I was an experimental synbio person for decades, and I did plenty of microbial pathogen work. I've also worked on frontier LLMs for the last decade. All of this stuff is gated by experimental effort, not AI!

Alphafold can't reliably predict thermal energy landscapes or make functional predictions - and how could it? It wasn't trained on anything that could capture structure - function relationships.

Again, most people just have no idea how hard - fundamentally hard - molecular physics is to predict, and how necessary experiments are for any development of biological systems.

It's the fact that the complexity of molecular physics scales exponentially in particle number. No amount of thinking is going to punch through that. You've got to do experiments. The slow loop through reality is not optional, and in the case of "superviruses" would require a lot of iterative experimental development in humans.

(And please knock off the bio infohazard act - I routinely get asked about scenarios that AIxBio safety people cook up and they always involve some howler misunderstanding of basic facts in biology or medicine. Just talk about an idea if you have it.)

The biorisk scenarios that the AI safety folks flog are fever-dreamed fantasies that have only the most tenuous connection to biological reality. As someone who cares about the real bio-risks of natural pathogens, I get pretty tired of fear-based marketing pretending that AI is a bigger threat than, say, animal agriculture.

JAX/XLA does offer some really nice tools for doing automated sharding of models across devices, but for really large performance-optimized models we often handle the comms stuff manually, similar in spirit to MPI.

The odd set of claims is that somehow biology has 1) figured out how to preserve long-range entanglement and coherent states at 300K in a solvated environment when we struggle to do so in cold vacuum for quantum computing and 2) somehow still manages to selectively couple this to the -known- neuronal computational processes that are experimentally proven to be essential to thought and consciousness.

This more or less amounts to assertions that "biology is magic" without any substantive experimental evidence over the last thirty years that any of the above is actually happening. That's why most biophysicists and neuroscientists don't take it at all seriously.

It's hard to buy that their proposed stories are the simplest explanation for these few measurements. Much more boring phenomena can influence QY. e.g. simply occluding fluorophores from the bulk solvent can have a huge influence on QY and spectra. (I used to design biological fluorescent reporter reagents...)

It's hard to buy that their proposed stories are the simplest explanation for these few measurements. Much more boring phenomena can influence QY. e.g. simply occluding fluorophores from the bulk solvent can have a huge influence on QY.

Fold prediction is an incredibly useful tool for scientists and genetic engineers to help design new proteins, but it doesn't magically solve molecular or cell biology. Designing new functions and mechanisms is still going to involve a huge amount of labor and brute-force experimentation.

I certainly don't think it will help at all with stability. Things like Q/K layernorm are better tricks for softmax stability when scaling: https://arxiv.org/pdf/2302.05442.pdf

As a 2-decade genetic engineer: there are no genetic "markers" pointing to a lab leak, there's really no sign of unnatural manipulation in the sequence.

What I've tried repeatedly to impress upon people here is that most routine cloning strategies leave pretty clear signatures, and the idea that a lab would go so far as to eliminate these signatures for such mundane virology work is tantamount to a much more elaborate conspiracy theory.

What they're observing is homologous recombination between strains - all the sites they're claiming are found in nature.

Again - there would be a genetic signal the strength of the noonday sun burning your eyes out if sars-cov-2 was made by cut-and-paste at these sites. You wouldn't need this ridiculous circular argumentation to prove that point.

If we're linking to tweets, these two go into great depth about how ridiculous this paper is: https://twitter.com/Friedemann1/status/1583519970902048768 https://twitter.com/acritschristoph/status/15834864034169692...

This paper posits a completely crazy cloning strategy that makes no sense (ie doing something far more convoluted than typical bsaI/bsmbi seamless cloning workflows that breaks the whole point of "seamless" workflows), and then tries to use that to make a case for a genomic signature that we could look for. They then look at a handpicked set of viral genomes, but leave a bunch out and duplicate others (I think WIV04 and WHu are the same), and largely seem to be observing without realizing it that yes, recombination occurs among these viral lineages.

This isn't even getting into the fact that a restriction-ligation based cloning strategy would leave glaringly obvious fingerprints behind in the form of the hundreds of nucleotide differences that are present outside the cutsites across the lineages... it would be blindingly obvious if someone just cut-and-pasted sars-cov-2 from other studied genomes.

Comments URL: https://news.ycombinator.com/item?id=32946389

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