Home » Darwinism, Intelligent Design » ERV’s challenge to Michael Behe

ERV’s challenge to Michael Behe

[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.

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145 Responses to ERV’s challenge to Michael Behe

  1. But there have been minor skirmishes … 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. …
    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.

    Certainly AS will receive a hearing fairer than in the PT’s and her site; but I suspect that she won’t appreciate your proposal. From the comments about him I think that she wouldn’t accept for Mike the definition of “one of today’s leading thinkers in the origins discussion”. But after all I find difficult to consider a student as “a scientist in the field” :-)

  2. If I can offer an observation of the diagram Abbie presented here:

    An Illustrated Guide to VPU

    That diagram is a supposed phylogeny (evolutionary history). It states that a new gene emerged just before getting inserted into humans. Is that correct.

    1. Did a new gene emerge AFTER getting inserted into humans

    2. Just for completeness, how do we know the phylogeny represents an emergence of a new gene and not a reduction of a pre-existing gene in the ancestral line leading to HIV-2.

    Phylogenies are prone to project the biases of the researcher, when in fact, all they have are sequence divergence measurements, not an actual timeline of events.

    Those would be good starting points.

    Salvador

  3. 1. Did a new gene emerge AFTER getting inserted into humans

    2. … how do we know the phylogeny represents and emergence of an new gene and not a reduction of a pre-existing gene in the ancestral line leading to HIV-2.

    Those would be good starting points.

    … or ending ones.

    Answers to 1.: NO ( => Mike is right)

    Answers to 2.: WE DON’T ( => Mike is right too)

    Sal, you are right; this is a minor skirmish.

  4. But after all I find difficult to consider a student as “a scientist in the field”

    But Panda’s Thumb, the leading light of Darwinian evolution on the internet, presented Abbie as important contributor to the discussion. I believe she’s the best PT has to offer on the subject.

    Any way, I’d appreciate hearing from Abbie. I hope she visits.

  5. … or ending ones.

    Answers to 1.: NO ( => Mike is right)

    Answers to 2.: WE DON’T ( => Mike is right too)

    Sal, you are right; this is a minor skirmish.

    Dang it. How can we keep the controversy alive in the public eye if we win these arguments with such ease. We gotta generate a little more drama than this.

  6. But Panda’s Thumg, the leading light of Darwinian evolution on the internet, presented Abbie as important contributor to the discussion. I believe she’s the best PT has to offer on the subject.

    Probably yes.

    “buy him for what he’s worth and sell for what he thinks he’s worth”

  7. “We gotta generate a little more drama than this.”

    But this would need other people to discuss with …

  8. Again with the circular reasoning:

    1. Something is different than how we saw something similar before.

    2. This change must have come about through neo-Darwinian mechanisms.

    3. Therefore, this difference proves neo-Darwinian evolution.

  9. Please hold off the snarkiness on this thread. ERV’s challenge is being held up as a simple, obvious refutation of Behe’s argument. Let this thread be a thorough, open, polite discussion on the merits (as scordova has properly initiated). The comments over at ERV’s website are snarky and childish. Don’t fall to their level. The style of how one argues speaks volumes about one’s intellectual ability, confidence, and trustworthiness.

  10. Smith has some major hurdles to get past to prove her point conclusively. I hope she comes and does debate her position on this blog. I will be very interested to watch the exchange.
    One thing for sure is that the truth will be hashed out to its most clear position and will not be covered over as it is on some other nameless blogs that could care less for free inquiry.

  11. I haven’t read Behe’s new book but I have read ERV’s post and Casey’s response.

    From reading those posts I get the “apples v oranges” feeling.

    Perhaps Dr Behe wasn’t clear enough in his book and ERV found a crack to wiggle in.

    Hopefully Dr Behe will respond.

    (from Dr Spetner’s PoV in “Not By Chance” he would call any gene duplication and subsequent modification and example of “built-in responses to environmental cues”)

  12. Zed, while there definitely is a mocking tone to some of these posts, they hardly compare to the venemous vitriole validated by the vicious vermin on the other side. I don’t see too many people actually saying, “God, what dumb s**ts those Darwinists are”, but that is exactly what passes for conversation in opposition sites. Ridicule is the proper response to a vacuous position, and at least here we don’t resort to name-calling (too often [ignore word "vermin" above {who are you to judge me anyway, I'm only human, geez}]).

  13. Zed,

    You of course are right. I meant no condescention aimed at Ms. Smith as I am a grad student myself, but because PT is UD’s mortal enemy, I couldn’t resist taking a pot shot at them.

    Salvador

  14. Sal, thank you for providing me a forum where I can answer your questions. That makes you two steps ahead of Behe. To answer your questions—fine. Lets say all viruses in the lentivirus family related to HIV-1 lost their Vpu. It probably cropped up millions of years ago—long before we were there with Qiagen kits to watch what was happening, so I will happily entertain that possibility*. HIV still does not have, quote, the ‘same number of genes.’ If we grant your premise, all branches of immunodeficiency viruses ‘lost’ a gene. ‘Same’ minus one. And, HIV-1 Vpu doesn’t look genetically or act biochemically like its ancestor, SIVcpz Vpu. They don’t ‘work in the same way.’ Behe is still wrong. Additionally, what has happened while we were watching is the evolution of the Subtype B and Subtype C sequences. Not only are HIV-1 Vpu sequences vastly different from SIVcpz Vpus, but B and C Vpus each have their own specific biochemical markers and specialties. We’ve watched that happen. Thus, Behe is still wrong. And we have barely scratched the surface of HIV evolution. Hes only going to get ‘more wrong’ from here on out. * We know Vpu is new in HIV-1 because of the directionality of necessity. As I referenced in my original essay, Vpu evolved in a very specific way in HIV-1 to overcome a cell specific and human specific host factor. Please see reference 10- I tried very hard to find PLoS/PubMedCentral references for this very purpose.

  15. Thanks for visiting this site Ms. Smith, I anticipate this will be a very interesting dialog.

  16. Sal, thank you for providing me a forum where I can answer your questions.

    You are more than welcome, and please alert me if any of your posts get caught in the spam buffer.

    My apologies for any snide remarks, they were not directed at you but some of my long-time sparring partners at younder site. It’s not my policy to be rude to my guests, and consider yourself my guest.

    Please feel free to add your datapoints here. I’m deeply appreciative, especially since it is your field of specialty.

    By the way, I am sincerely grateful for your involvement in the research of HIV and the treatment of AIDS. Although we may disagree on various issues, any one working to add to our knowledge base toward the healing of others is appreciated.

    regards,
    Salvador

  17. HIV still does not have, quote, the ‘same number of genes.’ If we grant your premise, all branches of immunodeficiency viruses ‘lost’ a gene

    That is true that the number of genes is different prior to the introduction into humans, but I believe Mike was referring specfically to human strains after the introduction into humans as he is trying to use the data gathered observationally to support his argument. He preferred to use directly observed evolution rather than using interpretations possibly biased by a preconception such as a phylogeny (an interpretation) superimposed on actual empircal data (sequence divergence measurements).

    Were new genes added to strains found in humans after the introduction into humans? It appears when HIV 1 was introduced into humans it already had the Viral Protein U (Vpu) gene in it. The Vpu protein did not emerge de novo after introduction into humans. Is that correct?

    I realize that Ian Musgrave provided a phylogeny diagram, but I just wanted to be sure I’m interpreting the diagram correctly.

    By the way, I appreciate your candor regarding the possibility of Vpu gene loss in ancient strains of HIV rather than gene emergence.

    Sincerely, I was quite ready to accept the possibility of novel gene emergence, because, surprisingly the work of James Shapiro almost suggests we should expect the emergence of novel genes.

    About half of UD authors are fans for front-loaded evolution, and such a development would be consistent with some of their ideas.

    regards,
    Salvador

  18. I believe Mike was referring specfically to human strains after the introduction into humans…
    You dont want to reinterpret what Behe said this way. HIV-1 and HIV-2 are entirely different creatures. Also, HIV-2 has a gene duplication– something Behe said ‘specifically’ hadnt happened in HIV.

    He preferred to us directly observed evolutions rather than using interpretations possibly biased by a preconception such as a phylogeny…
    How, exactly, do you explain the apparent phylogeny of primate lentiviruses, then? And, this doesnt help your case. Again, lets grant your premise– HIV-1 is not related to SIVcpz. HIV-1 and HIV-2 are entirely different creatures. This makes things worse for Behe.

    The Vpu protein did not emerge de novo after introduction into humans. Is that correct?
    Absolutely right, which I addressed in my essay: “Ah, Michael Behe, you might try to talk your way around Vpu now (though you were evidently unaware of its existence moments ago) by insisting that it is not *new* new.”

    By the way, I appreciate your candor regarding the possibility of Vpu gene loss in ancient strains of HIV rather than gene emergence.
    Anything is a possibility with HIV. But experimental evidence is normally used to figure out which possibilities are viable, and which can be discarded. Vpu is a new gene, not a ‘lost in everyone else’ gene.

  19. Also, HIV-2 has a gene duplication– something Behe said ’specifically’ hadnt happened in HIV.

    If he argues gene duplication didn’t happen, a charitable reading would indicate he was referring to HIV-1, not HIV-2, and further more he referred to HIV-1 only since introduction into humans.

    I think it appropriate for a book for a general audience to use language appropriate to the audience. When the general audience hears HIV, it is implicitly HIV-1, not HIV-2.

    Nonetheless, I understand your objection, but I think it is misplaced since Behe was not talking about observations of AIDs outside of the human strains.

    How, exactly, do you explain the apparent phylogeny of primate lentiviruses, then?

    They evolved via a common ancestral strain as a phylogeny would suggest, but as I pointed out, and as you conceded, the phylogeny does not necessarily say much as to when Vpu emerged or was deleted.

    Further, this evolution outside of humans is irrelevant to the analysis since Behe was not talking about primate lintivirus phylogenies.

    Again, lets grant your premise– HIV-1 is not related to SIVcpz

    That is not my premise, and I’m afraid you misinterpreted my position. That’s understandable since I don’t always express myself well.

    I did not say HIV-1 is not related to SIVcpz, it arguably is, I merely pointed out the assumption of novel Vpu after introdcution of HIV-1 into the human population was not indicated, in fact, contradicted even by the presumed phylogeny offered by Ian Musgrave.

  20. “But experimental evidence is normally used to figure out which possibilities are viable, and which can be discarded. Vpu is a new gene, not a ‘lost in everyone else’ gene.”

    If you do not mind, I would appreciate a link to PubMed, PLoS, etc., of such experimental evidence put forth in peer reviewed journals and any other references regarding phyologeny, etc., the two of you make. This will enable us to individually determine for ourselves the objectivity applied to HIV evolutionary history upon which either of you rely.

    Otherwise I feel I’m watching ping pong or tennis. Entertaining yes, but I desire the details of each volley and serve up to match point.

    Unlike tennis with a final score, evolutionary history changes daily for any number of phylum and I see it as a very subjective area of study influenced often by emotions.

    Thanks….

  21. erv

    Also, HIV-2 has a gene duplication– something Behe said ’specifically’ hadnt happened in HIV.

    Behe (EoE pg. 139) talking about HIV

    “No gene duplication has occured leading to a new function.”

    Consider this your first and only warning ERV.

  22. ERV,

    I’m trying to follow your argument.

    By way of background information, it would appear that vpu is similar to the mammalian TASK-1 gene according to sequence analysis. Vpu is also associated with SIV. Putting this together gives the impression that somewhere along the line, TASK-1 was included in the package of viral proteins in SIV (which isn’t a big surprise given the recombinant powers of IV), and was part of the package when the virus passed from simians to humans. TASK-1 codes for a potassium pump attached to the cellular membrane. One of the principal functions of vpu seems to be the release of the retroviruses from the cell membrane. This all seems to fit together.

    So, it’s easy to envision that a retrovirus that had five proteins, then scavanging a sixth (vpu), which gave it an advantage over the same virus minus this sixth gene. NS takes over, and we have HIV-1.

    Frankly, I don’t see how this affects Behe’s argument in the least. It appears that vpu is there from the start, and that it continues to do what it had done from the first time it was incorporated into HIV. What new function, what new “protein-to-protein” interactions have developed?

    It appears that there was an experiment done that pinpointed the critical a.a. residues for the vpu protein. There’s just a few. But given the reproductive rate, and mutation rate, of HIV, it would be well within a CCC to have several a.a. sites changed. Where does this argument go?

    Here’s what Behe says on pp. 138-139:

    As one study put it, “Each and every possible singlo-point mutation occurs between 10^4 and 10^5 times per day in an HIV-infected individual.” Every double point mutation, where two amino acids are changed simultaneously, would occur in each person once each day. (This means a chloroquine-type resistance mutation–where two particular amino acids has to appear before there was a net beneficial effect–would occur in each AIDS patient every day. Now that’s mutational firepower!) . . . . And exactly what has all that evolution of HIV wrought? Very little. . . . Over the years its DNA sequence has certainly changed. HIV has killed millions of people, fended off the human immune system, and become resistant to whatever drug humanity could throw at it. Yet through all that, there have been no significant basic biochemical changes in the virus at all.

    Yes, HIV’s DNA has changed. Vpu’s DNA has changed. But the virus is still no more than a virus, with several different forms of the basic vpu function competing with one another. That’s 10^20 viruses that have been generated—a number of individual organisms greater than all the mammalian forms produced throughout geologic time. AND, with a ‘mutation rate’ that is 10,000 higher than the mammalian lineage.

    As Behe says, “exactly what has all that evolution of HIV wrought?” Not much, it would appear.

  23. Sal– *quip, sorry* HIV-1 is not AIDS. You progress to AIDS after being infected with HIV-1. :)

    Again, I will grant your premise– Behe meant nothing happened in HIV-1 AFTER it was introduced to humans.
    Behe still has a de novo multiprotein complex to worry about, and several de novo protein-protein interactions. He says that hasnt happened. He even made a table to say it hasnt happened.

    I have never typed that Vpu is novel in humans. Its new in a branch of primate lentiviruses, again, look at reference 10. Its the sequence, biochemistry, and functionality that are different in humans.

    Michael– The number of phylogeny papers for HIV-1, 2, and SIV is massive (go to PubMed/PLos and search ‘HIV phylogeny’). The easiest thing would be to point you towards the Los Alamos National Laboratory HIV sequence database. There, you can get sequences to line up yourself, if you dont believe anyone!

    Dave– Yup! Thats the quote (I knew he said it at least once)! HIV-2 has a new gene with lots of fun functions.
    Here is a recent (free) paper on the topic!

    PaV– Sure! HIV-1 could have gotten Vpu from the chimpanzee genome! The sequence is so divergent (not only in humans, but in SIVcpz) that we have no idea where it came from at this point. Its not an obvious gene duplication like Vpx.

    But as I said in my essay and here– HIV-1 Vpu and SIVcpz Vpu are totally different genetically, biochemically, and functionally. The main difference is that HIV-1 Vpus can form ‘viroporins’. Thats pretty wild.
    The function they both have in common (destroying CD4 markers) is irreducibly complex in HIV-1… But not in SIVcpz. And then theres the evolution of novel protein binding/localization sequences in at least two subtypes (we havent looked at them all yet).

    But the virus is still no more than a virus…
    *frown* There is a reason HIV-1 has taken over this planet while HIV-2 has not. Vpu is part of that reason.
    The differential evolution of Vpu between the subtypes points towards a way of stopping the subtype that is out competing every other HIV-1 out there.
    Youre free to believe Vpu evolution is ‘insignificant’, but I doubt HIV-1 would agree with you.

    That is a very old Creationist Claim, btw.

  24. #13 Sal

    Zed, You of course are right. I meant no condescention aimed at Ms. Smith as I am a grad student myself, but because PT is UD’s mortal enemy, I couldn’t resist taking a pot shot at them.

    Sal you are very polite but IMHO the same criticism must concern ERV too, for ERV comments towards Behe and ID supporters are not (euphemistically) particularly kind. Concerning the graduate status you are a good example that not all graduate students lack in wisdom …
    Anyway I strongly think that to discuss does not mean to be, always and unconditionally, polite with the kind of people that currently write on PT site. Clearly, no offense towards people who spread offenses, but a bit of hirony :-)

    #22 PaV

    Frankly, I don’t see how this affects Behe’s argument in the least. It appears that vpu is there from the start, and that it continues to do what it had done from the first time it was incorporated into HIV. What new function, what new “protein-to-protein” interactions have developed?

    Agree. Sal was right when defined ERV criticism as a skirmish for a point in EoE that had apparently been misunderstood. It’s quite instructive that PT & Co. must resort to this sort of (misleaded) criticism about minor points to discredit the main devastating arguments by Mike.

  25. ERV

    You didn’t even read Behe’s book did you? If you had and you still wrote this

    There is no excuse for you to write an entire book on the premise of HIV not being able to do something, when it is clear that these impossible feats did happen.

    then that would make you (in the words of Richard Dawkins) ignorant, stupid or insane (or wicked, but I’d rather not consider that).

    HIV was barely mentioned in comparison to the focal point of the book – the eukaryote P. falciparum, the parasite that causes malaria. If you’d read the book you’d know that.

    And what exactly was the reason for all the sarcasm and insult directed at Professor Behe? Do you think that adds something substantial to your points? Here’s a clue, it doesn’t. It subtracts from any merit there might be. It’s juvenile and adds appeal only for the juvenile audience at Panda’s Thumb. Grow up. If you want to be a serious scholar some day then I suggest you start acting the part first, young lady.

  26. A question for ERV.

    It seems there’s an assumption you and some others are making that lentoviruses (in the form of HIV-1 and HIV-2) found for the first time a home in humans several decades ago at most.

    What on earth makes you think that primate lentoviruses haven’t been attacking humans for millions of years? For all you know the first primate lentovirus was in a human millions of years ago and then jumped to other primates and then back to humans again in recent history.

    Another unsupported assumption is that the current genetic survey of primate lentoviruses is somewhere near complete enough to make broad conclusions about its genetic diversity so that when something is newly discovered the discovery is conflated with newly evolved. The survey isn’t even close to that point. A few virus particles from a few individual organisms have been sequenced while uncounted trillions of lentovirus particles in dozens of primate species remain unsequenced. What’s claimed to be newly evolved is not necessarily so. It may have preexisted for a very long time. Taking a few facts and making wild extrapolations from them seems to be common practice in evolutionary theory. You’ve got that part of it down pat.

  27. ERV you stated:
    We know Vpu is new in HIV-1 because of the directionality of necessity. As I referenced in my original essay, Vpu evolved in a very specific way in HIV-1 to overcome a cell specific and human specific host factor.

    This is where the rubber is going to meet the road in your assertions. If you can show how this claim beats Behe’,s observationally backed capable for what evolution is capable of it would help your case.
    I don’t necessarily see you empirically backing your claim of “We know Vpu is new in HIV-1 because of the directionality of necessity.” because it is outside the scope of observed data and requires one to postulate to its origin, Yet this claim you make “Vpu evolved in a very specific way in HIV-1 to overcome a cell specific and human specific host factor.” is according to what you wrote within the realm of what has been observed. Thus it is simply a matter of stating your case clearly of how this has violated the limits Behe has set forth in his book. If your assertion truly withstands scrutiny then your claim will be validated.

  28. Forgive my oversight but perhaps this is the claim you feel violates Behe’s assertion with observational data?

    Not only are HIV-1 Vpu sequences vastly different from SIVcpz Vpus, but B and C Vpus each have their own specific biochemical markers and specialties. We’ve watched that happen.

    If you could please clearly elaborate the violation of Behe’s limit for the less educated onlookers who are watching this exchange, I’m sure it will be greatly appreciated.

  29. Forgive my oversight but perhaps this is the specific claim you feel violates Behe’s assertion with observational data?

    Not only are HIV-1 Vpu sequences vastly different from SIVcpz Vpus, but B and C Vpus each have their own specific biochemical markers and specialties. We’ve watched that happen.

    If you could please clearly elaborate the violation of Behe’s limit for those who are watching this exchange, I’m sure it will be greatly appreciated.

  30. Sal you are very polite

    Actually, to quote Ben Stein, I’m B-B-B Bad to the Bone, but thank you for the kind words.

    DaveScot wrote:

    Consider this your first and only warning ERV.

    DaveScot,

    If I could plead a bit of mercy here on behalf of Ms. Smith, even if she says something that may be untrue or an uncharitable reading or misinterpretation of Behe, for the sake of the readers, this debate would be the best place to address inaccuracies and cure any lingering doubts that may have been raised in the blogshpere.

    If we drive Ms. Smith away, others might think we had to resort to banning because we could not defend ourselves, or could not point out when her reading of Behe was inaccurate. This should be an easy thing to do, and no cause for getting rid of her.

    Besides, it was awfully nice of her to visit and show more courage than those spinless cowards at PT who have to hide behind her skirts to defend themselves. I applaud Ms. Smith’s courage and she puts to shame those spineless thugs at our rival website.

    Let the discussion continue since the semester is about to begin, and some of us will have to bail in a week or so anyway.

    Thank you for your consideration.

    Salvador

  31. It’s easier to look like you’re thrashing your opponents when you don’t allow them to speak.

    Umm they already spoke. Behe is responding to what they already said.

    And he has thrashed what they have said.

  32. factician,

    Behe’s weblog was being spammed by people who didn’t read his book and misrepresented what he had to say. It was classic spam tactics.

    The fair fight was Behe vs. Coyne, Behe vs. Miller, Behe vs. Carroll, Behe vs. Ruse, Behe vs. Dawkins. Not Behe vs. a mob of sockpuppet scum like John Kwak.

  33. factician,

    I’d prefer we stick to the discussion of HIV, as that was the main topic, the reason I even mentioned Ken Miller’s sophormoric mistakes (such mischaracterizing lipds as proteins) was to introduce the main topic.

    Feel free to discuss HIV and the topic at hand.

    If you want to hear more John Kwak, by all means start your own weblog and let Kwak speak and drink Kwak’s vomit to your fullest delight.

    But in this thread, the main topic is Behe’s arguments over HIV.

  34. #25 Dave

    “It’s juvenile and adds appeal only for the juvenile audience at Panda’s Thumb. Grow up. If you want to be a serious scholar some day …”

    Although Sal is right in asking to be fair towards ERV, your comment is OK to aid ERV to grow. After all “youth is a disease from which we all recover” (D. Fuldheim)

    #27 bornagain77

    “This is where the rubber is going to meet the road in your assertions. If you can show how this claim beats Behe’,s observationally backed capable for what evolution is capable of it would help your case.”

    Precisely, but this is just what it is not possible without the well-known circular reasoning.

  35. In general,

    1. A bundle of assumptions seems to be substituted for hard data. Reconstructing a speculative Darwinian pathway is not hard data. It would be best to stick to observed evolution known to have been caused by unguided Darwinian processes rather than perceived/inferred evolution.

    2. Behe only made an ESTIMATE for a generalized “edge of evolution” that can apply in all circumstances. I don’t see why this “edge” could be expanded a bit further under fortunate circumstances. Obviously I’m doubtful observation will expand this “edge” enough to save Darwinism but if there is a minor expansion everyone (especially Darwinists) needs to keep in mind that potentiality won’t hurt ID. So the current estimate need not be defended overly much by ID proponents. I for one will say right now that I think the estimate too low.

  36. It is clear we might have to agree to disagree with Ms. Smith, but let’s not lose the opportunity to get some clarificaitons and even tap her expertise.

    I for one did not know that Vpu gene loss is as much a possibility as gene emergence when interpreting the phylogeny. It could argue either way, and in light of the sea anome phylogeny being only rescued by appeals to “convergent losses” this interpretation of the phylogeny becomes more compelling.

    I would welcome a litte more discussion of the emergence of binding emergence or function change after introduction of HIV-1 into humans. Though I don’t think it will refute Behe’s arguments, I’d like to tie up some loose ends with Ms. Smith’s assistance.

  37. Art2:

    this moderating system leaves much to be desired

    Dr. Hunt,

    [I presume that now you are posting under your own name (as "Art Hunt") at Pandas Thumb and that PT circulated photos of you, I am free to make the readers aware that you are the same author from PT that is posting under your first name here at UD. I only wished to make the readers aware that you are from PT, and that you are something of an ambassadors from PT to UD.]

    My apologies for the fact your comments got trapped in the spam queue.

    Do you beleive that HIV-1 developed the Vpu gene before or after introduction into humans?

    It appears Musgrave thinks the Vpu gene did not emerge after HIV-1 enetered the human population but rather before. Is that how you read Musgrave’s phylogeny?

  38. Sal,

    Could you get clarification from Dr Behe? From reading your responses (as well as Casey’s) and comparing them to what ERV posts, there seems to be a misunderstanding.

    Sal said:
    I believe Mike was referring specfically to human strains after the introduction into humans…

    To which ERV responded:
    You dont want to reinterpret what Behe said this way.

    Obviously this is the crux of the matter and Dr Behe could clarify his position.

    Thanks

  39. Art2:

    Here’s a link to an abstract. In the abstract they talk about an homology between TASK-1 and vpu. It appears, though, that the upshot of the article is that TASK-1 and vpu interact with one another, with vpu inhibiting the function of TASK-1. So, it surely doesn’t appear that TASK-1 and vpu are, as now constituted, homologues. (I don’t have access to the article, only the abstract)

  40. Art2: “The example of VPu suggests a “value” of about 10^-6, the example of T-urf13 indicates a value of 10^-9.”

    Two things here: (1) what does the calculation look like wherein you arrive at these numbers; (2) in the case of T-urf-13, aren’t we dealing with: (a) mitochondrial plant DNA which, in the case of cms, is known to produce chimeric proteins, and (b) whose genetic mechanisms aren’t fully understood, and (c), in the case of ‘maize’, had to at some time been subjected to artificial selection, and therefore not a relevant comparison?

  41. If there were other human lentiviruses that infected humans, we would likely have found evidence of them by now…

    Here’s the scenario:

    An isolated village in Africa.

    One inhabitant of said village gets infected by a lentivirus that was inhabiting a chimp.

    That infected person, through time and contact, manages to get the whole village infected.

    Chimps go into the village while the villagers are dying.

    Those chimps get infected with the virus.

    The villagers die and do not leave a trace (scavenging, decay, weathering etc.).

    IOW no evidence is left behind in any humans.

  42. I hope people don’t find it confusing but I edited the timestamp on Art2′s comment so it wouldn’t be missed as an “old” comment.

  43. Obviously this is the crux of the matter and Dr Behe could clarify his position.

    Thanks

    I appreciate your desire to get the facts straight, but I sparingly resort to contacting authors because there might be a question someday where we really need their help, and so I’d rather inconvenience them only in extreme cases. I do not want to wear out my welcome…

    It is quite apparent from my reading of pages 136-139 that Behe is talking about HIV-1 in humans, not HIV-2 outside of humans. This is further confirmed by the bibliographic references by Behe to HIV-1.

    Gene duplication in HIV-2 or Vpu emergence in the common ancestor of HIV-1 and HIV-2 is irrelevant to the scope of Behe’s discussion, and therefore such events can’t be properly entered as counter examples to Behe’s claims.

    Ms. Smith offered a paper on gene duplication being the mechanism of Vpx origination. Unfortunately the paper assumes as true the very question at hand

    So this paper should not be cited as a counter example to Behe.

    Further, gene emergence through gene duplication does not in and of itself imply that a Darwinian mechanism is at play, because novel gene emergence via gene duplication could just as well support front loading!

    Let the reader note, I’m not saying Vpu was not novel at some point, as surely it was since it now exists. The question is how do such genes emerge in the first place, and then how are such genes incoporated once they exist.

    If one argues gene duplication as the answer to the question of how large scale biolgoical innovation occurred, it would be helpful to actually observe it directly in the lab as it unfolds. Behe’s citation of Malaria, HIV, and E. Coli are attempts to catalogue the experiments where there were sufficient controls in place to monitor the steps of evolution. Those are the closest experiments to making direct observation “in the lab”, and in Lenski’s case it actually was in the lab.

    Behe argues the observational evidecne does not support the operating presumptions in current literature such the assumption in the paper which Ms. Smith provided.

    And as I pointed out, one would be hard pressed to say successful utilization of gene duplication is inherently Darwinian since the work of Shapiro and others (like Sternberg) suggest teleological descriptions could be a more appropriate description than non-teleological ones. [see their papers on repetitive elements]

  44. Ms. Smith you state in your challenge to Behe on your blog:

    . SIVcpz Vpu and HIV-1 Vpu act in different ways, biochemically , which is predictable enough when you do something as simple as comparing amino acid sequences. For instance, if you compare a laboratory strain gag to SIVcpz gag, you get a similarity of ~75%3. Not too shabby. On the other hand, if you compare the subunit portion of env (the gene I use to create phylogenetic trees because it’s the most variable between viruses) you get an AA similarity of only ~59.5%.

    I just want to ask you Ms. Smith, “What specifically is the observational data you have for biochemical differences other than sequence comparisons?”
    I point this out because Behe doesn’t contest the fact that HIV is a “mutational powerhouse”. I believe Behe’s exact claim is that the number of protein-protein binding sites reached by 10^20 random mutations is vanishingly small in HIV (pg. 143-144 EOE) compared to the overall number of binding sites needed to produce positive evolution for HIV.
    Can you please clearly show us where this Protein Binding site limit, that Behe has tentatively established in his book, has been exceeded with observational data in HIV evolution?

  45. Sal,

    It looks like you have the situation in hand. Good job and thanks.

    To Factician:

    An isolated village in pre-20th century Africa fits the bill- no outside human contact.

    Then along comes the 20th century and humans make contact with the infected chimps. The virus didn’t kill the chimps- a successful virus wouldn’t. It just hung-out infecting the whole population.

    However once it got inside humans (again) it started hammering away on some people’s immune system.

  46. If we drive Ms. Smith away, others might think we had to resort to banning because we could not defend ourselves, or could not point out when her reading of Behe was inaccurate. This should be an easy thing to do, and no cause for getting rid of her.

    Thank you, Sal. And your readers have brought up wonderful questions. However, answers will only be posted to questions on my blog if my comments are going to be ‘held in moderation’ here.

    This is your blog– youre free to moderate as you see fit. But Im not wasting my time answering your readers questions if youre going to trash my responses.

    Dave– Im looking at a copy of ‘Edge’ right now. Would you like to read it out loud together?
    “Yet through all that, there have been no significant biochemical changes in the virus at all…”

  47. Ms Smith writes at PT:

    Vpu involves the evolution of at least two protein-protein interaction sites – one to interact with CD4, one to interact with the pathway that degrades the CD4.

    This was the more interesting of the assertions offered as a counter example to Behe. But there is a subtle Equivocation in this statement that only make it appear Behe’s points were refuted when in fact they weren’t.

    There are at least two notions of “protein-protein binding”:

    1. protein-protein binding within the same organism upon which a critical function depends.

    (i.e. see the bindings of a protein as function in Protein Dark Energy)

    2. protein-protein binding between one organism’s protein (like HIV) to another organism’s protein (like human CD4)

    Mike was referring to #1, and Ms. Smith to #2, therefore, because this is an equivocation, #2 cannot be used as a counter example to #1.

    Further Mike argued for a two-binding site problem, where a single function was tied to the existence of two binding sites. Formally:

    Function-A within an organism can only be true if binding site-B AND binding-site-C exist

    the situation Ms. Smith describes is:

    function-A from one organism to another exists because binding site-B exists

    function-C from one organism to another exists because binding site-D exists

    Thus the two situations are not identical. But the other problem is when did these binding sites emerge? Was it before or after introduction into humans?

    Finally, another problem again is whether there is a clear interpretation of the phylogeny:

    “gain of function in one strain” could in fact also be explained by “loss of function in other strains”. Thus a preconception could actually cloud what really happened.

    One must be careful when one compares a fish missing eyes with similar fish that have them. Were it not so obvious, one could almost think, “aha fish with eyes, and fish without eyes, thus an new eye emerged in evolutionary history.” But such an interpretation is thrown out becuase it is obviously wrong. But it is possible that we have a comparable situation (but not so obvious) with HIV. We may be asserting gain of function merely because of pre-conception, when in fact we could be dead wrong.

    Thus, it is premature to render these Vpu bindings as evolved novel functions, and moreover, they aren’t even the kinds of functions Mike was talking about.

  48. So Scordova I take it that this is all the observational proof she has so far:

    Vpu involves the evolution of at least two protein-protein interaction sites – one to interact with CD4, one to interact with the pathway that degrades the CD4.

    This seems sort of trivial “conclusive Proof” for evolution when Dr. Behe states on page 138 of EOE “Each and Every possible point mutation occurs between 10^4 and 10^5 times per day in a HIV infected individual” Every double point mutation, where two mutations are change simultaneously, would occur in each person once a day(…Now that’s Mutational Firepower!) In fact, just about every possible combination of up to six point mutations would be expected to have occurred in a HIV particle somewhere in the world in the past several decades… In addition to all those point mutations, enormous numbers of insertions, deletions, duplications and other sorts of mutations would occur as well.
    And exactly what has all that evolution of HIV wrought? Very little. Although news stories rightly emphasize the ability of HIV to quickly develop drug resistance, and although massive publicity makes HIV seem to the public to be an evolutionary powerhouse, on a functional biochemical level the virus has been a stick-in-the-mud…..there have been no basic biochemical changes IN THE VIRUS AT ALL.

    One of the points that Dr. Behe stresses after he writes this, is that even though HIV has undergone more mutations than the entire “hominid” line has since our split from apes the evolutionary effect is effectively zilch on the basic virus itself…It is still very much basically a HIV virus and only a HIV virus. The main point of the whole ID/evolution debate is that evolution is required to empirically demonstrate significant and positive morphological change with mutation and here we are quibbling over insignificant changes in a virus that has undergone extensive mutational pressure!. Ms. Smith someone sold you a bill of goods if you believe this is conclusive proof of positive evolution. If I were you I would demand my money back!

  49. Mike was referring to #1, and Ms. Smith to #2, therefore, because this is an equivocation, #2 cannot be used as a counter example to #1.

    Fine. Lets grant your premise again. Behe really meant ’1. protein-protein binding within the same organism upon which a critical function depends.’

    Vpu proteins interact with other Vpu proteins to create a tetramer– a viroporin. Its also integral for particle release in humans, requiring more HIV protein-protein interactions. Completely new function/molecular machine in HIV-1. It is NOT in SIVcpz. And, Subtype C evolved biochemically to form these viroporins better than other subtypes. References for all of this is in my original essay.

    Are you ready to start listing to what I say, or are you going to keep squirming?

  50. Oops! Typo– pentamers.

  51. This is your blog– youre free to moderate as you see fit. But Im not wasting my time answering your readers questions if youre going to trash my responses.

    No conspiracy involved…your comments are automatically being caught along with a bunch of other comments. And the delay is unfortunate because people have to wait until a moderator comes online. But it’s better than being spammed with ads for various products (over 115,000 and counting so far).

  52. Lets grant your premise again

    Vpu did not emerge as a brand new gene after HIV-1 entered humans but rather before it entered humans.

    That premise was as much yours and Ian Musgrave’s as it is mine and Michael Behe’s.

    So why do you refer to Human Vpu being a pre-existing gene as simply my premise. It is your premise as well.

    But let us do an accounting.

    1. When did a Vpu domain have the ability to degrade CD4 in the endoplasmic reticulum? Before or after HIV-1 was introduced into humans?

    2. When did a Vpu transmembrane anchor domain have the capacity to regulate virus release? Before or after HIV-1 was introduced into humans?

    I think those data points are important for the discussion to move forward.

    If you don’t know the answer, then I’d say it’s premature to assume those capabilities evolved after introduction into humans, and thus, at least with respect to those two capabilites, should not be used as counter examples to Michael Behe’s assertions.

  53. This is your blog– youre free to moderate as you see fit. But Im not wasting my time answering your readers questions if youre going to trash my responses.

    Ms. Smith,

    I am perfectly willing to ask my questions at your weblog if UD is unsuitable to you.

    I expect we will disagree in the end, but I would at least like greater clarity in the emprical facts as to time tables of events and distinctions between phylogenetic pre-conceptions versus actual hard facts of sequence divergence measurements.

    I have also perused the peer-reviewed literature and would like to count how many amino acids changes were involved in the formation of new functionality, and how many estimated trials were required to achive novel functioning domains.

    regards,
    Salvador

  54. For the sake of discussion, let’s assume Smith is correct in her assumptions. Now I haven’t had time yet to read all the referenced materials so perhaps someone could answer two yes/no questions.

    1. Would this go significantly beyond Behe’s current estimate for the edge?

    2. Would this be CSI?

  55. let’s assume Smith is correct in her assumptions.

    The problem is, I am not sure her assumptions are clearly stated. The areas needing clarification:

    1. What is her assumption about whether Vpu emerged before or after introduction into humans? She keeps saying it’s my premise, and I’ve argued that it was her premis first before it was mine. I was merely trying to get confirmation.

    2. When did CD4 functionality emerge? Before or after introduction into humans?

    3. When did transmembrane anchor domain regulation of viral release occur? Before or after introduction into humans?

  56. Are you ready to start listing to what I say, or are you going to keep squirming?

    It is true that I’ve been accused of being dense, so I hope you’ll be willing to assist my lack of understanding.

    I posed this question:

    2. When did CD4 functionality emerge? Before or after introduction into humans?

    I did this just to make sure that I’m interpreting this paper correctly which you reference:

    Vpu-mediated CD4 down-regulation and degradation is conserved among highly divergent SIV(cpz) strains.

    It would appear this paper suggests the capacity to degrade CD4 pre-existed the introduction into humans. Is that correct? In that case, it would be difficult to argue that this is really a new feature whatsoever in the time frame which Michael Behe was examing, but rather an inhereted feature.

    Thus CD4 down regulation and degredation cannot be used as an argument against Michael Behe’s claims. Is that correct?

  57. Ms Smith said:

    Subtype C evolved biochemically to form these viroporins better than other subtypes.

    But I looked at your comment at PT:

    Viroporin capabilities have not been found with SIVcpz Vpu. Knowing what we know about Vpu, this is not surprising. If you scramble the transmembrane region of HIV-1 Vpu (the portion responsible for the ion channel formation), viral release is crippled.9 And when you compare AA homology between SIVcpz and HIV-1 Vpu in the transmembrane region is unremarkable (roughly two) – that’s as good as a ‘scramble’.

    I’m having problems accepting that viropoin capability was novel after emergence in humans in light of this paper:
    Scrambling of the amino acids within the transmembrane domain of Vpu results in a simian-human immunodeficiency virus (SHIVTM) that is less pathogenic for pig-tailed macaques.

    To date, no studies have been performed to assess the role of this domain in virus pathogenesis in a macaque model of disease. Using a pathogenic molecular clone of simian human immunodeficiency virus (SHIVKU-1bMC33), we have generated a novel virus in which the transmembrane domain of the Vpu protein was scrambled but maintained hydrophobic in nature (SHIVTM), which presumably would disrupt any ion channel TM properties of this protein

    Thus, these results show for the first time that the TM domain of Vpu contributes to the pathogenicity of SHIVKU-1bMC33 in pig-tailed macaques.

    This paper would appear to weaken the claim that even if “Viroporin capabilities have not been found with SIVcpz Vpu”, that they emerged brand spanking new in humans.

    Thus, this would appear not to be an appropriate counter example to Behe’s claims. The fact that one may not see a function in one strain does not imply that it emerged brand new in another strain. It is entirely possible this was a loss of fucntion, and with respect to the issue of this viroporin capability, it was a loss of function (if at all).

    Speaking of which, were there even studies done on SIVcpz regarding scrambling of the TM domain? Can’t very well find them if one doesn’t even look for them.

  58. art (and art2) is no longer with us

    erv can also take her sarcastic mouth elsewhere

    factician has also been included in the housecleaning

  59. I think this site may be useful for those following this discussion on HIV evolution.

    http://pathmicro.med.sc.edu/lecture/hiv14a.htm

    Its an overview of the treatment of the HIV virus.

    This is an interesting excerpt from the paper;

    Protease inhibitors

    With the advent of protease inhibitors, there has been optimism that HIV might become a tractable disease since now we have the promise of a drug regimen that can suppress indefinitely the progress of disease. If, as seems to be the case, viral load is the key to the progression from infection to the clinical manifestations of the disease, combination therapy may make HIV infection manageable.

    Many aspartyl protease inhibitors are being developed but at present, only a few are approved. They are all substrate analogs, that is they mimic a peptide that can bind to the active site of the viral protease. The latter is a dimeric aspartyl protease (has catalytic aspartates at its active site). When used individually, protease inhibitors can drive down viral load to between one 30th and one 100th of initial value but sub-optimal doses of these inhibitors when used alone can result in loss of suppression after several weeks or months and an accumulation of multiple mutations in the protease gene giving a high level of drug resistance. However, patients with sustained suppression do not develop the resistant mutations. This is because replication must be maintained for the development of such mutations under the selective pressure of the drug.

  60. DaveScot,
    Remember these people actually believe whole heartedly that evolution of CSI is possible in HIV. We know for a fact, from rigorous math and the study of observational data of deleterious mutation rates in other organisms, that this is not possible. I think Sal is doing an excellent job of gathering the available observational data that is available in HIV in which to clearly show these people why it is not remotely possible.
    Their snide comments probably come from years of brainwashing in the Darwinism doctrine and the arrogant and mistaken assumption that they can’t possibly be wrong. But we have a surprise for them in the actual practice of hard science, So I ask that we may exercise a little patience with our guest until we have the observation data we need to destroy their case.

  61. For the sake of discussion, let’s assume Smith is correct in her assumptions.

    and this is what Sal is questioning.

    1. Would this go significantly beyond Behe’s current estimate for the edge?

    Absolutely NOT.

    2. Would this be CSI?

    Absolutely NOT.

    So, where did ERV take the certainty that Behe analysis is “fatally flawed”?

  62. #60

    Remember these people actually believe whole heartedly that evolution of CSI is possible in HIV.

    10% faith.

    But we have a surprise for them in the actual practice of hard science, So I ask that we may exercise a little patience with our guest until we have the observation data we need to destroy their case.

    This is a good argument.

  63. I think this following statement is very telling to the whole ID/evolution issue:

    However, patients with sustained suppression do not develop the resistant mutations. This is because replication must be maintained for the development of such mutations under the selective pressure of the drug.

    Therefore the only most successful way, so far, to arrest the disease is to dramatically suppress the HIV numbers and to thus restrict their access to the numbers they need to continue their RM/NS search for a “successful deleterious” mutation that will block the drug/virus interaction.

    Another thought that may be of use to this discussion: If RM/NS was truly the power behind the development of novel information of life on earth then “the survival of the fittest” would belong to the most lethal (non-living) viruses since they have vastly greater access to the powers of RM/NS than higher organisms above them. Lethal Viruses should rule the earth in this RM/NS scenario since any organism with which the viruses reacted would quickly be destroyed because they are vastly outclassed by this “hypothetical” power of the Virus to develop successful protein/protein binding sites with accelerated RM/NS.
    That is to say simply that the “fittest” organisms on earth would be the ones to have greatest access to this RM/NS power.
    Yet this is not what we see we see. We see higher organisms with access to arguably far less mutation firepower successfully coexisting with viruses. If RM/NS were truly a successful way to build proteins then life should never even arise past the lowliest organisms with the most “Mutational Firepower”. In a hypothetical “blind” world of natural selection only the fittest would survive and the fittest would definitely not be us it would be “mutational powerhouses”!

  64. Good point. In a certain sense (and provided that really it seems highly implausible that RM+NS could have produced them) only the more basic organisms, such as viruses and procariotes, should be the winners. In a more general sense this argument could be enhanced. The more an organism is complex the less is its number and the slower is its capacity to reproduce. How can a blind mechanism such as RM+NS hope to explain thie reverse pyramidal status?

  65. Waah!!!! The Darwinsits are gone. Sniff. They just couldn’t control themselves. Crying shame.

    I was just about to deliver the coup de grace to all 3. It would have been nice if I could have delivered it here before our fans. Our fans come to UD afterall for a bit of entertainment.

    I was about to ask Dr. Hunt about the phylogenies and the interpretation of various papers like SHIVTM. Same with factian.
    I was about to ask Ms. Smith too.

    But now I’ll have to wander to the slime pits to hunt my prey down rather than wage the battle on friendly territory. Man those guys make my life hard.

    Wish me luck man, as I’ll have to go it alone at PT, ERV, and the blogshpere, unless there is anyone who wants to join me on this glorious expedition.

    If anyone wants to help me on this expedition, come forward, or do I have to go it alone?

    I shall land my expedition
    here.

    Salvador

  66. LOL, you go get em SAL, But please do let us know exactly how you destroy their fallacies.

  67. Well here is the play by play so far at the comemnt section of Another Savage Blow to My Critique

    Salvador Cordova, Invasion Force Commander:

    Ms Smith,

    This is Salvador Cordova from UD. I had nothting to do with your banning and I lobbied DaveScot to allow you to stay.

    I was wondering if I could we could continue our dialogue. I only have a few more questions, and don’t intend to trouble you much over them.

    Salvador

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

    Anonymous Darwinist:
    Ooh, yes, please let Sal continue. He is about to deliver the coup de grace, don’t you know.

    Hey, Sal, since you seem to have insights not available to actual practitioners of biology, genetics, and virology you really should start your own biomedical research company based on the ID paradigm. I’ll bet you could attract lots of funding and wouldn’t it be a big splatter of egg on the Darwinists faces when you patented a breakthrough treatment.

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

    Salvador Cordova, Invasion Force Commander:

    Annonymous said:
    “since you seem to have insights not available to actual practitioners of biology,”

    Not at all, I’m just a dumb uneducated dolt who has an overinflated view of himself, that’s why I was hoping Ms. Smith could help me understand something.

    I looked at the phylogeny that was suggested by Dr. Musgrave here:
    Illustrated Guide to Vpu

    Is it Ms. Smith’s expert scientific opinion that Dr. Musgrave’s diagram indicates that Vpu was present in HIV-1 strains when they were first introduced into the human population?

  68. If RM/NS were truly a successful way to build proteins then life should never even arise past the lowliest organisms with the most “Mutational Firepower”.

    In fact this is what is revealed by computer simulations of RM+NS.

    Edge of Evolution pg. 276

    In Avida, acquiring new abilities is only one way for an organism to get computer food. Another way is by simply acquiring surplus instructions, whether or not they do anything. In fact, instructions that aren’t ever executed – making them utterly useless for performing tasks – are beneficial in Avida because they provide additional food without requiring any additional consumption. It’s survival of the fattest!

    It’s also very unrealistic. Biological organisms show the opposite behavior – genes that are useless in the real world are not rewarded; the genes are rapidly lost or degraded by mutation. Why, then, was Avida programmed to do the opposite? As explained on the Avida website, the counterbiological feature was needed, “Otherwise there is a strong selective pressure for shorter genomes.” In other words, otherwise the program wouldn’t give the desired results.

  69. #68 Dave

    are beneficial in Avida because they provide additional food without requiring any additional consumption. It’s survival of the fattest!

    In my opinion the high number of references to Avida by NDE supporters is one of the most evident signs of their hidden desperation. Please let us always remember that, fattest or fittest, anyway we are speaking of the evolution of trivially simple EQU operators …

  70. I’m going to skip reporting a lot of the spam at ERV’s website, but here was the latest:

    Salvador Cordova, Invasion Force Commander:

    Olegt said: “You have started graduate school. Tell us where and in what field. We’re dying to know.”

    I’m learning the science of Denial and Deception from the University of Charles Darwin.

    Ah, but I see Dr. Arthur Hunt of Pandas Thumb is here. YAY!

    You know Art, I’d like to answer your question, but there is something I need a little help with first so I can understand where you’re coming from.

    When you read those phylogenies Dr. Musgrave offered, does that suggest to you that Vpu existed in HIV-1 strains prior to their introduction into humans?

    I was hoping Ms. Smith could offer her expert opinion, but perhaps in the interim you could tell us what you think of Dr. Musgrave’s phylogenies with respect to that questin.

    Prediction:

    1. Dr.Arthur Hunt of PT will obfuscate the issue, accuse me of evasion etc., throw out red herrings and equivocations, literature bluffs

    2. Ms. Smith will do the same, through out red herrings and equivocations, literature bluffs

    3. More spam and ad hominems from the Howler Monkeys to try to derail the discussion

    4. I will keep hammering the phylogenies because they know they pulled a “literature bluff” and equivocated the notion of “new function”. Watch it unfold. They’ll be reluctant to admit when I catch them on something. Notice when they don’t respond to a simple question such as those I pose about Musgrave’s phylogenies.

    [Learn more about Darwinist literature bluffing and the fine art of countering it:
    Becoming a Jedi Master in the online ID Wars
    ]

  71. Sal

    You can’t reason with unreasonable people.

    The bottom line remains that rapid reproducers like falciparum and HIV have been observed in nature replicating and mutating in numbers orders of magnitude larger than all the mammals that ever lived and in all that opportunity to build complexity they accomplished almost nothing. So on the one hand we have a mechanism that is observed to do very little in billions of trillions of actual replications yet on the other hand chance pundits insist this same mechanism with far less opportunity built all the complexity in mammals that distinguish them from reptiles. This is the mother of all non sequiturs. Under actual observation in numbers sufficiently large to remove any doubt that we just haven’t observed it long enough, rm+ns does exactly what ID predicted it would do. RM+NS simply cannot defeat the statistical odds working against it. The only thing in nature with a known ability to choose desired outcomes from a virtually infinite set of equally probable undesirable outcomes – defeating at least temporarily the laws of entropy in thermodynamics and information – is intelligent agency.

  72. #67

    Sal you forgot to quote the “incipit” by ERV in its site. I quote it to show what’s the fairness of the person to whom you had kindly asked information.

    Dave is completely right: this person has to grow more and more to become (perhaps) a good scholar.

    —————————-
    from: http://endogenousretrovirus.bl.....tique.html
    Thursday, August 30, 2007
    Another savage blow to my Behe critique

    ERV, banned at UD for being *sarcastic*, aka repeatedly anticipating and demolishing Sallys attempts to move goal posts, and answering Davies attempts at being *mean* with cheer.

    Have fun scissoring each other, pussies.

    ROFL!

    Poor Tweedle-Dee and Tweedle-Dumb, too stupid to know Behe was trying to let my post blow over. Trying sooooooo hard to ignore my post, hoping others would forget I wrote it… And then Dee and Dumb plaster it on the front page of UD and let me smash their Creationist Claims on their own damn blog!

    AAAAAAAAHAHAHAHAHAHAHA! IDiots! AAAAAAAAHAHAHAHAHAHA!!!!

    Posted by ERV at 7:39 AM

    Labels: Creationism
    ————————–

  73. Here is an update in response to Olegt’s question as it will be inevitable:

    Well Oleg Tchernyshyov I’m in the unfortunate position of stuydying physics at your school, Johns Hopkins.

    Do you look forward to dismissing me?

    Salvador T. Cordova

  74. I’m someone who’s interested in ID but who frankly doesn’t know enough to weigh in on the merits. I follow the arguments on each side as best I can. One thing that has made me more likely to credit ID is the other side’s childish, dismissive manner in responding to ID arguments. It suggests defensiveness and lack of confidence in their position. On her webiste, ERV and her commenters are great examples of this and do their side no favors with their rudeness and snarkiness.

    That said, I don’t see why they were banned here. ERV’s comments here seemed within the bounds of acceptable argument. ERV’s ideas will never get a thorough vetting over there, and UD has now destroyed the chance for a real, fair debate here.

    Please — resist the temptation to sink to their level. It’s hard to ignore their juvenile attacks, but please remember how your responses will be interpreted by undecided people like me.

  75. Sal,

    LOL,,,LOL,,,LOL,,,LOL…

  76. So Sal, Is a literature bluff exactly what you got them on?

    If you get time I do want to know what they have that is supported by observational data (I suspect well within EOE) and what they tried to claim with unsupported postulations and literature bluffing.

  77. Well Oleg Tchernyshyov I’m in the unfortunate position of stuydying physics at your school, Johns Hopkins. Do you look forward to dismissing me?

    Congratulation Sal; this is genuine and fair psicological war :-)

    BTW, I’ve found the following biography of your (possible) future professor:

    “Oleg Tchernyshyov is a professor in the Department of Physics and Astronomy of the Johns Hopkins University. He is a condensed matter theorist interested in strongly correlated electron systems, such as high-temperature superconductors and **frustrated** magnets.”

  78. DaveScot:

    You can’t reason with unreasonable people.

    I am dealing with the questions for the sake of the people sitting on the sideline wanting to hear the debate, not because I believe Ms. Smith or Dr. Hunt will be convinced.

    If I don’t address the questions, that might instill lingering doubts amongst the readers.

    Oh well, it’s a moot point as the semester is about to start and I’ll be scarce in a little while.

  79. Zed, the problem is that, all too often, Darwinists attack ID for what it is not, and ignore what it is. Logically, one must be able to define a theory and understand what it is prior to attacking it.

    Note, for example, the way they criticize the concept of “specified complexity.” They will say, “well just because something is complex doesn’t mean that design was involved.” Clearly, statements like that prove that they don’t have a clue about what “specified” means. Everyone knows that complexity alone does not indicate design.

    This kind of ignorance does not occur on the other side of the debate. ID advocates understand every aspect of Darwinian evolution, its claims, and all the implications involved.

    We argue against their theory, and they argue against their false characterization of our theoory. If anyone has earned the right to be discourteous, it is us. Nevertheless, our side is usually much more civil.

  80. To sum this all up (adding to StephenB’s last paragraph in 79) :

    Both Sal & Casey are saying that Behe is talking about “apples” (HIV-1 only).

    ERV is saying that Behe is talking about “oranges” (xIV-x, with x being any letter denoting any known & “related” virus or no letter).

    If we can make any predictions about this debate we can predict this scenario.

    That is we can predict that when an IDist makes a claim someone will say that claim is falsified. Yet on closer examination they refuted a strawman. And they will cling to that strawman until they die, regardless of what the data demonstrates.

    They do this because they can always claim- “Sure, he says that NOOOWWWW! But we know what he meant before I corrected him.”

  81. Stephen B: This isn’t about who has the right to be discourteous. It is about how to be persuasive. ERV’s comments HERE didn’t cross the line into being discourteous, and the ID side lost points, in my view, for shutting down the debate. To be persuasive, the ID side needs to rise above the other side’s immaturity. The other side’s commetns may be hard to take, and it can be fun to engage in flame wars, but ask yourself, is it really helping to advance your argument?

  82. kairos #61,

    I agree completely and that’s the point. I was hoping to get Ms. Smith and Dr. Hunt to admit that even if their speculative scenario was correct it’s still not a challenge to ID. But now that they’re banned that’s unlikely…

    The worst assumption is the presumption that the only possible mechanism for this evolution scenario is unguided Darwinian processes. If they really want to challenge Behe they need to find evidence where the mechanism is KNOWN to be unguided Darwinian processes.

    That said, I don’t see why they were banned here. ERV’s comments here seemed within the bounds of acceptable argument. ERV’s ideas will never get a thorough vetting over there, and UD has now destroyed the chance for a real, fair debate here.

    Agreed. That said, it’s amazing the lack of maturity they’re showing in their responses on their own sites.

  83. So Sal, Is a literature bluff exactly what you got them on?

    It is possilbe Ms. Smith was very hasty to render judgement, and PT presenting her prominently as having destroyed Behe’s arguments, put her in a very precarious position.

    If someone comes along and finds major holes in her understanding, her friends will have to try to correct a few mistakes with even more. They can never admit that they are wrong since it is impossible they are wrong, if you know what I mean….

    At issue is the simple question I posed in various incarnations: “if you have two organisms with a common ancestor, one has an eye and the other doesn’t, how do you interpret the evolution? Did one line gain an eye, or did one line lose an eye?”

    I was willing to grant Ms. Smith’s claim that Vpu emerged recently. Her own diagrams suggest Vpu emerged just before HIV-1 entered humans, NOT AFTER.

    Actually, I’m now thinking I was too generous. It’s possible Vpu was in all the strains, and any strains lacking them may be through loss of function, not because they are more “primitive” than other strains!!!!!

    Same with the supposed novel emergence of ion channel capbility.

    My current hypothesis based on peer-reviewed literature:

    1. Vpu pre-existed HIV entry into humans

    2. CD4 degradation existed before HIV entry into humans

    3. viral relase regulation via Vpu existed before HIV entry into humans

    4. possibly even ion channel capability existed before HIV entry into humans

    Yet, all these 4 capabilities were presented as something new, when indeed the peer review literature argues the opposite.

    The reason I posed the question to Dr. Hunt is that for him to answer honestly might result in him refuting absolutely everything Ms. Smith said. Her whole essay would be discredited at the hands of one of her own.

    I for one had little to lose. And I already admitted, I have in my back pocket a minor error which Mike made, and I’m quite happy to disclose my finding later. I assure you all it is minor (on the order of a few typos), and does not refute his conclusions. So one can’t accuse me of always defending Mike, and in fact when I was on C-SPAN, I gently objected to Mike giving credit to Darwin rather than Blyth.

    I was sincere, if there was a mistake, what better thing than getting free public peer-review to help Mike with his next edition? We can acknowlege Dr. Hunt and Ms. Smith for helping us. I’m sure they’ll be appreciative of our public gratitude.

  84. Zed wrote:

    This isn’t about who has the right to be discourteous. It is about how to be persuasive.

    Well, my interaction with them has continued at ERV for the sake of the readers. I hope the exchange will be informative.

    Please consider these central questions I raised as I believe Ms. Smith was hasty to judgement, and doing so allowed her to arrive at badly mistaken conclusions. I will keep hammering the following points:

    1. Vpu pre-existed HIV entry into humans

    2. CD4 degradation capability existed before HIV entry into humans

    3. viral relase regulation via Vpu existed before HIV entry into humans

    4. possibly even ion channel capability existed before HIV entry into humans

    Therefore these points can’t be used to refute Michael Behe, and Ms. Smith was badly mistaken to appeal to them in the first place. I smelt something of a weak hand in her treatment of the TM domains. :-)

    Hammering the phylogeny by Dr. Musgrave is what I’ll do. If they avoid answering the 4 simple assertions, you’ll know I was right. :-)

  85. ERV’s comments HERE didn’t cross the line into being discourteous, and the ID side lost points, in my view, for shutting down the debate.

    Zed, one of the problems in these debates is that Darwinists have a very annoying strategy of using data dumps and lit bluffing. These replies always sound reasonable and almost always appear conclusive until someone takes the time to delve into what the lit cite actually says or to wade through the data provided to determine its reliablity and germaneness to the debate.

    I suspect that was the motivation of the mods for giving them the boot.

    And it looks like Sal has established that EVR was lit bluffing.

    Also, that EVR appeared to misrepresent Michael Behe’s position didn’t help.

  86. Patrick wrote:

    I agree completely and that’s the point. I was hoping to get Ms. Smith and Dr. Hunt to admit that even if their speculative scenario was correct it’s still not a challenge to ID.

    And I went for the opposite end showing the Ms. Smith didn’t ever correctly interpret the literature she listed as supporting her position.

    I took the time to wade through it, and it looks very embarassing to her position. I listed my findings above, and I have a feeling those knowledegeable in the field will have to conclude Ms. Smith’s position is indefensible, and they’ll have to avoid acknowledging I was right. Such a thing cannot be a conceded.

    I am still unsure of the SHIVTM paper, but if I’m right, that’s the final nail in the coffin as that would mean even her own lit search overlooked a very significant datapoint.

    Bottom Line: any suggestions of emergence of new functions after HIV got introduced into humans is suspect. Mike was right.

  87. Very Well done Sal,

    1. Vpu pre-existed HIV entry into humans

    2. CD4 degradation capability existed before HIV entry into humans

    3. viral relase regulation via Vpu existed before HIV entry into humans

    4. possibly even ion channel capability existed before HIV entry into humans

    Very, Very Well Done Sal,,, so this is the “tentative” observational evidence for degradation of SIV to HIV from these papers
    ,, correct?

    http://www.ncbi.nlm.nih.gov/si.....m%E2%80%9D

    http://lib.bioinfo.pl/pmid:15975620

    Well the evolutionists won’t like this development much at all will they?

  88. My comment about courtesy was an afterthought and should be understood in the context of my main point, which is that one side is simply more honest than the other. You are trying to make it the main point of my post, which is precisely the problem I am complaining about.

    The main process in winning an argument is to present sound arguments and be honest about what both sides are saying. Courtesy matters, but honesty matters more. Once one side proves that they are no longer arguing in good faith, what is the point of continuing.

  89. Dealing With the Backlash

    Critics and enemies are useful. The point is to use them effectively. In our case, this is remarkably easy to do. The reason is that our critics are so assured of themselves and of the rightness of their cause. As a result, they rush into print their latest pronouncements against intelligent design when more careful thought, or perhaps even silence, is called for. The Internet, especially now with its blogs (web logs), provides our critics with numerous opportunities for intemperate, indiscreet, and ill-conceived attacks on intelligent design. These can be turned to advantage, and I’ve done so on numerous occasions. I’m not going to give away all my secrets, but one thing I sometimes do is post on the web a chapter or section from a forthcoming book, let the critics descend, and then revise it so that what appears in book form preempts the critics’ objections. An additional advantage with this approach is that I can cite the website on which the objections appear, which typically gives me the last word in the exchange. And even if the critics choose to revise the objections on their website, books are far more permanent and influential than webpages.

    An illustration might be helpful here. As I was working on my book No Free Lunch, I wrote a section critical of Thomas Schneider’s article “Evolution of Biological Information,” which appeared in Nucleic Acids Research. I would have liked to get from Schneider a well-considered response to my criticisms. But with Darwin fish crawling over his website, I frankly doubted that he could serve as a fair-minded respondent. I therefore posted the relevant section on the science-religion listserve META, framing the discussion around some remarks on design by the German theologian Wolfhart Pannenberg. I posted my 3000 word critique one day. Wesley Elsberry immediately alerted Schneider. Schneider posted his rebuttal the following day. I love the Internet!

    Schneider failed to address the substance of my critique, but provided some useful details about his work that I was able to incorporate into my section. Also, he engaged in some hair-splitting that could only look ridiculous to outsider observers: no, he was not claiming evolution brought about biological complexity as a “free lunch,” but, yes, he was claiming that it brought about biological complexity “from scratch”; no, he did not generally find fitness a useful concept, but, yes, his research did require error-counting functions that scored errors monotonically with respect to survivability (that sure sounds like a fitness function to me). This hair-splitting made it into my book and made for amusing reading, though not at my expense.

    As far as possible, I try to steer the attacks of my critics by the judicious dissemination of information. This has the advantage that I know what to expect. Often, however, the attacks by our critics blindside us. A common feature is that they are vicious and personal. Sometimes they are written to employers to discredit us or even to destroy our reputations and careers (I write from personal experience). Our natural tendency in response to such attacks is to get upset and react in one of three ways, none of which is advised.

    One reaction is to placate: My, you really are angry. I must have done something wrong. Help me make things right with you. Another reaction is to flee: What did I get myself into? This kitchen is a lot hotter than I can stand. I don’t need to be dealing with this level of conflict. Let me out of here. Still another reaction is to fight: You no good so-and-so. I’ll show you. You want to play hardball? You came to the right place. I submit that none of these reactions is helpful in advancing our cause. The hardcore critics with whom I regularly deal are intellectual bullies, and they don’t deserve to be placated. What’s more, they are not very frightening, especially when you get past their initial defenses, so there’s no reason to flee.

    Fighting, however, is not advised either. The problem with fighting is that it consumes valuable energies and is motivated by anger, which always distorts mental clarity and distracts from the real issues. As John Cassian noted over 1,500 years ago,

    No matter what provokes it, anger blinds the soul’s eyes, preventing it from seeing the Sun of righteousness. Leaves, whether of gold or lead, placed over the eyes, obstruct the sight equally, for the value of the gold does not affect the blindness it produces. Similarly, anger, whether reasonable or unreasonable, obstructs our spiritual vision. Our incensive power can be used in a way that is according to nature only when turned against our own impassioned or self-indulgent thoughts.

    So, let’s put anger aside. Let the other side fume with indignation. Indeed, many of them have turned indignation into a full-time occupation. From our vantage, however, we need to take their vitriol as par for the course. These valiant defenders of evolution are just that — valiant defenders. It would be unworthy of them not to use every means at their disposal to try to stop us. They are as committed to their program as we are to ours (sometimes I wonder if they are not more so).

    Think of their no-concession policy in pure business terms. When, for instance, gas prices go down, we don’t congratulate oil companies for their generosity. So, when gas prices go up, we would be out of line to accuse them of greed. Oil companies and the prices they charge are constrained by market forces. So, too, the market of ideas is constrained by ideational forces (especially the inertia of entrenched ideas), and our opponents are simply playing their part. I find this perspective freeing. Far from wanting to curl up in a corner when attacked, I’m grateful for my critics. Truth be known, their attacks are my idea of a good time. Indifference is a far worse form of violence.

    The appropriate response to attacks by critics is to see the attacks as opportunities to advance our cause. Think of them as gifts. As a student of the Old Testament, I’ve always been fascinated with the Israelite conquest of the Promised Land. The pattern that kept repeating itself was this. The Israelites would approach a fortified city. Instead of entrenching themselves in their city and allowing their countryside to be ravaged, the inhabitants of the city would come out for battle. Once outside their positions of safety, however, they were fair game, and the Israelites were able to make short work of them. That’s the pattern I see in this debate. The proponents of evolution would very much prefer to stay in their fortified positions. They don’t want to dignify us by devoting time and energy to refute us. They would prefer to ignore us. They wish we would just go away. But the challenge to evolution in the schools and public square is real and threatens their monopoly. The unwashed masses are not with them. The evolutionists cannot leave these crazy design theorists unanswered. So, out they come from their positions of safety to challenge us. But, in the very challenge, they open evolutionary theory to a scrutiny it cannot withstand.

    Bill Dembski

  90. Ok people this is ERV’s claim to refute Behe:

    Vpu is a new gene, not a ‘lost in everyone else’ gene.

    And this is the observational evidence from the Paper Sal found:

    Human immunodeficiency virus type 1 (HIV-1) along with simian immunodeficiency viruses from chimpanzees (SIV(cpz)) and three species of Old World monkeys from the genus Cercopithecus have been shown to encode a Vpu protein. To date, the functional characterization of Vpu has been limited to a small number of subtype B and more recently subtype C Vpu proteins. Using a recently developed VpuEGFP reporter system, we have shown that the subtype B and C Vpus are capable of preventing CD4 from being expressed on the cell surface. Using the same reporter system, we report here on the expression and functional analysis of Vpu protein from four SIV(cpz) isolates (CAM13, ANT, TAN1, and GAB1). All four SIV Vpu fusion proteins were efficiently expressed and prevented CD4 expression on the cell surface and induced CD4 degradation. This was surprising as three of the SIV(cpz) Vpu fusion proteins had only one canonical casein kinase II (CK-II) site (CAM13, ANT, TAN1) while previous studies with laboratory adapted HXB2 had indicated that both CK-II sites were required for CD4 degradation.

    Thus claim number 1 of ERV is invalid!

  91. And this is the observational evidence from the Paper Sal found:

    Actually, that paper was listed in Ms. Smith’s bibliography. :-)

    I could be a little mean and ask how an expert like herself could possibly mis-read so badly a paper which she herself cited.

    Should I do that? I haven’t visited the site. I invite the UD readers to read for themselves and report what the hear from that site. Tell me the responses of:

    1. Dr. Hunt
    2. Ms. Smith

    See if the could provide a simple “yes” or “no” to my question about pre-existence of Vpu in the HIV which infected humans.

    If they dodge, I invite readers to pose the question again and again until they fess up. They only have to say “yes” or “no”.

    If they answer “yes”, ask Ms. Smith whether my interpretation of that paper was accurate with respect to it suggesting the pre-existence of Vpu prior to entry into humans. If she says, “yes”, ask her why then did she mis-read it, and moreover why did she mis-report it at PT. :=)

  92. I wonder Sal is it possible to actually prove the HIV lost some protein functions or functional genetic information from SIV?
    It is very possible that Genetic Entropy will play a role if there was any sort of major change from the original form of the virus since it first appeared as SIV?
    In other words it very well may be possible to nail the evolutionists with conclusive proof of degradation instead of evolution in this matter!

  93. Sal, I wouldn’t go Unless you like being slandered. I don’t think they will be to happy to see you right now that their cornerstone claim is so easily dismissed,,,, with their own evidence no less,,,LOL,,,LOL

  94. bornagain77 wrote:

    Sal, I wouldn’t go Unless you like being slandered.

    Well, maybe I’m a glutton for punishment, but I want my name and the name of my colleagues cleared.

    I posted the following here:

    smokey wrote: “I think Sal was lying when he claimed to want to continue his dialogue with Abbie.”

    We can continue the dialogue. I invited the readers to visit here to hear Ms. Smith’s case. Because she is banned this is the most that I can do.

    I would hope Ms. Smith will articulate the details of what she believes Musgrave’s phylogeny says and what the peer-reviewed papers say.

    The first question I posed was, “did HIV-1 have Vpu when it entered humans?”

    A simple “yes”, “no”, or “I don’t know” would suffice.

    Hermagoras here has fiercly criticized me.

    But what is his answer to that question? How does he think Ms. Smith will respond?

    How about Dr. Hunt? What is his answer to this simple question?

    How about anyone else who has labeled me a liar? What is your answer to the question?

    When Ms. Smith articulates her position on the matter, then we can proceed as that question is fairly central to this discussion.

    I encourage the doubters to monitor Ms. Smith’s response to this simple question. It is fairly central.

    In the mean time, I expect her supporters to build a smoke screen of spam and red herrings to protect her and keep every other issue alive EXCEPT my question.

    Note, I posed the question to the others. Observe what they say, especially Dr. Arthur “Art” Hunt of PT (a plant biologist) and Dr. Hermagoras (some English professor somewhere).

    If Ms. Smith answers my question, I’ll will pose the simple questions of the pre-existence of CD4 degredation, viral release regulation, and ion channel functionality, and that should do it.

    We’ll see. Keep me posted guys.

  95. Sal,
    I found some “tentative” evidence that HIV is degrading instead of evolving, At this site:

    http://www.eurekalert.org/pub_.....071307.php

    Citing some laboratory research that suggests HIVs from the late 1980s are more virulent than HIVs from the 2000s, Worobey added, “For HIV, the really cool thing is that these changes can take place on a more rapid timeline that previously thought.”

    I looked for the laboratory research on the web but could not find it :(

    Maybe one of you guys can help me find the paper-s :)

    If the virus is in reality slowly degrading into a less virulent form it would be hard evidence for the Genetic entropy of the virus and would effectively refute any assertions of evolution occurring in the virus..

    They also assert in the paper that SIV is less virulent today than it was in the past for monkeys!

  96. http://www.whale.to/vaccines/decline1.html

    This page is very interesting in that the data shows all infectious diseases were declining prior to the introduction of immunization. The author attributes it to a drop in poverty. Yet I see that another connection may be able to be drawn that validates the postulation of Genetic Entropy of infectious diseases.
    I believe, if my memory serves me right, all known infectious diseases, such as flu, appear suddenly (perhaps luckily finding a single protein/protein binding site) Then the liness of the infectious agent slowly decreases with time (genetic entropy to infectious agent) until it disappears.
    This FACT stands out to me since the liness of the disease should increase, or at least stay constant, if evolution were truly driving it to find better protein binding paths in its host.
    Thus from the past natural gradual DECLINE of all other infectious diseases studied BEFORE IMMUNIZATION, HIV infection should show a gradual decline in the future due to its natural genetic entropy!

    Some may try to attribute this to the human immune system, yet the immune system is known to have a limited memory.
    Of course other factors could very well be involved, yet I think my postulation is highly feasible in the over scheme, none-the-less

  97. I wrote:

    I am still unsure of the SHIVTM paper

    ERV provided a data point:
    Shiv vs hiv vs siv creationists know

  98. Ok Sal, In all their evidence I see this is the only one that comes close to being anything that would remotely challenge Behe’s EOE limit of 2 novel protein/protein binding sites.

    2. CD4 degradation capability existed before HIV entry into humans.

    And ERV told us that in her first post: “The feature both Vpus have in common, CD4 degradation, is carried out in completely different ways. HIV-1 Vpu requires two casein kinase II sites. You could almost call it irreducibly complex– If you dont have both CKII sites, CD4 isn’t degraded. Yet some SIVcpz Vpus have only one CKII site, and instead utilize a simple string of negatively charged amino acids in place of the second site 11. Different ways of performing similar tricks with totally different amino acids. I think that’s biochemically significant as well.”

    Same capapbility; novel method.

    The VPU protein already has the ability to bind to the host CD4 protein and degrade CD4, Thus no new protein/protein binding site is generated, neither is a novel function created!
    ERV and her friends are calling an inhanced function of one VPU protein significant. It may be significant in a very limited way of a already bound protein and already existing function, yet this enhancment of a already existing function does absolutely nothing to establish a violation of the Limit set forth by Behe for the tentative protein/protein binding limit of 2. Enhancing a preexisting function is small potatoes compared to finding the correct match in a novel protein/protein binding search.
    So I still don’t see where this has anything to do with violating Behe’s EOE limit. So Sal maybe you can get them to tell us where the violation is.

    I mean Aren’t they trying to claim Behe’s protein binding limit is violated with observational data?
    I still don’t see it. Maybe they just forgot to post it. Could you see if this was a oversight on their part Sal?

  99. Sal, you appear to have them squirming

    Your question: Did Vpu pre-exist in the HIV strain prior entry into humans?”

    Now, all that’s needed here is a yes or no. But you got:

    9:46 PM
    ERV said…
    Why dont you start with reading my (potty-mouth word) post from a month ago that explained that clearly. Then why dont you read the proceeding posts that reiterated my answers to that question. Then why dont you read the comments that I wrote for you answering that question. Then you can read the posts OTHER people wrote answering that question by TELLING YOU EXACTLY where I wrote comments AND posts for you before.

    Are you retarded?

  100. bornagain77:
    I found some “tentative” evidence that HIV is degrading instead of evolving…

    Decreasing virulence is not a sign that the virus is ‘devolving’ or ‘degrading’. It’s textbook natural selection. A greater mortality rate does not make the virus more successful or ‘evolved’.

    If the rate of transmission is high, strains with a faster reproductive cycle are favoured over their slower cousins. This might mean greater mortality for the host but not necessarily so – HIV does not gain in any way from killing it’s victim. When the rate of transmission goes down the reverse occurs.

  101. Ah, so this thread is no longer the original but has evolved into the counter part of ATBC and the Infidels Peanut Gallery.

    I responded to Ms. Smith:

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

    Ms Smith asks “Are you retarded?”

    Apparently so, that’s why I just wanted to make sure that you are indeed answering “YES” because you kept accusing me that it was “my premise” that Vpu pre-existed in HIV prior to entry into humans.

    So is it your premise as well that Vpu pre-existed in HIV prior to entry into humans?

    For the sake of retarded individuals like myself and the mentally impaired readers who do not quite have the ability to appreciate your literary flourishes, a simple “YES” will clarify the matter greatly.

    Thank you in advance.

    regards,
    Salvador

  102. ERV apparently is having a hard time answering a simple question:

    See: Sal buys ‘Where’s Waldo’ book, never seen again

    =========

    The fact that Vpu exists in SIVcpz and HIV-1 today suggests that Vpu existed in HIV-1 already when it infected humans.

    The VPUs are different today but one still calls it Vpu. This fact argues for the very point I’m trying to be certain of, namely Vpu already existed in HIV-1 when it first infected humans.

    I really don’t want to misrepresent your position on a simple question. So I asks this simple question again:

    “Is it your premise that Vpu pre-existed in HIV prior to entry into humans?”

    If you’d answered it already, my apologies in advance, but a simple YES or NO to that question would help clarify the matter greatly.

    Thank you in advance.

    regards,
    Salvador

  103. Sal,

    For the sake of retarded individuals like myself and the mentally impaired readers who do not quite have the ability to appreciate your literary flourishes, a simple “YES” will clarify the matter greatly.

    Be careful about admitting to being mentally retarded, they might try to force you into compulsory sterilization.

  104. The question is putting ERV in an extremely difficult position.

    She must concede a major point, namely, the Vpu gene existed already in HIV prior to entry into humans.

    When this point is conceded it will also lead to other difficulties. Because if Vpu existed already when HIV infected humans, then the question arises: “what other sorts of machinery came along for the ride?”

    ERV went off into tangents without answering the very simple question directly and cleary on behalf of the debate.

    ERV appears unwilling to make it explicit that the Vpu gene existed already when HIV first infected humans.

    This simple question has bearing on Behe’s book:

    page 139:

    no new gizmos or basic machinery…

    no gene duplication leading to a new function

    I pointed out ERV’s invocation of gene duplication in HIV-2 has no bearing on Behe’s claims because Behe is talking about HIV-1 after HIV-1′s introduction into humans. He is not talking about HIV-2.

    The simple question I posed remains unanswered:

    Is it your premise that Vpu pre-existed in HIV prior to entry into humans?

  105. Ah yes, the question is still not answered. Here is my interaction with Dr. Hermagoras

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

    Hermagoras said:

    “What part of “Vpu is only found in one group– Chimpanzee SIV (SIVcpz) and its descendants—including HIV-1″ do you not understand? The question was answered before you asked it”

    I very well understand that this means I’m right. I’m not even being bashful that the reason I keep hammering this issue is that Ms. Smith will have to make a major concession, namely: “the Vpu gene already existed in HIV-1 when it first infected humans.”

    She can articulate that clearly or let the discussion drag on with pictures and insults. Fine. The question still remains:

    “Is it your premise that Vpu pre-existed in HIV prior to entry into humans?”

    A simple YES or NO for the sake of the audience to this debate will suffice, and spare the readers any more tedium.

  106. http://www.eurekalert.org/pub_.....071307.php

    In the above paper the authors state this:

    Citing some laboratory research that suggests HIVs from the late 1980s are more virulent than HIVs from the 2000s, Worobey added, “For HIV, the really cool thing is that these changes can take place on a more rapid timeline that previously thought.

    I can’t seem to find any references on the web to this laboratory research.

    Does anybody know where I can get the paper on the web?

    This research will go a long way in establishing the overall “genetic entropy” of HIV and effectively refute claims of positive evolution in HIV by evolutionists!

  107. #105 Bornagain77

    Here is the ful text of the paper:

    http://pathogens.plosjournals......at.0030095

    A Challenge to the Ancient Origin of SIVagm Based on African Green Monkey Mitochondrial Genomes

    Joel O. Wertheim*, Michael Worobey

    1 Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, Arizona, United States of America

    While the circumstances surrounding the origin and spread of HIV are becoming clearer, the particulars of the origin of simian immunodeficiency virus (SIV) are still unknown. Specifically, the age of SIV, whether it is an ancient or recent infection, has not been resolved. Although many instances of cross-species transmission of SIV have been documented, the similarity between the African green monkey (AGM) and SIVagm phylogenies has long been held as suggestive of ancient codivergence between SIVs and their primate hosts. Here, we present well-resolved phylogenies based on full-length AGM mitochondrial genomes and seven previously published SIVagm genomes; these allowed us to perform the first rigorous phylogenetic test to our knowledge of the hypothesis that SIVagm codiverged with the AGMs. Using the Shimodaira–Hasegawa test, we show that the AGM mitochondrial genomes and SIVagm did not evolve along the same topology. Furthermore, we demonstrate that the SIVagm topology can be explained by a pattern of west-to-east transmission of the virus across existing AGM geographic ranges. Using a relaxed molecular clock, we also provide a date for the most recent common ancestor of the AGMs at approximately 3 million years ago. This study substantially weakens the theory of ancient SIV infection followed by codivergence with its primate hosts.

    Funding. This work was supported by the NSF-IGERT (Integrative Graduate Education and Research Traineeship) in Evolutionary, Functional, and Computational Genomics at the University of Arizona, NIH/NIAID (R21 AI065371 to MW), and the Department of Ecology and Evolutionary Biology at the University of Arizona.

    Competing interests. The authors have declared that no competing interests exist.

    Editor: Edward C. Holmes, The Pennsylvania State University, United States of America

    Citation: Wertheim JO, Worobey M (2007) A Challenge to the Ancient Origin of SIVagm Based on African Green Monkey Mitochondrial Genomes. PLoS Pathog 3(7): e95 doi:10.1371/journal.ppat.0030095

    Received: March 12, 2007; Accepted: May 17, 2007; Published: July 6, 2007

    ….

  108. #101

    The question is putting ERV in an extremely difficult position.

    Go on Sal. It’t too fun that a handful of “retarded IDiots” (IDiots because retarded or retarded because IDiots?) shows as “fatally flawed” the brilliant arguments of a brilliant and promising graduate student …. :-D

  109. The stone walling continues….Since Ms. Smith wouldn’t answer the question, I posed the simple question to her colleagues.

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

    factian said: “You’re making a very simple error. I suspect you’re doing it on purpose,…..

    Naming something vpu doesn’t make it the same thing as vpuSIV.”

    Where did I the Vpu’s are necessarily identical in any strain where Vpu’s exist?

    Now then, let’s move on. I said: “I very well understand that this means I’m right.”

    Dr. Hermagaoras asked:
    “Right about what, exactly, Sal?”

    Right about the fact that Vpu existed in HIV prior to HIV entering the human population.

    So, the question remains to Ms. Smith, and I’ll even simplify the wording so any one here can answer it:

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

    I phrased it so you can answer it Hermagoras, and clarify it for me.

    You seem to argue I’m dense. Fine. For the sake of argument I’m dense.

    I suppose a simple YES or NO to this central question is not too difficult to articulate, especially for you Dr. Hermagoras.

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

    YES or NO?

    We’ll see if a PhD English professor can spell the word “YES” ! :=)

  110. This research will go a long way in establishing the overall “genetic entropy” of HIV and effectively refute claims of positive evolution in HIV by evolutionists!

    I don’t know if becoming less virulent is a sign of genetic entropy. If you think about it. An HIV strain that does not kill its host has a better chance of reproducing than a fatal strain. In that sense, becoming less virulent is a selective advantage.

  111. #110,

    Agreed.

    In general, while it’s “interesting” to watch the verbal gymnastics being employed I’d rather focus on subjects like that made in comment #98. This is like arguing whether the TTSS came before or after the flagellum when there are more deadlier arguments to Darwinism.

  112. We must be careful to assert becoming more or less virulent or more or less selectively advantage has much to say about complexity or functional increase or decrease.

    For example, dysfunctional systems (like sickle cell anemia) confer selective advantage in certain contexts.

    As Scott Minnich pointed out in Icons, sometimes the selective advantage for bacteria as it develops anti-biotic resistance is the result of damage, not functional improvement. When the selective pressure is removed (i.e. level of anti-biotics decreased in the environment) the absence of selection will favor the more functional strains.

    Thus by way of slight extrapolation, there could be cases where decrease in virulence could possibly be an indication of the prevalence of more functional forms rather than genetic entropy.

    This is the odd fact: “Genetic Entropy may lead to selective advantage in some cases”. We should not be fooled into thinking because genetic entropy decreases function, that decrease in function necessarily leads to disadvantage in a Darwinian world.

    Consider cases where dysfunction is selectively advantageous:

    1. Cave fish losing the ability to see (they are more metabollically efficient, no need for eyes if you can’t use them any way)

    2. Moles losing vision

    3. Speigelman experiment

    4. Some forms of anti-biotic resistance

    5. Sickle cell anemia

    etc. etc…..

    At first glace it looks like the ancestors of HIV possibly had more functionality than today. It is possible specialized adaptation to the host may have occured through loss of function rather than acquisition of function. This is speculation at this time, but well, given the pro-Darwin climate, it unfortunately can’t be explored.

    My reading of the papers suggests that there were levels of redundancy that are now lost. In some strains Vpu performs a certain function, and in other strains another protein does the job. Why? Is that evolution of new function or is it really loss of 1 function in one lineage and loss of another function in another lineage? The Darwinian paradigm is not allowing the question to be raised because it would violate orthodox views.

    Salvador
    PS
    Can Hermagoras spell the word “YES”? What sort of sweet things are they saying about me over at ERV? Keep me posted.

  113. This link at bottom is a graph showing declining mortality rates for infectious diseases through time. It seems to have a fairly constant mathematical decay curve through time for all the different infectious diseases, indicating a very possible mathematical correlation to the (constant?) genetic entropy of the infectious agent. My main gripe with the criticism I’ve received, concerning this postulation, is that a infectious disease becoming less virulent in order to survive is still ignoring the proven hard fact of the overwhelming, if not what very well may be complete, negative mutation rate to an organisms DNA, all the while, creating a loophole for evolutionists to escape through and claim positive results for evolution. No I don’t like it at all! Especially when we got hard evidence in our corner to back up our claims for the deleterious nature of any mutations to the DNA itself!

    Please take a look at the graph and see if any of you can spot a fairly constant pattern. My main point is that all new infectious diseases should follow this same decay curve of the old diseases as well.

    http://www.healthsentinel.com/....._list_item

  114. Sal, I just went over there.

    I don’t think they understand Behe’s work.

    As bornagin77 said way back in post 28 “If (they) could please clearly elaborate the violation of Behe’s limit” it would give something concrete to discuss.

    But they can’t even give a yes or no

  115. bornagain77, you wrote:

    “It seems to have a fairly constant mathematical decay curve through time for all the different infectious diseases, indicating a very possible mathematical correlation to the (constant?) genetic entropy of the infectious agent.”

    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.

  116. 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.”

  117. “Let your ‘Yes’ mean ‘Yes,’ and your ‘No’ mean ‘No.’ Anything more is from the evil one.”

    Yup.

  118. It looks like they finally answered, btw.

    YES

  119. 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”. :-)

  120. I suppose ‘Piss off’ was too hard for you to understand too?

    A classy lady :-)

  121. 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?”

  122. 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.

  123. 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/....._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)

  124. 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.

  125. 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.

  126. 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/....._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!

  127. 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.

  128. 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!

  129. #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.

  130. #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 .-D

  131. 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.”

  132. #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.

  133. 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”.

  134. 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.

  135. 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!

  136. 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?

  137. 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
    ======

  138. 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.

  139. DaveScot, I remember it well. It is the origin of the “liar liar, pants on fire” objection.

  140. 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.”

  141. 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 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?

  142. 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 ;-)

  143. 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.

  144. 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??

  145. 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.

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