Uncommon Descent Serving The Intelligent Design Community

ERV’s challenge to Michael Behe

Salvador Cordova
August 28, 2007
Darwinism, Intelligent Design
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[continued from Dr. D.A. Cook’s thread, Where Did Sea Anemones Get Human Genes?]

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

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

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

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

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

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

Comments
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. DaveScot
August 29, 2007
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#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.kairos
August 29, 2007
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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.ERV
August 29, 2007
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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.PaV
August 29, 2007
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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.DaveScot
August 29, 2007
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"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....Michaels7
August 28, 2007
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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.scordova
August 28, 2007
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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.ERV
August 28, 2007
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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, Salvadorscordova
August 28, 2007
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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, Salvadorscordova
August 28, 2007
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Thanks for visiting this site Ms. Smith, I anticipate this will be a very interesting dialog.bornagain77
August 28, 2007
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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.ERV
August 28, 2007
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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. Salvadorscordova
August 28, 2007
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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}]).Charles Foljambe
August 28, 2007
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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")Joseph
August 28, 2007
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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.bornagain77
August 28, 2007
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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.Zed
August 28, 2007
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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.Charles Foljambe
August 28, 2007
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"We gotta generate a little more drama than this." But this would need other people to discuss with ...kairos
August 28, 2007
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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"kairos
August 28, 2007
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… 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.scordova
August 28, 2007
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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.scordova
August 28, 2007
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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.kairos
August 28, 2007
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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. Salvadorscordova
August 28, 2007
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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" :-)kairos
August 28, 2007
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