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ERV’s challenge to Michael Behe

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[continued from Dr. D.A. Cook’s thread, Where Did Sea Anemones Get Human Genes?]

Michael Behe has certainly given his critics a thrashing at his Amazon weblog. When I saw Mike taking Ken Miller to task for Miller mischaracterizing Lipids as Proteins (a sophomoric mistake by Miller), I knew Mike was slamming the best the Darwinist could muster onto the floor. Behe single handedly defeated Ken Miller, Sean Carroll, Jerry Coyne, Michael Ruse, and Richard Dawkins, and thus earned the title “Darwin Slayer”.

But there have been minor skirmishes between Behe’s supporters and detractors. One such skirmish was between Casey Luskin of the Discovery Institute and Abbie Smith of the ERV weblog. Abbie is an AIDS/HIV researcher. We’re pleased to have Abbie visiting with us, and I’d like to grant her a fair hearing regarding what she has to say, especially since she is a scientist in the field.

The skirmish involved this post at Pandas Thumb ERV & HIV versus Behe. Behe loses.

Later Casey Luskin joined in with: Pandas Thumb Fails to Refute Michael Behe on HIV Evolution.

I invite discussion and research on the topic. I am aware of one minor error in Mike’s books, so I’m glad to help the editorial process for any subsequent editions, and if Abbie has some useful corrections to suggest, I certainly welcome them.

I’d like to thank Abbie Smith for volunteering her expertise and time in providing public peer review for the work of one of today’s leading thinkers in the origins discussion.

Comments
Here is a very peripherally related article. (since we are estimating probabilities in various places) A biologist has made a calculation on what he calls the "origin of replication and translation" or OORT. This an euphemism for the OOL. 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.jerry
September 3, 2007
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Patrick: "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??PaV
September 3, 2007
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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.Patrick
September 3, 2007
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Very good point PaV. Everyone who has actually read EoE is aware of the fact that Mike is mainly arguing about cells with high DNA content. At this point a question arises; did PT crew and people blattering about "fatal flaws" really read the book they are acritically attacking? Only 0.0000000001 cent for the correct answer ;-)kairos
September 3, 2007
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I've been over at ERV's blog trying to discuss her 'challenge'. ERV has been, for the most part, AWOL. (In her defense, she's a student. OTOH, she's started up a thread or two in the meantime). 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 3x10^-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?PaV
September 2, 2007
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And the strenuous objection
"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."
Charlie
September 2, 2007
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DaveScot, I remember it well. It is the origin of the "liar liar, pants on fire" objection.BarryA
September 2, 2007
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For the reader's benefit this phrase is a abmiguous:
“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.scordova
September 1, 2007
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In deference to Hermagoras I provide the following from here. ======================== 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 ======scordova
September 1, 2007
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Here is what I wrote at ERV ================================= 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?scordova
September 1, 2007
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Thanks Gareth, I truly do appreciate your insights into the weaknesses of my postulation. Yet, I will have to dig just a little deeper and "follow the evidence" to wherever it goes, and truly see what the empirical evidence may reveal about what I consider a very fascinating topic. Thanks again for your insights,,,I will definitely use them in my discernment of the evidence that is available on this matter!bornagain77
September 1, 2007
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bornagain77, you wrote: "Many of the diseases listed show the (constant?) decay curve before vaccinations, thus vaccinations are ruled out due to non-existence." Actually, that doesn't rule out vaccinations. It could just mean that other factors (nutrition, hygiene) began the decline and vaccinations added to the decline later. That is, after all, just common sense: get the easy wins first (get out the old disinfectant, chuck some fruit at the patients), then do the more involved stuff later as and when you have the medical capability. "The only options left on the table are nutrition, hygiene, general health care and Genetic Entropy. I believe hygiene, general health care and nutrition are “the easy way out” and don’t adequately explain the constancy we see in the graphs!" Well, I'll take the easy way anytime, especially when it comes to improving health! And we shouldn't forget Occam's razor: the simplest explanation typically being the best, it strikes me that hygiene, health care and nutrition fit the bill better. "If memory serves me correctly there are numerous diseases in mans history that have wrecked havoc and then quietly drifted into oblivion." True. Although they often have the ability to come right back at us (e.g. tubercolosis, typhoid, cholera) once we get complacent about our medical practices or some disaster strikes that leaves us unable to take as much care as we should. That suggests to me that genetic entropy is not a factor: once the disease is down genetically then it shouldn't make reappearances. " And very few such as leprosy that have had a continual presence with man and even leprosy may have followed a decay curve since it seems to be less prevalent than in ancient times." Which would also be explained by the other factors mentioned. "If an infectious agent was operating by evolutionary rules we would expect to see flare ups throughout history as the “evolutionary powerhouses” of infectious agents found novel protein/protein binding sites!" But that is what we DO see. Take a look at the graph you linked to, and check out the influenza line. That shows the spikes you would expect to see in an evolutionary scenario, and they appear all the way along the influenza history. The year 1919 in particular needs a lot of explaining if you want the keep to the genetic entropy theory. "We would probably also expect to see a continual presence as the infectious agent eventually “found a evolutionary niche”. Yet we see the infectious agents drifting into oblivion. This is not at all compatible with any evolutionary scenario I know of!" Yes, it is compatible - with extinction. Smallpox was effectively eradicated, but throught the control of the infectious agent rather than through genetic entropy. "My inference to Genetic Entropy comes from Dr. John Sanford’s book Genetic Entropy;2005. It is a powerful book and lists many studies establishing this foundational principle of biology! If you have not read it, I highly recommend it so that you may better understand the concept I’m postulating." Thanks, I'll add it to the (already too long)list of books for me to read. But as things stand, I think the graphs you put up are better explained by other factors.Gareth
September 1, 2007
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Barry The point about novice trial lawyers making a fuss over damaging evidence thus bringing more attention to it was made in a courtroom scene in the movie "A Few Good Men".DaveScot
September 1, 2007
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#128 Behe made an estimate. Personally I've figured for a while that a generalized maximum attributable to all cases would be 3 or 4. But it's still a fact that they're cherry-picking a preferred speculative scenario in order to attempt to make a point. Never mind that they're conflating the circumstances surrounding viruses with other cells and even higher organisms.Patrick
September 1, 2007
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kairos (#129). Indeed. Ms. Smith's behavior is akin to a mistake many young lawyers make when they make strenuous though clearly futile objections to evidence they know will come in. It is like say to the jury, "Pay close attention to what the witness is about to say. It is very damaging to my case."BarryA
September 1, 2007
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#121 Sal
Ms. Smith responded: “You stupid, stupid cow. I suppose ‘Piss off’ was too hard for you to understand too?”
As an addendum to my previous message, also this kind of reaction is highly welcome to show to the undecided who's really in pain in this debate.
I have no intention of proceeding. I will let your comrades pressure you to say YES or NO. Of course, which ever way you answer you know I’ll be able to successfully take issue. If you say YES, I will win the argument. If you say NO I will win the argument. If you avoid the question, you avoid the coup de grace.
This is one of those situations in which I love aristotelaen logic .-Dkairos
September 1, 2007
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#125 BarryA
Just admit the damaging fact as quickly as possible and make him move on, because when you dance and squirm you are just drawing attention to the damaging information without doing yourself any good.
This is one of the reason why the behavior of people such as ERV has to be welcome.kairos
September 1, 2007
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Sal,,, art said over at ERV... So apparently Sal is of the opinion that the appearance, from scratch, of 4 "CCC"'s in an HIV lineage before it "found" humans does not contradict Behe. This is laughable. Dr. Behe clearly talks of observational data of HIV since the HIV is found in Humans. This 4 CCC claim is clearly not a violation of Behe's limit and to infer that the limit is violated is to go beyond the bounds of observational data and postulate the origination of the very point under debate. Thus ERV's claim of a violation of Behe's limit is based on her own philosophical bias in interpreting the "suggestive" evidence and is not based on actual observational evidence! Since ERV has gone beyond observational data, ERV has no case against Dr. Behe!bornagain77
August 31, 2007
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Gareth you wrote: These are interesting sites, but I’m not entirely sure I understand what you are saying. There are other potential (and perhaps more likely) factors that may be involved here, such as better vaccines, nutrition, hygiene, general health care. Many of the diseases listed show the (constant?) decay curve before vaccinations, thus vaccinations are ruled out due to non-existence. The only options left on the table are nutrition, hygiene, general health care and Genetic Entropy. I believe hygiene, general health care and nutrition are "the easy way out" and don't adequately explain the constancy we see in the graphs! If memory serves me correctly there are numerous diseases in mans history that have wrecked havoc and then quietly drifted into oblivion. And very few such as leprosy that have had a continual presence with man and even leprosy may have followed a decay curve since it seems to be less prevalent than in ancient times. If an infectious agent was operating by evolutionary rules we would expect to see flare ups throughout history as the "evolutionary powerhouses" of infectious agents found novel protein/protein binding sites! We would probably also expect to see a continual presence as the infectious agent eventually "found a evolutionary niche". Yet we see the infectious agents drifting into oblivion. This is not at all compatible with any evolutionary scenario I know of! My inference to Genetic Entropy comes from Dr. John Sanford's book Genetic Entropy;2005. It is a powerful book and lists many studies establishing this foundational principle of biology! If you have not read it, I highly recommend it so that you may better understand the concept I'm postulating.bornagain77
August 31, 2007
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Jehu, I conceded your point to a certain degree in my original post, Knowledge and prevention do play a large role in declining numbers! Yet the most important point I'm making is that the mortality transition is smoothly downward for all the other diseases in this graph; http://www.healthsentinel.com/graphs.php?id=23&event=graphs_print_list_item This should not be so! If "evolutionary powerhouses" can't cause a ripple here then it is very a strong indication that no "dramatic" evolution is occuring in the infectious agent itself. This is further evidence that indicates very strongly that no new protein/protein binding sites are being found! A novel binding site, if truly as common for Darwinian evolution to find as evolutionists claim it is, (hippos into whales don't forget) then we should clearly see its effects with a fluctuating mortality rate for all diseases that are in the study. It should definitely be a very noticeable characteristic on these graphs! Also, though I concede education and prevention an important role in the decline, Genetic entropy is still very much on the table as a contributing factor to the gradual decline we find in all the other diseases plotted on the graph! In other words I find the existing data sufficient to warrant this inference!bornagain77
August 31, 2007
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Sal, I was in court today and I thought of your little dust up with Ms. Smith. I had a hostile witness pinned down; whichever way he answered the question he looked bad (trapping witnesses on cross is one of the most satisfying experiences in the practice of law). He knew this; I knew this; his lawyer knew this; most importantly, the judge knew this. So what did the witness do? Of course, he danced around. In my experience very rarely will a witness allow you the ultimate pleasure of the coup de grace. On the other hand, it is good to realize that all you are seeking is just that (i.e., pleasure, the emotional satisfaction that comes when someone finally admits the truth). As far as the truth is concerned, it is out and plain for all to see. So I tell my clients that when the other side pins you down, don't squirm or dance. Just admit the damaging fact as quickly as possible and make him move on, because when you dance and squirm you are just drawing attention to the damaging information without doing yourself any good.BarryA
August 31, 2007
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bornagain77, HIV hasn't become any less contagious. It is spread the same way it always has. True, it hasn't become an air born pathogen but it hasn't lost any contagiousness either. Any decline in the spread is do to preventative measures and changes in behavior.Jehu
August 31, 2007
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http://pathmicro.med.sc.edu/lecture/sc-stats.jpg The above graph is example of how the overall HIV mortality rate should look world wide. Notice the gradual decrease in time after the initial rapid rise..This finding matches the (constant?) slow decay of the "old" infectious diseases in this following graph. http://www.healthsentinel.com/graphs.php?id=23&event=graphs_print_list_item Some may argue that prevention and education played a large role, And indeed, to a certain degree, I will buy that. Yet the main point is that if the "mutational powerhouses" of infectious agents where truly finding novel protein/protein binding sites then there should be noticeable spikes in the graphs for various infectious agents as we go through time. Yet this is not what we see, we clearly see a nice, clean, and fairly smooth gradual decline. I steadfastly maintain that the infectious agents are NOT FINDING ANY novel protein/protein binding sites as stipulated by Dr. Behe and are in fact losing demonstrable potency as infectious agent in large part due to the degradation of their genome through time! (Genetic Entropy; Sanford, 2005)bornagain77
August 31, 2007
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Sal and tribune7 (or other following along)... I haven't been able to keep up with the developments concerning Ms. Smith's paper...I just have been catching glimpses of the exchange here and there...so: Since, Sal, you have declared that if your questioned is answered either "Yes" or "No", you will win the argument, will you write up a post showing the details of this? A refutation paper of sorts, showing how her paper fails on either count, so therefore, the paper is erroneous. I, for one, would appreciate the recap. It will also be a clean place to point to when people link to Abbie's PT paper. Just a suggestion.Atom
August 31, 2007
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Below is the latesest, and I really should go. Have a nice weekend everyone. May the Wedge of Truth be with you. ========
With respect to the question: "Is it Ms. Smith's premise that Vpu existed in HIV prior to entry into humans?" Ms. Smith responded: "You stupid, stupid cow. I suppose 'Piss off' was too hard for you to understand too?" Does that mean YES? YAY! I was right, Vpu existed in HIV before it entered humans. But just to be sure, when you said, 'Piss off', that was an admission that: "Vpu existed in HIV prior to entry into humans?" Right? YES or NO? If you say YES, then I can move forward with Hermagoras's objection, but until you acknowledge "Vpu existed in HIV prior to entry into humans?" I have no intention of proceeding. I will let your comrades pressure you to say YES or NO. Of course, which ever way you answer you know I'll be able to successfully take issue. If you say YES, I will win the argument. If you say NO I will win the argument. If you avoid the question, you avoid the coup de grace. Such is life when one must protect and indefensible position and admit an essay published at PT was erroneous and too hasty in its conclusions. Oh well, have a nice labor day weekend. The question remains: "Is it Ms. Smith's premise that Vpu existed in HIV prior to entry into humans?"
scordova
August 31, 2007
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I suppose ‘Piss off’ was too hard for you to understand too? A classy lady :-)tribune7
August 31, 2007
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What! Ms. Smith said "YES" --- Uh actually she said here:
"Is it Ms. Smith's premise that Vpu existed in HIV prior to entry into humans?" You stupid, stupid cow. I suppose 'Piss off' was too hard for you to understand too?
Why Ms. Smith, does that mean YES. :=) Maybe her friends are realizing we're just getting too much good mileage out of this. Hermagoras said:
So the answer to your question is Yes
The question remains to Ms. Smith, “Is it Ms. Smith’s premise that Vpu existed in HIV prior to entry into humans?” YES or NO? And contrary to Hermagoras claims, it is highly relevant, but I see little point in going on until MS. Smith grants the coup de grace and admits I'm right. She can say so by simply saying, "YES". :-)scordova
August 31, 2007
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It looks like they finally answered, btw. YEStribune7
August 31, 2007
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“Let your ‘Yes’ mean ‘Yes,’ and your ‘No’ mean ‘No.’ Anything more is from the evil one.” Yup.tribune7
August 31, 2007
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But they can’t even give a yes or no.
Do you remember the following phrase? "Let your 'Yes' mean 'Yes,' and your 'No' mean 'No.' Anything more is from the evil one."kairos
August 31, 2007
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