Well yes, all this begs the question that the outcome is in doubt at all - which it isn’t, as Dawkins demonstrated with WEASEL. We also have a problem with basic probability calculation (which I feel duty bound to try to sort out 
).
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Some binding != binding specificity. So it is new.
You yourself claimed that Exon-1-encoded Sia-recognizing domains of human and ape Siglec-9 was an example of a new protein-protein interaction, even though your referenced paper was discussing the evolution of CD33rSiglec binding specificity.
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Technically, you don’t understand undergraduate biochemistry, as affinity (the amount of binding) is not the same as specificity.
He is not. He even admitted that he hadn’t read the relevant immunology literature UNDER OATH.
But he’s not doing that, and it’s not a justification for ignoring how evolution works, because the immune system uses random variations (which are not limited to mutation, but include mutation).
Do you not realize that many of us have far more and more relevant expertise and experience than Behe?
So what? Does you not being aware of something mean that it does not exist? How much of the primary HIV literature have you read, Lee?
But Behe ignores them in his silly calculation.
I don’t see that they were required to be simultaneous, as Behe claimed.
Again, how much money are you willing to bet that there is no data showing that a single mutation confers measurable resistance? How much faith do you really have in Behe?
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The distribution of the outcomes of rolling a die twice, or two dice simultaneously, being the same set of outcomes in both cases.
No, I don’t have successes in mind, I’m only insisting that rolling one die twice, or two dice once, gives the same set of outcomes.
I try to respond to your posts, and everybody else’s posts point by point.
No, I was asking, not claiming.
I got off track, I would mean affinity, are we still talking about the paper by Wang? "Viruses might take advantage of this low affinity to invade a host cell by evolving a stronger binding affinity to the surface receptors than that associated with physiological ligands.”
But he did say that the advantage of scientific publications is that you can read recent papers and get a good idea of the state of the art, without reading all the past publications.
Have you read his book? His argument is about how evolution works, one of the chapters is entitled “What Darwinism Can Do.”
That’s fine, but Behe’s arguments are still out there to be evaluated.
Well, I expect if someone I have discussed Behe’s ideas in the past was aware of this in HIV, I would have heard of it, early and often.
What do you keep referring to as Behe’s calculation, specifically?
You may need to explain what a ‘distribution’ is in statistics, I don’t think @lee_merrill is familiar.
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And yet you didn’t respond to my points in the post I was talking about. And you appear to understand nothing about quantitative characters or genetic variance, notably as they apply to Nilsson & Pelger.
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That’s utterly false.
Here are some of my points to which you have not responded:
Please respond to those.
You’re trying to avoid the track, from my perspective. What are the mechanisms underlying what evolution actually does?
How can you talk, in good faith, about a paper you haven’t read?
That’s not responsive, as Behe hasn’t read recent papers either.
Yes. It’s ludicrous.
And it’s full of misrepresentations.
You didn’t answer the question. Behe’s arguments cannot be evaluated without familiarity with the relevant evidence, which you avoid.
Given your record here, you could have heard of it 10 times, but still not acknowledged it.
The one you referred to as his calculation, of course.
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Glad to catch up if I missed something important.
We have discussed Nilsson and Pelger’s paper extensively, I do still think it’s going to be difficult to complete 1800 steps in sequence, especially repeatedly in multiple populations.
And they don’t even address the corresponding neural changes that would be needed for vision!
But again, Behe is observing what evolution did, which includes intermittent selection.
And Behe is observing what evolution did, which includes all these factors.
No, the truth about the disease is important, and I’m sure Behe cares about this.
Mutation and natural selection, primarily, but there can be other factors too, such as you and others have listed.
Because the abstract seems clear.
Now you’re just starting to be pejorative. How do you know this?
But these are not arguments.
i mean Behe’s calculation of two mutations required for resistance, due to observing (not modeling) 1 in 10^40 organisms. But you seem to be thinking Behe is modeling evolution, and producing a number from a model.
All that shows is that you haven’t read much of what I’ve told you. I don’t know if it’s worthwhile repeating anything.
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They don’t need to be done in sequence. That’s the thing you’re missing. The ~1800 number is the number of 1% changes. Many of the stages of evolution require many combined 1% changes to a single feature. But you could have 100 such mutations occur in a single generation, and then combine through recombination. So there is no need for them to be sequential.
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Note that 1% is an arbitrary figure used to facilitate computation. It’s not supposed to be the result of a single mutation or, in fact, of any mutation at all, just selection acting over some number of generations (and that number is computed in the paper) on existing quantitative variation. Mutations aren’t mentioned, and their only importance is that selection reduces quantitative variation, so evolution will eventually stall out unless mutations recharge that variation. Eventually.
And the steps (which, remember, are not mutations) are sequential by definition, each step being a 1% change from the immediately previous state. But again, this isn’t 1% in one generation but is summed over many generations.
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Behe has observed nothing of the sort. He stopped publishing in the primary scientific literature 27 years ago. Your retort is incoherent, because the question is Behe’s claims about the mechanisms underlying what evolution does, which are laughable. That’s why you don’t even try to support them.
Please stop repeating falsehoods.
False. Behe is misrepresenting the work of others regarding how evolution did what it did, while making zero observations himself.
Please stop repeating falsehoods. It doesn’t make them more credible.
I’m not. Neither of us knows him, so we can only judge by his action or inaction. He stopped doing any science long ago.
Why does Behe pretend that these are the only two, then? Is that honest? Competent?
You were making claims about what was NOT in the paper. You can’t possibly make such claims in good faith without reading it.
How does bearing false witness help to support a religion that commands us to not bear false witness?
He admitted it under oath.
Speaking of pejorative, what about your claims of understanding genetics, virology, and biochemistry better than I do?
Correct, arguments are not misrepresentations. Arguments that depend on misrepresentations, like Behe’s and yours, are ludicrous.
Behe has observed no organisms. He doesn’t even read the relevant primary literature. Please stop repeating falsehoods.
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It’s true that one can consider rolling one die twice as equivalent to rolling two dice once. But that equivalence is lost when considering longer sequences of rolls and different collation of outcomes, both of which apply to your eye evolution scenario.
That is not true. You have never provided a total number of lineages, only a total number of organisms.
Either you’re completely missing the point, or you’re now saying that every population would evolve eyes. The futility of engaging you is clear in either case
If you can’t work it out, no explanation would help.
It’s very germane to the current discussion.
You are making claims about the probability of eyes evolving. If you can’t even manage the much easier calculation of the probability of drawing a full house in poker (and your avoidance of the question and the ineptness shown in your other calculation attempts suggests that you can’t), then more complex calculations involved in eye evolution are beyond your ability and the claims you make about them are baseless.
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Please explain how Behe observed that chloroquine resistance occurred only once in 10^40 organisms, if that is the total number there have been in all life’s history.
Did Behe, for instance, observe that chloroquine resistance did not evolve in trilobites? Or in Albertosaurus fleas? I’m fairly sure Behe wasn’t around to observe whether Arthropleura was chloroquine-resistant.
Or have you merely forgotten your own previous claims, as usual?
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Depends on the model. If you roll 20 dice at the same time the chances of having two matching sixes is much higher than when you roll just 2 dice. It is also much easier to match two sixes if you start with 20 already rolled dice and only need one more six.
You keep forgetting that the vast majority of adaptations are not limited to just two mutations. You also ignore all of the existing genetic variation in a population as well as the accumulated genetic diversity over the 100’s of millions of years in any given lineage.
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Those calculations would only apply to that one adaptation in that one species with that specific genetic background, not to all life and all adaptations.
Can Behe or any ID proponent point to a specific known adaptation that involved the appearance of specific mutations which could not occur through evolutionary mechanisms? If you are going to cite something like the bacterial flagellum, then we need to see the exact DNA sequences before and immediately after the feature appeared and the list of mutations that were required.
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