Jeffb asks for examples of beneficial mutations

Yes, this is the one I was referring to. I was being lazy and didn’t feel like looking up what I was called - N501Y.

It doesn’t discredit Sanford’s ideas as far as I understand his hypothesis. There can be increased fitness in the model in the initial evolution of the strain - Fitness will just decrease eventually as mutations accumulate.

I had read the Vox article earlier. It definitely was the best popular article I’ve read on the subject. I’m definitely trying to keep up anything new written about it. If I find anything of significance I’ll post it. :slightly_smiling_face:

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But there is the usual problem with this. Was the initial baramin a benevolent virus perfectly created 4004 BC, or the pandemic inducing monster unleashed in 2019? Given the accumulation of mutations, in Sanford’s model we have past extinction, not present virulence. The unleashing of this plague does, however, fits perfectly well with evolutionary principles. And here the issue is more explicit, because recombination in corona is not as routine a mechanism as H1N1.

As for the mutations by which the virus has adapted to human transmission, do you really think that these are just “loss of function”, as in jettisoning clutter that was just getting in the way? Or from the standpoint of the virus, are real time examples of beneficial mutation and gain of function as per @jeffb OP?

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The lack of recombination makes this a better virus to examine observable evolution. That’s why it interests me; hopefully we’ll learn a lot more about viruses even through all the sadness of the pandemic because of all the sequencing being done. I’m very interested now to see how the science progresses based on what I’ve learned the last few months. So I did find @Timothy_Horton comments silly.

Not enough info to know, though some indications maybe the latter.

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I wonder if this is the type of thing that you had in mind, and if those qualified to assess this in the forum (not me) thought this would be an appropriate example: “A single splice site mutation in human-specific ARHGAP11B causes basal progenitor amplification” talking about a mutation leading to neocortex expansion of the brain.


I can see why the fitness of a highly letal virus may increase if its virulence decreases. But how could it be the case for a virus such as Sars-cov-2 who kills no more than 0,05% of the population and whose CFR is probably less than 0,5%?

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This is one of my favorite examples that has been discussed in other threads here on the forum. This example is clearly beneficial in the context, but also serves as an example of de novo gene generation.


Here is a cool example of a mutation conferring hypoxia tolerance in a group of humans whose culture is intimately associated with water and diving:


Ah, that’s a good one! It also reminded me of this.


I don’t know how you got that idea:

Its behavior to date is consistent with what we know about virology. If it interests you, there are decades of studies that have been done and are highly relevant.


@jeffb, here’s a mind-blowing and clinically important example of the complexity of the science, which does not neatly fit your very stereotypical (sorry, can’t resist) request. The human MYH7 gene encodes the primary cardiac myosin that is also the major myosin in slow-twitch skeletal muscle. It is incredibly polymorphic:

1189 entries on 2 pages.
Unique variants in the MYH7 gene - Global Variome shared LOVD

While many of the variants are listed as “pathogenic” in this table, most dominantly causing inherited cardiomyopathy, with only a few exceptions their penetrance is very low, meaning most people with them are healthy. A simplistic understanding of evolution would predict extreme conservation, not polymorphism.

In your view, what hypothesis explains this polymorphism? I have an unpublished, empirically testable one.

The great thing about this case is that there’s really nothing one can copy/paste to address it. You know, the most devastating rebuttal conceivable would be for you to simply ignore what you perceive as sniping and dig into the science…


Agree that the baseline here is such that decreased virulence would not be as big a factor as transmission with regards to the fitness of this virus. But as a species, we are not very tolerant of even those numbers, so payback is coming for Sars-cov-2.

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Virulence cannot be reduced to mortality. It includes morbidity.


Sure. Let’s see if we can figure out how far to extend the x-axis to the right so we can place a 50-60% increase in transmissibility mutation. I’m pretty sure a mutation with an effect of that magnitude shouldn’t even exist according to Sanford. One has to wonder when mutation are supposed to result in a net fitness loss if mutations of beneficial effects of such magnitude keep occurring. 100 million years from now?



Here’s another fine example of beneficial mutations at the protein level:

McCracken KM et al. 2009. Signatures of high-altitude adaptation in the major hemoglobin of five species of Andean dabbling ducks. Am. Nat. 174(5):631-50.

Of course one can’t say these are mutations unless one allows that ducks are related by descent. @jeffb needs to define the limits of the “kind” before we can talk about most of the evidence for such things.


You and I both know this % increase number is probably reckless. It’s based on modeling, which could be a founder effect or chance. There’s some information it is more prevalent in kids so I wonder if it gained function to infect kids more readily. That means there’s a huge population that wasn’t getting infected very easily but now is. Anyway, there’s too many unknowns to draw conclusions. It may not even have increased fitness at all and it could all be hype. I’m doubting that too, but it’s still within the realm of possibility.

I would anticipate this will fall under the Jeanson’s speciation by heterozygosity. So then a YEC “duck baramin was created with high-altitude heterozygosity genes in reserve” clause. Voila, variation with limited common descent, unstained by beneficial mutation.

Don’t forget to also narrow the “No Selection Zone” from an effective population size of ~10^3 to an effective population size of ~10^7.

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We don’t, but I’d be happy to say the number is subject to change as more data is collected.

Of course, even at a mere 10% increase it’s still essentially outside the realm of possibility given Sanford’s “Correct distribution”. You’d have to extend the x-axis to be over 50 times wider than what is shown. Please try to calculate the probability of a mutation with a fitness effect of 10% given an exponential decline, with that depicted curve for beneficial mutations Sanford has drawn inside the “zone of no selection”.

At one tenth of one hundreth of a percent increase in fitness, Sanford has drawn the curve at effectively zero probability that a mutation has so large a positive effect. He clearly considers it so low as to be impossible to even show on a figure. So how infinitesimal must the probability of a mutation with a 2%, or 5%, or 10% increase in fitness be in his imagined reality?


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