It is at

http://www.biology-direct.com/content/2/1/15

As a conservative estimate he calculates 10^-1018 for the possibility that such a system could have arisen.

Someone might want to start a thread on this and also unpack all his assumptions. This is a pro Darwinist who presented these calculations.

“I haven’t had a chance to read everything involved so a comment from one of the Darwinists had me under the impression they were discussing four a.a.s.”

The two a.a.s have to do with one of the interactions with CD4+. But the claim is that there are other mutations, CCC’s, if you will, that have also occurred.

As I pointed out in my earlier post, the probabilities of a two a.a. change (or its equivalent) is not 10^20 in HIV. As well, there’s the question as to whence the vpu in HIV-1—was it from the M2 gene of Type A influenza or not. And, then, finally, what was the point that Behe was making? Well, he was saying we don’t see any “biochemical novelty” in HIV. It replicates the same. It has the same gene component. It enters the cell in the same way, etc. Where Behe certainly opened up a can of worms when he addressed HIV (almost in passing), I think his remarks, if properly understood, are correct. I mean, how interested are we, really, in the “biochemical life” of viruses. Now, certainly we should be as far as the human damage they inflict. But for an understanding of how life began, how life evolved, I, for one, am certainly more interested in what eukaryotic cells do.

If looked at in context, this whole imbroglio about HIV only points out the desperation that Darwinists must feel. If you have to resort to the “amazing” changes that have taken place in HIV to defend Darwinism, well….. I think you have to be in pretty bad shape. IOW, where are their examples from eukaryotic life? Where??

My brief literature search suggests to me that in some of the changed interactions between host and HIV that ERV mentions, that the “essential” changes (remember, there can be lots of so-called “neutral” substitutions) involve two a.a.s. Rather ho-hum, don’t you think?

Thanks, PaV! I haven’t had a chance to read everything involved so a comment from one of the Darwinists had me under the impression they were discussing four a.a.s.

In any event, it seems to me that there’s several issues involved here.

ERV’s basic challenge–although it wasn’t formally accepted as such on her blog–is that, contrary to what a.) Behe says in EoE, and contrary to what he should clearly have been aware of, b.) HIV presents an example of multiple protein-to-protein binding sites (4) in c.) much less the number of replications in a CCC (10^20), thus d.) falsigying Behe’s claims.

I’ll start with d.) and work backwards.

The argument Behe makes in EoE deals exclusively, and consistently, with eukaryotic cells. Viruses aren’t even classified as “life”. We’re not even dealing with prokaryotic life. So, to take what Behe claims about “cells” (meaning eukaryotic cells) and then to turn that around and claim that this is falsified by what is found in a virus, is, I believe, to completely miss the point of the book. Behe wants to compare the number of replications (progeny) that eukaryotes need simply to come up with a two a.a. change to its genome (in the case of the malarial parasite) to the number of mammals that have ever arisen. If an argument is to be attacked, that’s where one should start.

I think this is so self-evident, that I won’t comment any further.

As to c.)—where it is being claimed that novel complexity is seen occurring in far less replications than a CCC (10^20)—I think we have to step back and remember point d.), that Behe claims a CCC limit in eukaryotic cells—not in any kind of virus; and then we need to try and remember how Behe arrived at his CCC in the first place.

His CCC is based on a review written by Nicholas White. In that review, quoting EoE, White “[multiplied]the number of parasites in a person who is very ill with malaria times the number of people who get malaria per year times the number of years since the introduction of chloroquine, then you can estimate that the odds of a parasite developing resistance to chlorquine is roughly one in a hundred billion billion. In shorthand scientific notation, that’s one in 10^20.” (p. 57)

Now, to get an idea of Behe’s thinking on this, here’s what he wrote on p. 59:
“The odds [of achieving atovoquone resistance and of chloroquine resistance] are, respectively, one in a trillion (10^12) and one in a hundred billion billion (10^20). The ratio of the two numbers shows that the malarial parasite is a hundred million times (10^8) less likely to develop resistance to chloroquine than to atovaquone. This is reasonable since the genome size of the malarial parasite is in the neighborhood of a hundred million nucleotides. The implication is that if two amino acids in a protein have to be changed instead of just one, that decreases the likelihood of resistance by a factor of about a hundred million.”

As I pointed out at ERV’s blog, it’s quite obvious that Behe sees a connection between genome size and the level of improbability of getting particular point mutations in that same genome. But why, then, isn’t the CCC one in 10^16 (i.e., 10^8 for the first mutation, times, 10^8 for the second), and not, as Behe presents, one in 10^20? Well, it’s because Behe is using actual in vivo numbers. The fact is that the in vitro (what is seen in the lab) resistance to atovaquone is one in 10^10 or lower, but because of some kind of in vivo (the more life-like scenario) effect (for some of the reasons that White points out in his paper, and especially host immunity) inerfering with the development of resistance to atovaquone. So we end up with one in 10^20. But Behe’s remark about one in 10^8, linked as it is to genome size, makes it legitimate (in my view, at least) to sort of guess how Behe would approach the case of the virus. In EoE, he tells us that the mutation rate of the HIV virus is 10,000 greater than eukaryotes (which ought to be a warning about comparing the two). The figure, per Wikipedia, is in the area of 3×10^-5. The actual genome of HIV is roughly the inverse of this number. For two mutations, then, a simple calculation would be (3 x 10^-5) x (3 x 10^-5)= 9 x 10^-10=approx. 10^-9. Well, this 10^-9 number is the very number that Ian Musgrave (I believe it was he who made the calculation) gives for HIV-1 and the changes it has undergone. I hope this makes clear that it would be wrong to simply carry over the one in 10^20 CCC number that Behe uses for eukaryotes and apply it to the case of HIV.

Let’s now discuss b.): HIV presents an example of multiple protein-to-protein binding sites. Again, the starting point has to be EoE. It is very clear that Behe was talking about protein-to-protein interactions arising within the eukaryotic cell. If you look at his book, and the language that he uses, he’s always talking about the “cell”. Well, HIV isn’t a cell. For most scientists, it doesn’t even represent “life”. But what one also finds is that Behe is preoccupied with the development of novel cellular structures. In the case of P. falciparum, the malarial parasite, the a.a. changes happened to IT. The PARASITE changed. Two transporters have changed, allowing IT to survive. In the case of HIV, the vpu protein has changed, protecting it from the human immune system, in fact debilitating it. But the effect is exogenous, not endogenous, as in the case of P. falciparum.

Now this could be misconstrued as being too nitpicky: what does it matter if the changes are inside or outside? Well, to be consistent with Behe’s argument, it should technically consider only internal changes. When Behe addresses HIV, he says he see no novelty in it, meaning, I’m rather sure, that you have the same complement of genes now as you did 50 years ago; and, if you look at HIV microscopically, it doesn’t appear to be any different than before. This, pretty much, is what a.) is all about: simply understanding what Behe meant in his comments about HIV.

But, for the sake of the argument, let’s leave this solid understanding of Behe’s argument to the one side, and simply begin to examine just how many a.a. substitutions are involved in the changed function of vpu in HIV-1 versus, let’s say, vpu in SIVcpz. The first thing we have to consider is just how highly variable HIV is, as Behe rightly points out. Wikipedia says this: “HIV differs from many other viruses as it has very high genetic variability. This diversity is a result of its fast replication cycle, with the generation of 109 to 1010 virions every day, coupled with a high mutation rate of approximately 3 x 10-5 per nucleotide base per cycle of replication and recombinogenic properties of reverse transcriptase.”

HIV’s genome size is in the tens of thousands of nucleotides—very small. So, at 10^9 to 10^10 virions per day, and with the high error rate associated with reverse transcriptase (HIV’s genome is basically RNA, which is then “transcribed” [in reverse fashion] to DNA) all kinds of things can happen to HIV in very short order. So why should we be surprised that vpu in HIV is different from that of SIVcpz? There are all kinds of possibilities that can be explored mutationally in any of HIV’s gene complement. But, again, what about genetic, biochemcial novelty? Do we see it? Well, no. What we do see, though, are changes in the effects its gene’s products have on its hosts; and, thus, its survivibility. Yes, it’s NS at work. And so it would be no surprise at all that different “types” (subtypes) of HIV could co-exist. And they do. Again, no surprise here. Well, what about these changes, what’s involved? How complex are they? My brief literature search suggests to me that in some of the changed interactions between host and HIV that ERV mentions, that the “essential” changes (remember, there can be lots of so-called “neutral” substitutions) involve two a.a.s. Rather ho-hum, don’t you think?

I must confess, though, that what was not so ho-hum, and which actually startled me at first about ERV’s claims was that vpu (she writes Vpu; BTW, this stands for viral protein U) HIV’s vpu, that is, could now form an “ion-channel”, and that it did so by forming a viroporin (a composite structure). Well, this deserved some examining. And upon a very brief examination (you can look here and here, for example) interestingly, vpu is found to be structurally similar to the M2 gene of Type A influenza, and, in turn, M2 proteins, more or less, spontaneously form “ion-channels”. This then brings up the whole question as to whether what makes HIV the unique virus it is (different, that is, from the vpu in SIVcpz), is that somewhere along the line, whether in a human or a simian, it replaced its original vpu gene with this M2 gene. HIV is known to form hybrid viruses. M2 is also known to interact with CD4+T-cells. So, are we dealing with a case here where two viruses swapped genes? In all honesty, I can’t say (and I have no desire to spend all the time and effort that would be needed to run this down); but what little I have looked at is very suggestive. In Dembski’s terms, maybe all we’re seeing is the Law of Conservation of Information at work, where the information of the M2 gene is simply being “added” to that of SIV/HIV (really, replacing the previous information with this different information). I’m sure our Darwinian friends would strenously disagree with this view. But I don’t think it unreasonable in the least. I think the burden of proof is on them to demonstrate unequivocally that vpu does not have its origins in M2.

To summarize, then, the probability of a CCC occuring in a eukaryotic cell is far different from that of HIV. The challenges that ERV makes to Behe and EoE, fall outside the import of what Behe was saying about HIV in his book. The supposed novelty(ies) in HIV-1 may not, in some cases, be real novelties at all, but may in some way be linked to the phylogenetic history of the vpu gene itself. And, in those instances where some kind of novel interactions with the host are involved, in those changed interactions between host and HIV, what is seen represents, at least preliminarily, no more than an equivalent viral CCC; i.e., a two a.a. change within 10^9 replications of HIV.

[[As a kind of addendum to all of this, let me make a point here that I briefly alluded to at ERV’s blog. The current cry of OOL Darwinists is that DNA didn’t get everything started; that life began as a RNA-world. And they would argue that all that would be needed is for replication to start happening. Well, are those ingredients found in retroviruses, where you have RNA replicating itself at will? And don’t you have even much more than that, given that the replication takes place in an eukaryotic host which has an abundance of RNA and DNA among its constituents? Think of the speed of replication. Think of its high error rate (mutation rate). Think of its high recombinant rate. And what do we have after millenia of interactions between viruses and their hosts? Viruses and their hosts. And, viruses haven’t even made it to the starting gate: they’re still not considered “life”.]]

BTW, have we heard from kairosfocus since that hurricane swept through the Carribean?

“I strenuously object?” Is that how it works? Hm? “Objection.” “Overruled.” “Oh, no, no, no. No, I STRENUOUSLY object.” “Oh. Well, if you strenuously object then I should take some time to reconsider.”

“HIV-1 Vpu and SIVcpz Vpu are totally different genetically, biochemically, and functionally.”

Of course there are differences, but it is still Vpu, and what will be damaging to ERV’s case is the examination of similarities.

We of course can’t get to that point until Ms. Smith makes the concession of admitting that Vpu existed in HIV before it entered humans.

But she knows up front that I will call her on an equivocaqtion that was in the minds of some PT’ers when she made an appeal to HIV-2 to make it seem that HIV-1 developed a new Vpu gene after it entered humans.

I alluded to it here

From that point, ERV probably knew I would be able to successfully challenge her equivocation of the notion of “new Vpu gene”.

Hence, the central question:

“Is it Ms. Smith’s premise that Vpu existed in HIV prior to entry into humans?”

became more significant, and I would win the argument when she answered YES.

If she answered NO, I would win the argument simply because the evidence points to the fact the answer is YES.

Either way, Ms. Smith claims are discredited on empirical evidence and shown to exemplify equivocation, mis-interpretation and faulty inferences.

I am perceived by the other side as loathsome because my rather unsporting behavior of rubbing it in.

She could make a retraction, but we are aware of the “Zero Concession Policy” that are in their operating guidelines, so I’m not expect ERV to make a retraction.

========================

Hermagoras said:

“And then you do the same thing again. After I’ve asked you not to.

It’s a simple request. Let me say it again: quote the whole of my answer or don’t quote. It’s irresponsible. ”

My apologies Hermagoras, allow me to make a remedy. I will post this at UD as well along with links to this discussion in deference to you, so they can see everything in exact detail from the source of the discusison.

Hermagoras said:

======

Hey, Sal: I already spelled Yes, and I already clarified it for you. Let me repeat it, with added emphasis:

my understanding from ERV’s first post is that the novelty is found in HIV-1 Vpu, and that, as ERV puts it, “HIV-1 Vpu and SIVcpz Vpu are totally different genetically, biochemically, and functionally.” So the answer to your question is Yes, but it’s not a relevant question, and never was.

10:10 AM
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=================================
I asked:

“Is it Ms. Smith’s premise that Vpu existed in HIV prior to entry into humans?”

YES or NO?

Hermagoras said: “YES”

Smokey said:

“she’s already answered it already”

She may have, but I guess I’m a a little slow, Smokey, and I probably missed it, so can you spell it out. Did she say YES or NO?

Could you clarify the matter for us and affirm that Hermagoras is correct that the answer is YES?

But a little re-iteration and clarification from Ms. Smith would be most helpful. I’m having to appeal right now to secondary sources like Dr. Hermagoras. I would prefer something more authoritative from Ms. Smith, wouldn’t you?

How about Dr. Hunt, I’m glad to get his opinion of what Ms. Smith’s answer was. Was it YES or NO?