we knew about the existence of the virus.
In China before there was a huge outbreak there is absolutely no way you can expect a small number of cases of a virus that nobody knows exists to be picked up. By the time of the big Wuhan outbreak there are already different variations in the virus. It had been in some population for a while before it broke out.
So the first outbreak in NYC is analogous to Wuhan. It could have started in Wuhan or it could have started anywhere else and then Wuhan had the right combination of factors for the outbreak to surge. We don’t know for sure.
We do know for sure that it started in Wuhan. The viral phylogeny is extremely clear. We have hundreds of thousands of viral sequences that describe a tree that is rooted in Wuhan around October 2019. That's incontrovertible. No evidence has arisen to contradict this despite an extensive search by thousands of scientists.
>There are two subclusters of A which are distinguished by the synonymous mutation T29095C. In the T-allele subcluster, four Chinese individuals (from the southern coastal Chinese province of Guangdong)
This reply only makes sense if covid-19 popped up at a random spot in Wuhan....and not literally right next to their coronavirus research lab.
It's not hard to believe that there could be another spillover event, and I don't have any certainty where covid-19 came from, but you're unfairly downplaying the level of circumferential evidence that does exist. There has been a significant effort against evaluating the lab-leak as a reasonable hypothesis (I say that in the scientific meaning of the word), and that effort has significantly damaged the reputation of scientific institutions around the world, and for good reason.
Yes I have read more than the articles, which is why I’m correctly saying it was unlikely to come from the lab.
I’m not saying it is impossible, just unlikely. And automatically degrading the opinions of experts who have detailed their arguments because you think they are biased is not proof of anything either.
Other pertinent data point, how many epidemics have been positively traced to a lab leak since virology has been widely studied? The Wuhan lab was founded in the 1950s. You can say the likelihood that a virus would one day escape from one of these labs is pretty high. The likelihood that a given virus would be from a lab is very low. All of which brings us back to where we were at the start. It's plausible and possible but not really likely.
A 2007 outbreak of foot-and-mouth disease (an important virus affecting cattle) was traced to effluent released from a laboratory in the UK [1].
A small number of SARS infections in 2003-2004 are also believed to have been due to laboratory accidents [2].
This article [3] gives an introduction to the subject from the perspective of a journalist who has reported on laboratory safety in the US.
This article [4] published in Nature in January 2012 by members of the US National Science Advisory Board for Biosecurity reviews the risk of a release of an engineered form of H5N1 influenza. It includes some alarming remarks such as:
'We found the potential risk of public harm to be of unusually high magnitude' and;
'A pandemic, or the deliberate release of a transmissible highly pathogenic influenza A/H5N1 virus, would be an unimaginable catastrophe for which the world is currently inadequately prepared'
The authors take the possibility of release of a dangerous pathogen from a laboratory seriously, though the article is prospective rather than retrospective.
For an epidemic to occur, you need not just a lab leak, but a population sufficiently naive to the pathogen. H1N1 was displaced by H2N2 in the late 1950's pandemic, which in turn was displaced by H3N2 in the late 1960s pandemic. Thus it hit the cohort of people aged 25-6 or less who'd never been exposed to H1N1.
That article doesn't support your argument. It just says it was suspected.
I found an NIH article that says the likelier origin is that the 1950 virus was used to produce a weakened live virus vaccine candidate that lead to the reemergence and not an accidental leak. It also concludes by saying there has never been a likely lab leak epidemic ever observed.
That article's definition of "lab accident" seems narrow and legalistic to me. In either case, the virus spent 1950-1977 in a lab freezer. It ended up in the wild, with ~700k people dead. The only question is whether it escaped in an infected researcher (or in infectious lab waste, or in whatever else you'd consider a proper lab accident) vs. in that failed vaccine candidate.
Those details do inform some details of the correct policy response. For example, they determine the relative importance of better PPE at the bench vs. better QA before allowing the vaccine to leave the lab. They don't change the overall question of whether scientific research has ever caused a pandemic, though. That causality is what matters, not whether the sign on the door said "lab" vs. "experimental vaccine nurse".
For example, if the pandemic originated from a WIV researcher who became infected in the field (during their many expeditions to remote bat caves that no other humans would routinely enter), was that a "lab leak"? Literally no, since they weren't in the lab. The causality would still be the same, though--if not for that scientific research, that virus would likely have never left the cave.
To avoid such confusion, it's probably better to say something like "unnatural origin", or "origin arising from scientific research". A much bigger mouthful than "lab leak", though.
I'd add that the article does not state that there have never been cases of accidental releases of pathogens from laboratories, only that such accidents had likely not led to a 'global epidemic' as of the date the article was written (2015).
The article's abstract opens with the statement 'The 1977-1978 influenza epidemic was probably not a natural event'.
These labs are in major cities. Epidemics are likely to be detected in Major cities. The chance of an outbreak being near a research lab aren't as long as you seem to think.
As pointed out in the article, there were exactly 3 cities in the world working on gain-of-function research related to bat-originated coronaviruses. Galveston, Texas, Chapel Hill N.C, and Wuhan. It’s way more narrow than just being near a biological laboratory.
That's not what the person you are responding to said at all. Please stop dishonestly conflating the two theories. You can believe that a coronavirus accidentally leaked from a lab that was studying coronaviruses without believing that it was intentional, or that the disease was a bioweapon.
Honestly, this is not a difficult distinction to understand. You have to wonder why people are so eager to conflate the two.
If it's nothing to do with an engineered virus conspiracy then there's no reason to constrain ourselves to the 1 or 2 labs doing that kind of research. If we don't have that constraint then appearing in Wuhan is much less coincidental.
Listen, if the virus originated in a city that simply had an infectious disease lab, that’s one thing.
For a virus to originate in a city with one of three labs in the entire world conducting heavy-duty researching involving the exact kind of virus that unleashed this pandemic, with the stated intention of working with said viruses to make them more infectious (NOT for the purposes of making a bioweapon) that deserves special consideration. Especially with the fact that the animal the virus is thought to come from ranges 1500 miles south from said city, and started during a time that animal is typically hybernating.
You do know that there's genetic evidence that seems to point to an origin 600 miles from Wuhan?
> Of 23 samples that came from Wuhan, only three were type A, the rest were type B, a version two mutations from A. But in other parts of China, Forster says, initially A was the predominant strain. For instance, of nine genome samples in Guangdong, some 600 miles south of Wuhan, five were A types. [0]
> with the stated intention of working with said viruses to make them more infectious (NOT for the purposes of making a bioweapon)
Why is this relevant unless you're claiming that the virus that we've observed has been engineered in that way? Otherwise it seems like the chance of a coronavirus outbreak caused by poor handling in a lab is the same for any lab that's studying them for any purpose.
Good point, now that you mention it, it does now seem possible that SARS-CoV-2 is the result of some sort of engineering tests. Not saying it’s a certainty, but it’s surely at least a plausible consideration.
Why? Im not passing judgement on whether it was engineered as a bioweapon. But there was a lab that was actively engaged in research of viruses that are exactly what COVID is. They were conducting research on making said viruses more infectious. I’m not sure why the more likely thing is that it was just a virus sitting in a lab that spilled out, as opposed to a virus that was actively being worked on using the techniques the lab was known to be studying.
You've artificially limited the number of possible labs to those doing bioweapon research. If this isn't your claim there is no reason to do so and if there are more labs studying coronavirus it's far less coincidental.
There is zero evidence that anyone, anywhere in the world was working to develop SARS-like bioweapons. The gain-of-function research in question would have been basic research, intended to develop more dangerous variants of the viruses in order to predict future pandemic emergence, develop more universal vaccines, etc. I believe this research was reckless and should never have been funded (by the USA!) or permitted, even considering only what they knew at the time. It wasn't malicious, though.
In any case, beyond gain-of-function, the WIV and Wuhan CDC also had the biggest program in the world to sample novel SARS-like coronaviruses from nature, from remote bat caves that no other humans had any reason to enter.
If SARS-CoV-2 is a naturally-evolved virus accidentally released by scientists, then Wuhan is the obvious place for it to emerge. That could have been directly from a lab, or a researcher could have become infected on a sampling trip, traveled home from the sampling sites (~900 miles away, to be clear; Wuhan was not an expected natural spillover region), and seeded the infection there. None of this is anywhere close to proven, but the previous dismissal of any unnatural origin as a "conspiracy theory" was an outrageous, unscientific smear.
> There is zero evidence that anyone, anywhere in the world was working to develop SARS-like bioweapons
How do I square that with this claim from the article?
> Eleven of its 23 coauthors worked for the Academy of Military Medical Sciences, the Chinese army’s medical research institute. Using the gene-editing technology known as CRISPR, the researchers had engineered mice with humanized lungs, then studied their susceptibility to SARS-CoV-2. As the NSC officials worked backward from the date of publication to establish a timeline for the study, it became clear that the mice had been engineered sometime in the summer of 2019, before the pandemic even started. The NSC officials were left wondering: Had the Chinese military been running viruses through humanized mouse models, to see which might be infectious to humans?"
What this describes seems like it could be circumstantial evidence of the PLA developing bioweapons. Certainly it isn't proof of anything, and as evidence it's not very strong. But I wouldn't call it 'zero.'
"Running viruses through humanized mouse models" is a pretty normal (though frightening) part of virology. For example, Ralph Baric was doing it back in 2005:
So if the Chinese military had in fact been doing this, I'd guess it was just basic research, in the same way that lots of American basic research links back to DARPA. Of course they fund it because they believe there might be a military application, but I see no reason to think that application would be bioweapons (vs. the same kind of beneficial applications described in the open literature).
Perhaps "no evidence" would have been better phrasing than "no reason"? I do think it's possible that some Chinese (or American, or British, or ...) military officer has at some point wondered if coronaviruses would make good bioweapons, but there's still no evidence.
They don't seem like obvious candidates to me, though. Both SARS v1 and SARS-CoV-2 show unpredictable, stochastic person-to-person spread, via super-spreader events. For a bioweapon that would ideally infect all the enemy but no one else, that's the last thing you want, hard to reliably get started and hard to reliably stop once it starts. So that reinforces my belief that if SARS-CoV-2 was of unnatural origin, it was almost certainly an accident during basic research.
Non-scientists obviously go into bat caves all the time, for guano collection, mining, etc. This certainly is a possible pathway for the emergence of zoonotic diseases, including SARS-CoV-2. Those aren't the bat caves I was referring to, though.
The WIV and Wuhan CDC sent grad students to hike through the wilderness to remote bat caves too far from any road or farm to have been exploited yet for any practical use. They chose those caves based on their expert predictions of where they expected to see the greatest diversity of novel coronaviruses.
There's obviously far fewer WIV grad students than guano harvesters; but the risk per person seems orders of magnitude higher, for an expert deliberately seeking a virus vs. a merely indifferent laborer. So that seems like a new and non-negligible risk to me, and thus one that requires investigation. Note that I'm not alone in this; Marc Lipsitch, for example, often mentions this possible pathway.
Very easily, you can get to the other side of the world before you even become infectious, which can be days after contracting the virus. Even if there were a trail of infectious they were probably chalked up as the flu and is likely to be undetected. If it was spreading then the virus may not have been adapted enough for the explosive growth we saw in Wuhan.
Good question; I would guess that like SARS and MERS, whichever viruses they picked up, assuming that's what happened, didn't transmit well.
That's one of the independent vectors the author mentions that makes so many of us suspect very specifically a lab leak of a gain of function experiment: the virus started out very well adapted to humans.
A lot of emerging viruses are well adapted to humans… that’s why become outbreaks. How can you judge what level of adaption is expected vs unexpected in a virus.
Most virologists say the way this virus works is unlike anything they’ve seen or expected so they can’t imagine how a human would have engineered it. Why do you think your feeling about the virus’s level of adaptation trumps the experts opinions?
"A lot of emerging viruses are well adapted to humans…"
This is literally not true.
Most virologists say the way this virus works is unlike anything they’ve seen or expected so they can’t imagine how a human would have engineered it. Why do you think your feeling about the virus’s level of adaptation trumps the experts opinions?
1) Citation on "most" please. The world is a big place, so you will be able to find a citation for any opinion. If you are going to say "most" then please back it up with a source.
2) gain-of-function research doesn't require a human to engineer a new virus. It is a way to essentially speed up evolution and allow nature to do the heavy lifting. You're arguing points that no on here is making.
How can you judge what level of adaption is expected vs unexpected in a virus.
It's a long article so I don't expect you to find the argument in it; it highlights the work of Alina Chan who compared a fast mutation rate of SARS-CoV as it better adapted itself to human to SARS-CoV-2. Here are titles of three of them I've saved but not read, May through September of last year:
SARS-CoV-2 is well adapted for humans. What does this mean for re-emergence?
Single source of pangolin CoVs with a near identical Spike RBD to SARS-CoV-2
COVID-19 CG: Tracking SARS-CoV-2 mutations by locations and dates of interest
The lab wasn’t conducting bioweapon research. Gain of function research isn’t to create a bioweapon, nominally. It’s to examine the behavior of viruses under manipulation in order to better understand how we can respond to them given an outbreak. It’s not nefarious by nature, though it does seem like its usefulness hasn’t panned out as was thought.
But again, you really should read the article to understand what gain of function research is instead of insinuating I said COVID was a bioweapon.
They may be, but the WIV wasn't. In the words of Dr. Shi herself:
> We have done bat virus surveillance in Hubei Province for many years, but have not found that bats in Wuhan or even the wider Hubei Province carry any coronaviruses that are closely related to SARS-CoV-2. I don't think the spillover from bats to humans occurred in Wuhan or in Hubei Province.
The closest animal virus to SARS-CoV-2 was found in nature about 900 miles from Wuhan (RaTG13, in Mojiang), closer to Chongqing, Chengdu, Guangzhou, Shenzhen, or HK.
According to Wikipedia the lab had been established many decades ago, "The WIV was founded in 1956 as the Wuhan Microbiology Laboratory" and got its current name in 1978. For better or worse, open, public labs tend to be set up in urban areas, see the insane move of the work done at the Plum Island Animal Disease Center to college town Manhattan, Kansas https://en.wikipedia.org/wiki/Manhattan,_Kansas in the heartland of American agriculture.
Ebola Reston evolved naturally, and emerged in humans due to an infected lab monkey imported from the Philippines to a contract research organization in Reston. Anyone who guessed that it came from Fort Detrick would have been wrong about which lab it came from, but right that it came from a lab.
Put differently, if scientists there hadn't been experimenting with monkeys, Ebola Reston wouldn't have entered humans there. We don't absolve exotic wildlife traffickers or farmers of the consequences of their actions in releasing novel, naturally-evolved viruses; so I'm not sure why we'd absolve scientific researchers.
The lab leak theory doesn’t imply that the virus was created, or gain of functioned, in the lab, merely that it was studied there and escaped. The lab leak theory doesn’t imply unnatural origins.
An example of this would be the Marburg virus (unrelated to CoVs): leaked from a lab, but of natural origin, through an infected lab animal caught in the wild
When bats weren't even being sold in that market? When the nearest ones were hundreds of kilometers away and in hibernation? No it was just easier to call a guy racist and bury your head in the sand.
So when we find Anthrax outside its normal "range" but close to a lab we can just say, yeah, no, while it's not endemic to this location it is 1000 miles away, so nothing to worry about? Oh, and never mind the lab.
This is not remotely comparable. Russia uses Novichok as a signature "we did it, don't F around".
This one was, yeah, this is a virology institute, we study corona viruses, we were hiring for corona virus experts, we do GoF work, but trust us, just because it first appeared blocks from our facility, it did not come from us. Also, don't believe our former virologists who skipped town.
Doesn’t it seem likelier that zoonotic transmission from an animal in Yunnan would infect a local and result in an initial local outbreak, which we have no evidence of? What do you think the ratio of locals in Yunnan are to visitors from Wuhan or potential visitors to Wuhan are at any given time? 100 to 1, 1000 to 1? I have no idea, but excuse the incredulity. It’s less likely that a virus from Yunnan would break out somewhere other than Yunnan, perhaps by a couple of orders of magnitude or more.
I mean sure, anything’s possible, but we have only circumstantial evidence right now and this observation isn’t a smoking gun, but it ain’t worth nothing.
This presumes COVID-19 had to evolve in the place people are looking for possible coronaviruses and had to jump directly from bats to people, and not in surrounding or isolated areas where the bats might roam. Or that their wasn't - as is suspected now - one or several interim species.
SARS after all was found in civets, and then later several other species as well despite originating in bats.
It doesn’t presume that it had to, it just conjectures that it is either more likely or not significantly less likely than the scenarios you listed.
We can’t rule it out, ie. we only have evidence right now to try to make a determination based on the preponderance of evidence, not beyond a reasonable doubt. The story that is emerging is that we may never be able to prove something beyond a reasonable doubt because the debate was quashed for a year by political concerns, institutional biases, and motivated reasoning.
You're taking this the wrong way. You have to update your priors and calculate a joint probability knowing everything we know about the origins of this particular virus.
We know enough to calculate a joint probability. Just update your estimate with new information. This should be pretty non-controversial. Everybody does this every day especially in the face of uncertainty.
Are you expecting a number? The joint probability of low-probability events is itself very low.
I'm not saying you should calculate it like P(10 000 tails coin flip) * P(1 000 000 tails coin flip). That can be done numerically. I'm saying that based on everything I've read, the highest probability hypothesis according to my own evaluation is the unintentional lab leak. To me, that's as uncontroversial as it gets. Human error happens _all the time_. Arguing against the lab leak, knowing what we know about China's refusal to allow an actual thorough scientific investigation into it, seems quite a bit more controversial to me.
Labs burn down, medical errors happen, bridges collapse, whatever. That's just reality.
Yes, but, I've seen people try to do that both on here and on rootcause, and the probabilities are anything but objective. It's just people math-washing what they already thought
Anybody who has ever worked in a wet lab, or a lab of any sort, knows that accidents happen. All the time. Things catch fire, things are dropped, labeling issues happen, anything you can think of.
I worked for many years in a lab, the accidental leak hypothesis was and still is what I consider the most probable. Calculate the joint probability of everything we know about the origin of SARS-CoV-2 happening and it should be obvious that the "lab leak" should be _thoroughly_ investigated before dismissing it.
With SARS-Cov1 and MERS they were able to identify the cross-over host and find transitional stages that are somewhat adapted to human hosts but more successful in other host animals. It is not too late to find that of course, but it is becoming conspicuous in its absence. Also, the lab in Wuhan was basically trying to create SARS-Cov-2 and that isn't speculation its what their grant proposal says they were doing.
It also differs from every betacoronavirus backbone that had been used for genetic modification (and there’s no clear reason somebody would want to come up with a new one), which is basically the same problem but in reverse.
We’ve never, despite years and years of trying, been able to identify an origin for Ebola. The basic reality is we don’t know anywhere near all the diseases that animals have.
I’d guess several small teams have received single digit million dollar grants to look for the origin of Ebola. Maybe one or two got double digit millions.
China put sanctions on Australia that will and have cost their economy billions for implying that the lab leak hypothesis is plausible. Reasonable or not the Chinese government believes suppressing this theory to be a major policy goal. So I expect they’ve either spent orders of magnitude more effort than we ever spent on looking for Ebola’s origins, or they have some reason to believe they wouldn’t find anything.
This isn’t a smoking gun, but it is a dog that didn’t bark.
by guess, do you mean estimate, or just a real guess? Is there somewhere I can read more about the teams that have looked for the ebola origin and how they're funded?
p(Epidemic started in Wuhan) * p(origin in market right next to lab) * p(lab is one of 3 in the world to conduct gain-of-function research on conronaviruses) * p(lab scientists were notably sick prior to outbreak) * p(no accident ever happening in a lab) * p(et cetera) = very small number.
That's not evidence per se, but it does show you how probable a human error is.
I can’t help but feel you’re taking all the “for” factors and none of the “against”, then bending the “for” factors even further.
Calling the market “right next to the lab” is a bit of a stretch - it’s a three and a half hour walk.
The scientists getting sick early doesn’t actually seem to be confirmed - there’s still debate in the US intelligence community whether it’s true. And going to the hospital because you’re sick means something a bit different in China where primary care is rare.
And as for “against”... no mention of the virus not matching any backbones in use for genetic experimentation, or the suboptimal binding to humans, both of which would suggest against engineering.
Let me make this clear: I don't know for certain what happened. But after updating my priors, I believe it's highly probable that the outbreak came from human error.
Also, I never once mentioned engineering. There's a lab 280m away from the market that has one of the largest bat virus samples in the world.
I would have no problem revising my priors, but for the moment I still consider the lab leak human error hypothesis still the most reasonable explanation.
Every published backbone used for genetic experimentation was at some point unpublished. The WIV had the biggest program in the world to sample novel SARS-like coronaviruses from nature, plus the ability to engineer them in the lab. In the words of David Relman:
> This argument [that SARS-CoV-2 must be natural since it doesn't use a known backbone] fails to acknowledge the possibility that two or more as yet undisclosed ancestors (i.e., more proximal ancestors than RaTG13 and RmYN02) had already been discovered and were being studied in a laboratory—for example, one with the SARS-CoV-2 backbone and spike protein receptor-binding domain, and the other with the SARS-CoV-2 polybasic furin cleavage site. It would have been a logical next step to wonder about the properties of a recombinant virus and then create it in the laboratory.
Note also that the WIV's public database of viral genomes went offline in Sept 2019, and hasn't come back.
As to the binding, Andersen looked at the binding of SARS-CoV-2's RBD to human ACE2 in silico, and found that it was suboptimal. But that proves only that the RBD wasn't designed in silico using his software workflow. Among unnatural origins, it's far more likely that the RBD either evolved naturally (as Relman proposed above) in a different virus, or evolved quasi-naturally in the lab during culture in human cells or in humanized mice. Andersen's argument doesn't address these more likely possibilities.
> no mention of the virus not matching any backbones in use for genetic experimentation, or the suboptimal binding to humans
Are you going to cite sources? And then are you going to cite the other sources which have addressed both of these weak counter arguments? Some of us have done a lot of homework on this one, so you need to bring your A game.
There is a vast amount of unpublished research, not because of malicious intentions, but because it's either still ongoing, or abandoned, or postponed, or waiting for other results, or for review, or qualified specialists to help, whatever.
The VF article specifically mentions that the closest known virus was 96% similar (vs 90% for SARS-CoV-1), and had actually been renamed by the scientists studying it and that fact hadn't been put forward to the community.
It can still be shown that this has a completely natural (i.e. no human error involved) origin, but the burden of proof gets higher every day. It's much more probable that human error is involved, which is something that happens every day.
