Michael Behe's Amazon Blog

So help me understand this. Novel protein-protein interactions that evolve in a pathogen are off limits when we are talking about HIV ("I'm considering just cellular proteins binding to other cellular proteins, not to foreign proteins. Foreign proteins injected into a cell by an invading virus or bacterium make up a different category.") but novel protein-protein interactions are what you say never happen if the pathogen is P. falciparum... I'd appreciate your explanation of the difference beyond just the hand-waving "Destructive protein-protein binding is much easier to achieve by chance". From the point of view of the virus, evolution has produced a PRODUCTIVE novel protein-protein interaction, don't you think?

Can you tell me why the novel protein-protein interactions that have evolved multiple times in the past 60-70 years in Vpu (including changes that result in a novel re-location to the membrane) are not "novel virus systems or machinery"? Seems to me that the virus switched to a new host (humans) partially as a result of those changes in Vpu. In just a few decades.

Two and a half months.

For that.

Readers, I refer you to my blog for my reactions to this post, as I doubt Behe will be responding here, and this comments section being open is a fluke.
http://endogenousretrovirus.blogspot.com

Mike, you are a complete sell out who has betrayed his science in an "end satisfies the means" fashion to promote your personal, fundamentalist and intellectually void religion. In short, you are an idiot who behaves like a chess club geek who has just had his queen taken and would rather throw a tantrum than resign like a man.

But I'm not going to bring any of that up. Because that's the kind of guy I am.

Instead, I'm just going to stick to commenting on your book. It has a lot of words.

Of course, since it was written by a woman (or "Mean Girl", refering to that awful teen movie) it has junior high tone.That's very sexist of you. I expected more from a scientist.

"Mean Girls" wasn't an awful movie. Not the best, but not awful.

Behe's reply, on the other, hand was an awful and horribly sexist relpy, months after the fact. It was also unworthy of anybody with multiple neurons firing in the ol' cranium.

I'm no biologist, but it seems to me that Behe thinks that fitness and adaptation are irrelevant, and he expects that HIV should have become a mammal by now. If not for all of his shabby strawmen (and the witless sycophants who stand in line to shine his shoes), Behe would be a very lonely guy.

[Deleted by Amazon on Oct 12, 2007 8:41 AM PDT]

Abbie Smith,
It seems Behe was very clear in his refutation of you, He wanted to see the virus (or malaria) itself build up complexity and thus prove evolution...I see exactly what he means...Is not evolution suppose to build up the complexity of individual organisms? Yet, despite fantastic mutational firepower that far exceeds what happens in higher organisms, he found only trivial results in many more generations and mutations than occur for higher organisms.. Where is the the novel complexity Abbie?

To give a little more background to the uphill struggle evolution is facing let's break it down to the protein level.

"Each cell with genetic information, from bacteria to man, consists of artificial languages and their decoding systems, memory banks for information storage and retrieval, elegant control systems regulating the automated assembly of parts and components, error fail-safe and proof-reading devices utilized for quality control, assembly processes involving the principle of prefabrication and modular construction and a capacity not equaled in any of our most advanced machines, for it would be capable of replicating its entire structure within a matter of a few hours" Geneticist Michael Denton PhD.

To give an idea how impossible "simple" life is for naturalistic blind chance, Sir Fred Hoyle calculated the chance of obtaining the required set of enzymes for just one of any of the numerous types of "simple" bacterial life found on the early earth to be one in 10^40,000 (that is a one with 40 thousand zeros to the right). He compared the random emergence of the simplest bacterium on earth to the likelihood "a tornado sweeping through a junkyard might assemble a Boeing 747 therein". Sir Fred Hoyle also compared the chance of obtaining just one single functioning protein (out of the over one million protein molecules needed for that simplest cell), by chance combinations of amino acids, to a solar system packed full of blind men solving Rubik's Cube simultaneously.

The simplest bacteria ever found on earth is constructed with over a million protein molecules. Protein molecules are made from one dimensional sequences of the 20 different L-amino acids that can be used as building blocks for proteins. These one dimensional sequences of amino acids fold into complex three-dimensional structures. The proteins vary in length of sequences of amino acids. The average sequence of a typical protein is about 300 to 400 amino acids long. Yet many crucial proteins are thousands of amino acids long. Proteins do their work on the atomic scale. Therefore, proteins must be able to identify and precisely manipulate and interrelate with the many differently, and specifically, shaped atoms, atomic molecules and protein molecules at the same time to accomplish the construction, metabolism, structure and maintenance of the cell. Proteins are required to have the precisely correct shape to accomplish their specific function or functions in the cell. More than a slight variation in the precisely correct shape of the protein molecule type will be fatal for the life of the cell. It turns out there is some tolerance for error in the sequence of L-amino acids that make up some the less crucial protein molecule types. These errors can occur without adversely affecting the precisely required shape of the protein molecule type. This would seem to give some wiggle room to the naturalists, but as the following quote indicates this wiggle room is an illusion.

"A common rebuttal is that not all amino acids in organic molecules must be strictly sequenced. One can destroy or randomly replace about 1 amino acid out of 100 without doing damage to the function or shape of the molecule. This is vital since life necessarily exists in a "sequence-disrupting" radiation environment. However, this is equivalent to writing a computer program that will tolerate the destruction of 1 statement of code out of 1001. In other words, this error-handling ability of organic molecules constitutes a far more unlikely occurrence than strictly sequenced molecules." Dr. Hugh Ross PhD.

It is easily demonstrated mathematically that the entire universe does not even begin to come close to being old enough, nor large enough, to accidentally generate just one small but precisely sequenced 100 amino acid protein (out of the over one million interdependent protein molecules of longer sequences that would be required to match the sequences of their particular protein types) in that very first living bacteria. If any combinations of the 20 L-amino acids that are used in constructing proteins are equally possible, then there are (20100) =1.3 x 10130 possible amino acid sequences in proteins being composed of 100 amino acids. This impossibility, of finding even one "required" specifically sequenced protein, would still be true even if amino acids had a tendency to chemically bond with each other, which they don't despite over fifty years of experimentation trying to get amino acids to bond naturally (The odds of a single 100 amino acid protein overcoming the impossibilities of chemical bonding and forming spontaneously have been calculated at less than 1 in 10125 (Meyer, Evidence for Design, pg. 75)). The staggering impossibility found for the universe ever generating a "required" specifically sequenced 100 amino acid protein by accident would still be true even if we allowed that the entire universe, all 1080 sub-atomic particles of it, were nothing but groups of 100 freely bonding amino acids, and we then tried a trillion unique combinations per second for all those 100 amino acid groups for 100 billion years! Even after 100 billion years of trying a trillion unique combinations per second, we still would have made only one billion, trillionth of the entire total combinations possible for a 100 amino acid protein during that 100 billion years of trying! Even a child knows you cannot put any piece of a puzzle anywhere in a puzzle. You must have the required piece in the required place! The simplest forms of life ever found on earth are exceedingly far more complicated jigsaw puzzles than any of the puzzles man has ever made. Yet to believe a naturalistic theory we would have to believe that this tremendously complex puzzle of millions of precisely shaped, and placed, protein molecules "just happened" to overcome the impossible hurdles of chemical bonding and probability and put itself together into the sheer wonder of immense complexity that we find in the cell.

Instead of us just looking at the probability of a single protein molecule occurring (a solar system full of blind men solving the Rubik's Cube simultaneously), let's also look at the complexity that goes into crafting the shape of just one protein molecule. Complexity will give us a better indication if a protein molecule is, indeed, the handi-work of an infinitely powerful Creator.
In the year 2000 IBM announced the development of a new super-computer, called Blue Gene, that is 500 times faster than any supercomputer built up until that time. It took 4-5 years to build. Blue Gene stands about six feet high, and occupies a floor space of 40 feet by 40 feet. It cost $100 million to build. It was built specifically to better enable computer simulations of molecular biology. The computer performs one quadrillion (one million billion) computations per second. Despite its speed, it is estimated it will take one entire year for it to analyze the mechanism by which JUST ONE "simple" protein will fold onto itself from its one-dimensional starting point to its final three-dimensional shape. In real life, the protein folds into its final shape in a fraction of a second! The computer would have to operate at least 33 million times faster to accomplish what the protein does in a fraction of a second. That is the complexity found for JUST ONE "simple" protein. It is estimated, on the total number of known life forms on earth, that there are some 50 billion different types of unique proteins today. It is very possible the domain of the protein world may hold many trillions more completely distinct and different types of proteins. The simplest bacterium known to man has millions of protein molecules divided into, at bare minimum, several hundred distinct proteins types. These millions of precisely shaped protein molecules are interwoven into the final structure of the bacterium. Numerous times specific proteins in a distinct protein type will have very specific modifications to a few of the amino acids, in their sequence, in order for them to more precisely accomplish their specific function or functions in the overall parent structure of their protein type. To think naturalists can account for such complexity by saying it "happened by chance" should be the very definition of "absurd" we find in dictionaries. Naturalists have absolutely no answers for how this complexity arose in the first living cell unless, of course, you can take their imagination as hard evidence. Yet the "real" evidence scientists have found overwhelmingly supports the anthropic hypothesis once again. It should be remembered that naturalism postulated a very simple "first cell". Yet the simplest cell scientists have been able to find, or to even realistically theorize about, is vastly more complex than any machine man has ever made through concerted effort !! What makes matters much worse for naturalists is that naturalists try to assert that proteins of one function can easily mutate into other proteins of completely different functions by pure chance. Yet once again the empirical evidence we now have betrays the naturalists. Individual proteins have been experimentally proven to quickly lose their function in the cell with random point mutations. What are the odds of any functional protein in a cell mutating into any other functional folded protein, of very questionable value, by pure chance?

"From actual experimental results it can easily be calculated that the odds of finding a folded protein (by random point mutations to an existing protein) are about 1 in 10 to the 65 power (Sauer, MIT). To put this fantastic number in perspective imagine that someone hid a grain of sand, marked with a tiny 'X', somewhere in the Sahara Desert. After wandering blindfolded for several years in the desert you reach down, pick up a grain of sand, take off your blindfold, and find it has a tiny 'X'. Suspicious, you give the grain of sand to someone to hide again, again you wander blindfolded into the desert, bend down, and the grain you pick up again has an 'X'. A third time you repeat this action and a third time you find the marked grain. The odds of finding that marked grain of sand in the Sahara Desert three times in a row are about the same as finding one new functional protein structure (from chance transmutation of an existing functional protein structure). Rather than accept the result as a lucky coincidence, most people would be certain that the game had been fixed." Michael J. Behe, The Weekly Standard, June 7, 1999, Experimental Support for Regarding Functional Classes of Proteins to be Highly Isolated from Each Other
"Mutations are rare phenomena, and a simultaneous change of even two amino acid residues in one protein is totally unlikely. One could think, for instance, that by constantly changing amino acids one by one, it will eventually be possible to change the entire sequence substantially... These minor changes, however, are bound to eventually result in a situation in which the enzyme has ceased to perform its previous function but has not yet begun its `new duties'. It is at this point it will be destroyed - along with the organism carrying it." Maxim D. Frank-Kamenetski, Unraveling DNA, 1997, p. 72. (Professor at Brown U. Center for Advanced Biotechnology and Biomedical Engineering)

Even if evolution somehow managed to overcome the impossible hurdles for generating novel proteins by totally natural means, Evolution would still face the monumental hurdles of generating complimentary protein/protein binding sites in which the novel proteins could actually interface with each other in order to accomplish specific tasks in the cell (it is estimated that there are least 10,000 different types of protein-protein binding sites in a "simple" cell). What does the recent hard evidence say about novel protein-protein binding site generation from what is actually observed to be occuring on the protein level of malaria and HIV since they have infected humans? Once again the naturalists are brutally betrayed by the hard evidence that science has recently uncovered!

The likelihood of developing two binding sites in a protein complex would be the square of of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 binding sites being generated by accident) in the history of life. It is biologically unreasonable. Dr. Michael J. Behe PhD. (from page 146 of his book "Edge of Evolution")

[Deleted by the author on Oct 13, 2007 7:34 PM PDT]

[Deleted by the author on Oct 13, 2007 7:33 PM PDT]

Behe's mendacity in this essay is breathtaking:

"where a woman named Abbie Smith..."

Abbie Smith is an HIV researcher. Behe isn't. Behe, who makes a big deal of his own dubious expertise, deliberately omits her qualifications to speak about HIV. Does Behe have a problem with her gender? How is it relevant?

"...questioned whether results from HIV research actually square with the claims I made that little fundamental change has occurred in the virus, even though it attains enormous populations sizes and has a much increased mutation rate."

And nowhere does Behe inform his audience of the very specific claims he made in the book: "It still has the same number of genes that work in the same way. There is no new molecular machinery." He elides this because Ms. Smith demolished both of these claims. IOW, Behe knows that his claims are false.

"Although she calls herself a "pre-grad student," the tone of the post is decidedly junior high, the tone of someone who is trying hard to compete with all the other Mean Girls on that unpleasant website."

Wow. The sexism in this attack is astounding.

"I'll pass over all that and try to stick to the substance."

In fact, Behe brought it up as his first ad hominem attack, so he can't honestly claim to have passed it over at all.

"Her post mainly concerns a small protein coded for by HIV-1 called Vpu. She first points out that the amino acid identity between the homologous chimp SIV protein with HIV Vpu is 39%, much less than that of other homologous viral proteins, and she seems to regard that fact by itself as remarkable."

It is, because it shows how quickly HIV has evolved the new functions that Behe claimed couldn't evolve.

"Yet the alpha and beta chains of human hemoglobin are only about 44% identical, and have virtually superimposable structures and very similar functions."

This is a truly idiotic comparison, given that Behe doesn't dispute common descent. Alpha and beta hemoglobin are homologous; they diverged ~500 million years ago. Vpu of SIV and Vpu of HIV are orthologous, and diverged ~50 years ago.

"The fact that the chimp and human versions of VPU have 39% identity indicates they are structurally virtually identical."

No competent biochemist would make such a preposterous claim, so Behe must be deluded, dishonest, or (my opinion) both. The normal and pathological forms of the prion protein are 100% identical in sequence, and they have very, very different structures. The reality (and Behe knows this) is that sequence identity does not correlate well with structure. Proteins can be 10% identical and have superimposable structures, or as with prions, be 100% identical with radically different structures. A lot of biochemistry is about huge changes in structure and function caused by the binding of very small molecules to very large proteins.

"That doesn't seem like a fundamental change to me."

Behe defined fundamental changes in his book: "It still has the same number of genes that work in the same way. There is no new molecular machinery." Both of those claims are utterly false, as Abbie Smith demonstrated. Watch Behe dance!

"She goes on to write that Vpu acts to degrade CD4 molecules by binding to them and recruiting the pathway that degrades CD4. Unfortunately, she seems not to have read the beginning of chapter 8 of The Edge of Evolution ("Objections to the Edge"), where I make some careful distinctions:..."

Behe's distinctions are irrelevant. If Behe was still a scientist, he'd be publishing actual data from experimental tests of his own hypotheses. Instead, he has given up being a scientist in favor of writing books that deceive laypeople.

"Another, more important point to note is that I'm considering just cellular proteins binding to other cellular proteins, not to foreign proteins."

This is spectacularly false, as Behe's criteria were offered in the explicit context of HIV.

"Foreign proteins injected into a cell by an invading virus or bacterium make up a different category."

Behe's ignorance is showing. HIV doesn't "inject" Vpu into a cell, it enters by endocytosis, and Vpu is translated from transcripts of the viral genome *after* it integrates into the host genome. (Behe also falsely claims that the HIV genome is DNA, when in fact, it has an RNA genome.)

"[emphasis added here] The foreign proteins of pathogens almost always are intended to cripple a cell in any way possible."

This is absurdly ignorant. Viruses evolve to replicate themselves more efficiently. There is no "intention to cripple a cell," because they must parasitize the cellular machinery to replicate themselves. If pathogen proteins crippled the cell in any way possible, viral pathogens couldn't replicate. "Crippling" and death of cells are a byproduct, not an "intended" purpose. In fact, most of the clinical symptoms of a viral infection are caused by your immune response, not any destruction caused by the virus.

"Since there are so many more ways to break a machine than to improve it, this is the kind of task at which Darwinism excels. Like throwing a wad of chewing gum into a finely tuned machine, it's relatively easy to clog a system - much easier than making the system in the first place. Destructive protein-protein binding is much easier to achieve by chance."

Its destructiveness, real or imagined, is irrelevant.

The point is that protein-protein binding is trivially easy to evolve by random genetic variation and selection. Every reader of this post can personally evolve many new, incredibly specific protein-protein binding site in only two weeks, using nothing but (random wrt binding affinity) genetic variation and selection. These proteins are called antibodies. Apparently Behe is not familiar with them!

"So the example she chose is from exactly the category that I excluded in the above paragraph. My exclusion isn't arbitrary. As I wrote, there are many more ways to cripple a machine than to build one, so destructive Darwinian processes can appear to accomplish more."

Behe's exclusion is laughably arbitrary, because HIV's "goal" is to replicate itself, not cripple/destroy its host. Viruses in our real world tend to become less pathogenic as they evolve, not more.

"She goes on to list several other properties of Vpu, but, while interesting, none at all are what one should call "fundamental" changes."

All of them fulfill the criteria Behe explicitly specified but is concealing from his audience, because Behe's intent is to deceive: "It [HIV] still has the same number of genes that work in the same way. There is no new molecular machinery."

"Plenty of differences do exist, and some are "interesting", but not all that great."

Note that Behe is running away from his own criteria, because he knows that what he wrote is false.

"...And because of its much increased mutation rate, it has undergone in the past half century as many of some kinds of mutations as all the cells have undergone in the history of the world."

This comparison is laughable. The HIV genome has strict length constraints because it has to be packaged. Human genomes don't. That leaves out the most rapid means of evolution: gene duplication followed by divergence. Still, HIV evolved what Behe said it couldn't evolve (completely new biochemical functions) in mere decades of real-time observation.

"If Darwinism had the power that its boosters claim, we should expect to see truly fundamental changes. Yet despite the enormous number of opportunities, only minor changes have appeared. That is very strong evidence of the strict limits on what Darwinian processes can accomplish."

Behe's handwaving rhetoric isn't evidence. If Behe had even a smidgen of faith in what he writes, he would be working in his lab producing new evidence to cure/prevent AIDS and malaria, not grubbing for money by selling a book that bamboozles lay people about these horrible diseases.

Let's approach this as science, and hypothesize that Behe really believes that all the malaria researchers of the world are totally wrong in the way that they approach the evolution of drug resistance in Plasmodium, a horrendous problem. If this hypothesis is correct, Behe would be raising money from all the Christians who also passionately believe in ID to try and prevent the deaths of millions of children by doing actual research and generating real data, starting from his own hypotheses. Instead, Behe does nothing and will continue to stay out of his own laboratory, because writing these pseudoscientific books is lucrative and Behe, in whatever bit of soul he might have remaining, doesn't believe what he's trying to sell his readers at all.

My thoughts can be found here: http://afoolsexperiment.blogspot.com/2007/10/michael-behe-are-you-kidding-me.html

Smokey covered it in detail, though.

Dr. Behe,

While I agree with Smokey's analysis of your unfortunate reply to Abbie I am taking advantage of the ability to comment here and publicly asking you something that has bothered me. You have focused on the microscopic level to suggest that randomness is insufficient to explain observations. It is obvious that you are dealing at a level of detail that involves quantum mechanical effects. Experiments have shown quantum effects aren't random. Why was there so little discussion of quantum physics in your book Edge of Evolution when many scientists have been linking quantum physics to life processes? Examples of such scientists include Stapp, Patel and those at Berkeley lab who, this year, demonstrated photosynthesis is a quantum mechanical mechanism.

Both you and Abbie Smith could be correct. Her observations could be correct and your analysis visa-vie randomness could also be correct. Random Mutation would turn out to be impotent if, in fact, non-random quantum effects are fundamental to life at the microscopic level.

I would have thought you and CSC fellow, Henry F. Schaefer III, would have discussed something like this.

[Deleted by the author on Oct 12, 2007 2:08 PM PDT]

Some lowlights from Philip's rant:
"In real life, the protein folds into its final shape in a fraction of a second! The computer would have to operate at least 33 million times faster to accomplish what the protein does in a fraction of a second."

This is ridiculous. The computer isn't *doing *what the protein does (folding), it's calculating what a protein will do based on our incomplete knowledge. Are you claiming that computer weather simulations produce real hurricanes?

"That is the complexity found for JUST ONE "simple" protein. It is estimated, on the total number of known life forms on earth, that there are some 50 billion different types of unique proteins today."

Can any one explain the oxymoron "types of unique proteins"? I'm sure Philip can't.

"It is very possible the domain of the protein world may hold many trillions more completely distinct and different types of proteins."

There are very few distinct types of proteins. In fact, about 20% of your genes encode proteins of the P-loop NTPase family. Evolution doesn't produce random proteins; very little of "sequence space" is explored by evolution.

"The simplest bacterium known to man has millions of protein molecules divided into, at bare minimum, several hundred distinct proteins types."

Simply false. The number of distinct types is very small.

"Individual proteins have been experimentally proven to quickly lose their function in the cell with random point mutations."

False. Let's see how you do at prediction. If I mutate an almost universally-conserved residue in the active site (that even touches the substrate) of a protein to a residue not found in any member of its large superfamily, will I:
a) destroy all activity;
b) lose the original activity, but create a new activity; or
c) retain the original activity while creating a new activity?

"What are the odds of any functional protein in a cell mutating into any other functional folded protein, of very questionable value, by pure chance?"

Extremely high.

"...It is at this point it will be destroyed - along with the organism carrying it." Maxim D. Frank-Kamenetski, Unraveling DNA, 1997, p. 72. (Professor at Brown U. Center for Advanced Biotechnology and Biomedical Engineering)"

Oh, and by the way, we "knocked in" this radical substitution in the mouse genome. Were our homozygous mutant mice:
a) dead, or
b) normal?

"...Evolution would still face the monumental hurdles of generating complimentary protein/protein binding sites in which the novel proteins could actually interface with each other in order to accomplish specific tasks in the cell (it is estimated that there are least 10,000 different types of protein-protein binding sites in a "simple" cell)."

Your body evolves incredibly specific protein/protein binding sites IN ONLY TWO WEEKS using nothing but random genetic variation (primarily recombination, with point mutations added for spice) and selection, which isn't random, no matter how many times antievolutionists lie and claim it is.

"What does the recent hard evidence say about novel protein-protein binding site generation from what is actually observed to be occuring on the protein level of malaria and HIV since they have infected humans?"

You wouldn't know, because you've only skimmed Behe's gross misrepresentation of the evidence.

[Deleted by Amazon on Oct 12, 2007 5:24 PM PDT]

Behe: "She first points out that the amino acid identity between the homologous chimp SIV protein with HIV Vpu is 39%, much less than that of other homologous viral proteins, and she seems to regard that fact by itself as remarkable. Yet the alpha and beta chains of human hemoglobin are only about 44% identical, and have virtually superimposable structures and very similar functions. The fact that the chimp and human versions of VPU have 39% identity indicates they are structurally virtually identical. That doesn't seem like a fundamental change to me."

What a horrendous logical gaffe! He's arguing that because two particular proteins that share only 44% identity are nevertheless structurally superimposable, that any two proteins that share a similar level of identity will also be structurally identical. That's not quite the dumbest thing I've encountered from this "brilliant" mind, but it's close.

Behe also fails to explain how it is that the Antarctic antifreeze protein, whose stepwise evolution he presented so eloquently, also evolved a new protein-to-protein interaction (that he conveniently omitted from his discussion) that results in its modification with sugars to its mature form.

[Customers don't think this post adds to the discussion. Show post anyway. Show all unhelpful posts.]

Philip: "The likelihood of developing two binding sites in a protein complex would be the square of of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 binding sites being generated by ) in the history of life."

You have fallen into Behe's intellectual trap. It's really very simple. His calculations are based upon the false assumption that evolution works through the occurance of multiple, simultaneous mutations without the benefit of selection between genetic events. This assumption has an enormous impact on the probabilities. He is not only wrong in theory, he is wrong on the facts. There are some excellent examples of novel protein-to-protein interactions having evolved. Behe inadvertently provides one in his description of the evolution of the Antarctic antifreeze protein (pages 77-81, but leaves out the important fact of a new P-P interaction), which is actually a glycoprotein--a protein that is modified by sugar addition. The protein must be processed by an enzyme, through a specific protein-to-protein interaction. This interaction evolved as part of the evolution of the antifreeze protein.

I just wanted to add to Dr. Behe's great points:

Abbie's comment:

"Five Vpu proteins come together to form a Na+K+ viroporin."

The exact number of Vpu proteins assembling is not experimentally confirmed.

Also "Na+K+ viroporin" is a missleading statement. I would prefer 'a channel forming protein with preference for cations'.

Abbie also stated:
"Viroporin capabilities have not been found with SIVcpz Vpu."

And that therefore they evolved de novo, but thats a non-sequitor. It is since very recently that we know that Vpu-mediated CD4 down-regulation and degradation is conserved among highly divergent SIV(cpz) strains. As Behe's quote states, it's murky waters in here.

With regards to CD4 downregulation, recently in it has been shown that both HIV subtypes NL4-3 and R5 Vpu proteins in U937 downregulate CD4 to similar extents