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Comment by dnautics | Hacker News Reader

the HIV-1 protein sequence is the same but not the DNA sequence. The moderna DNA sequence is identical. The odds of HIV-1 mixing with bat coronavirus, and then somehow finding the moderna DNA sequence, while not astronomically low, are pretty low.

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How are you calculating those odds? And then once you have calculated them, what are you using to determine your threshold for "low" odds? The odds that a bunch of atoms ended up turning into you and me and the rest of humanity are extremely low or extremely high depending on what your criteria for "low" odds are.

Given the number of bats in the world, the number of human hosts, and probably most importantly, the number of individual virions within each infected host (and therefore the number of replication cycles) is...astronomically high. There are somewhere between 1 and 100 BILLION virions of COVID in each infected person. Now imagine a few thousand bats infected...we are already talking about maybe 1 QUADRILLION different virions (1,000 trillion). It only takes one virion to incorporate some very handy and fitness-increasing HIV-1 RNA into its genome and it is off to the races.

> How are you calculating those odds?

I truly have no idea what the answer is, but as someone well versed in economics, econometrics,and statistics, to me the relevant odds are not about independent coin tosses etc. I would like to know P(A|B) where:

A: sequence of 30 nucleotides appears in a virus identified in nature

B: sequence appears in a patent application that predates discovery in nature

Seems to me that would involve a whole bunch of arithmetic, but that ought to be calculable using this database.

the mutation rate simply is not as high as you imagine it to be. If it were, then we would (likely) see more wobbling around the wobble pairs in the cleavage site coding region.

I never mentioned mutation rate so your gotcha is not as crafty as you might think. Also a mutation in the sense you seem to be implying (random base pair changes due to lack of proof reading) is not really what I am talking about. I am talking about HIV-1 genome being incorporated into SARS-CoV-2 by the host cell or either virus during replication. That is not that crazy when you have quadrillion of replication cycles and a selective pressure to mutate and incorporate new RNA.

we're talking about the odds of the founder event. My guess is odds are about 1 in 3^{5-6} (3-ish wobble options, five to six wobble sites, haven't looked at the sequence to confirm this. Probably someone can do a better analysis based on codon usage in humans. I suggest doing it as an exercise in understanding molecular biology.

Besides an enormous number of people now infected with both HIV and COVID-19. That alone increases the chances of this happening naturally enormously.

my favorite part about your response here is how you didn't answer any of the questions and gave a hand-wavey response about how they're wrong.

alright, do you want a specific answer? My guess is it's somewhere around one in 3^{5-6}-ish, for the singular founder event that establishes and fixes that sequence as the canonical sequence for the furin cleavage site of COVID-19.

Well sure, but given that viruses mutate on the order of millions of times a day (since they replicate on the order of gazillions of times a day) it's not terribly unreasonable that this sequence could have developed by accident, even through the relatively winding path you described.

Hell, the entire genetic code of every variant of COVID-19 exists somewhere in the digits of Pi, but that doesn't mean that mathematicians created COVID. This reeks of a slightly more advanced form of numerology to me.

While viruses do mutate a lot, if the sequence were that labile, then you would expect there to be a lot of divergence around the furin cleavage site. We don't really see that, so the site is stable. So, is there something special about that DNA sequence (including the synonymous wobble pairs) that make this a random walk gradient descent minimum? Or is the mutation rate lower than you think.

All I'm saying is when people say "this mutation is super rare therefore it MUST have been manmade!", I'm skeptical. Even the most stable DNA sequences have mutations occasionally, because mutations happen for a bunch of totally uncorrelated reasons. It could have been manmade, but it could have also been made by a stray cosmic ray. To say a particular sequence "proves" that the virus is manmade is...sketchy at best.

Nobody is claiming proof. Don't move the goalposts.

This article is....suggestive, to say the least. So I'm at least responding to the article.

This article is worse than useless because it places a pseudoscientific veneer around something (to make it sound plausible) while still being almost certainly wrong.

Only gatekeepers would want to keep scientific evidence from commoners, instead of teaching them that said evidence isn't anywhere close to proof yet.

every major university in the us contains physical copies of all the published articles (IE, people who wanted to learn more, but couldn't afford to subscribe to every journal), annd the rest are on arxiv. Nobody is gatekeeping the evidence.

The reality is that average people simply aren't qualified to deal with the subtlety and complexity of ambiguous data, and the adversaries of public health can just make a video that lies and convince millions of people with seductive, but wrong, ideas. It's extremely rare to have a society which is scientifically savvy enough to understand these sorts of things.

What evidence?

The mutation rate for proofreading ssRNA viruses is, affair, about 10^-7 per nt per replication. If we don’t see a particular variant nt it is (from the top of my head) because it didn’t “survive” the drift events or that there is strong positive selection on the sequence.

(Preemptive) Synonymous mutations are able to be selected, as they affect speed of translation and protein folding due to stalled ribosomes.

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