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

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.Gareth_{August 31, 2007
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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 BeheÃ¢â‚¬â„¢s limit" it would give something concrete to discuss. But they can't even give a yes or notribune7_{August 31, 2007
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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/graphs.php?id=23&event=graphs_print_list_itembornagain77_{August 31, 2007
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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.scordova_{August 31, 2007
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#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.Patrick_{August 31, 2007
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This research will go a long way in establishing the overall Ã¢â‚¬Å“genetic entropyÃ¢â‚¬Â 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.Jehu_{August 31, 2007
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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" ! :=)scordova_{August 31, 2007
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#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 .... :-Dkairos_{August 31, 2007
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#105 Bornagain77 Here is the ful text of the paper: http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.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 ShimodairaÃ¢â‚¬â€œHasegawa 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 ....kairos_{August 31, 2007
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http://www.eurekalert.org/pub_releases/2007-07/uoa-ctf071307.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, Ã¢â‚¬Å“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!bornagain77_{August 31, 2007
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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 descendantsÃ¢â‚¬â€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.
scordova_{August 30, 2007
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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?
scordova_{August 30, 2007
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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 Ã¢â‚¬Å“YESÃ¢â‚¬Â will clarify the matter greatly.
Be careful about admitting to being mentally retarded, they might try to force you into compulsory sterilization.Jehu_{August 30, 2007
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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
scordova_{August 30, 2007
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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
scordova_{August 30, 2007
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bornagain77: I found some Ã¢â‚¬Å“tentativeÃ¢â‚¬Â 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.guppy_{August 30, 2007
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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?
tribune7_{August 30, 2007
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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?bornagain77_{August 30, 2007
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I wrote:
I am still unsure of the SHIVTM paper
ERV provided a data point: Shiv vs hiv vs siv creationists knowscordova_{August 30, 2007
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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-lessbornagain77_{August 30, 2007
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Sal, I found some "tentative" evidence that HIV is degrading instead of evolving, At this site: http://www.eurekalert.org/pub_releases/2007-07/uoa-ctf071307.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!bornagain77_{August 30, 2007
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bornagain77 wrote: Sal, I wouldnÃ¢â‚¬â„¢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.scordova_{August 30, 2007
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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,,,LOLbornagain77_{August 30, 2007
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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!bornagain77_{August 30, 2007
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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. :=)scordova_{August 30, 2007
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Ok people this is ERV's claim to refute Behe: Vpu is a new gene, not a Ã¢â‚¬Ëœlost in everyone elseÃ¢â‚¬â„¢ 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!bornagain77_{August 30, 2007
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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 IÃ¢â‚¬â„¢ve done so on numerous occasions. IÃ¢â‚¬â„¢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 criticsÃ¢â‚¬â„¢ 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 SchneiderÃ¢â‚¬â„¢s article Ã¢â‚¬Å“Evolution of Biological Information,Ã¢â‚¬Â 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 Ã¢â‚¬Å“free lunch,Ã¢â‚¬Â but, yes, he was claiming that it brought about biological complexity Ã¢â‚¬Å“from scratchÃ¢â‚¬Â; 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 donÃ¢â‚¬â„¢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. IÃ¢â‚¬â„¢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 donÃ¢â‚¬â„¢t deserve to be placated. WhatÃ¢â‚¬â„¢s more, they are not very frightening, especially when you get past their initial defenses, so thereÃ¢â‚¬â„¢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 soulÃ¢â‚¬â„¢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, letÃ¢â‚¬â„¢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 donÃ¢â‚¬â„¢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, IÃ¢â‚¬â„¢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, IÃ¢â‚¬â„¢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. ThatÃ¢â‚¬â„¢s the pattern I see in this debate. The proponents of evolution would very much prefer to stay in their fortified positions. They donÃ¢â‚¬â„¢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
scordova_{August 30, 2007
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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.StephenB_{August 30, 2007
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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/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15823605&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum%E2%80%9D http://lib.bioinfo.pl/pmid:15975620 Well the evolutionists won't like this development much at all will they?bornagain77_{August 30, 2007
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Patrick wrote: I agree completely and thatÃ¢â‚¬â„¢s the point. I was hoping to get Ms. Smith and Dr. Hunt to admit that even if their speculative scenario was correct itÃ¢â‚¬â„¢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.scordova_{August 30, 2007
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