I just sent an email to Dr. Behe letting him know that in my showdown with Dr. Musgrave over at ERV’s blog I had already pointed out to Ian that the development of viroporin activity happened in the 20′s and 30′s, well before anyone had ever heard of HIV. Thus, if one considers the time period for which Table 7.1 was constructed, the viroporin activity should not be included.

The ZERO should remain ZERO.

Thus Dr. Musgrave must conclusively prove the development of two more protien/protein binding sites to defeat Dr. Behe’s estimate of a limit of 2.

eh? Don’t fall into Musgrave’s trap of conflating the two examples of minor Darwinian evolution. The whole point is that something like this might be expected to be within the powers of Darwinism for viruses. The problem is that they’re taking the factors surrounding viruses and extrapolating that as somehow providing evidence for higher organisms even though the situation is very different.

Really, the only reason Darwinists are gaining any mileage at all on this minor issue is because it was not originally included in EoE. You don’t hear them crowing over the other minor examples of Darwinian evolution that were discussed in the book. The oddball part is that none of these examples have enough informational bits to be CSI. Even before Behe took the time to look at this example I was wondering what the commotion was about since even to me it was rather obvious after a cursory reading it would not present a challenge. So why make a mountain out of a molehill?

Since Dr. Musgrave was so blatant on this distortion, I looked at what Dr. Behe said about this binding site that Dr. Musgrave is so impressed with.

One should, however, also make some distinctions with this example. First, although there apparently are five or so copies of Vpu in the viroporin complex, that does not mean that five binding sites developed. Only one new binding site need develop for one area of a protein which binds to a different area of the same protein, to form a homogeneous complex with, say, C5 symmetry. That is all that is required for a circularly symmetric structure to form. Second, the viroporin is not some new molecular machine. There is no evidence that it exerts its effect in, say, an ATP- or energy-dependent manner. Rather, similar to other viroporins, the protein simply forms a passive leaky pore or weak channel. (4,5) This situation is probably best viewed as a foreign protein degrading the integrity of a membrane, rather than performing some positive function. And third, I explicitly pointed out in Chapter 8 of The Edge of Evolution that HIV had undergone enough mutating in past decades to form all possible viral-viral binding sites, but commented that apparently none of them had been helpful (now I know that one of them helped). This I discussed as the “principle of restricted choice”:

From my limited knowledge of the subject, it seems the protein/protein binding site he is so excited about, is actually a additional “refining” protein binding site of the one that actually allowed the HIV to gain access to humans in the first place.

Yet even conceding this point Dr. Behe comments: So the square point in Figure 7.4 representing HIV should be placed on the Y axis at a value of one, instead of zero, and Table 7.1 should list one protein-binding site developed by HIV instead of zero.

Thus Dr. Musgrave must conclusively prove the development of two more protien/protein binding sites to defeat Dr. Behe’s estimate of a limit of 2.

To me the whole debate is laughable , because the conservative estimate of number of protein/protein binding sites in a cell in Dr. Behe’ book is 10,000.
Yet in a number of replication events that far exceeds the proposed mammals split from reptiles (which requires far more than a paltry few binding sites to develop), we see this quibbling over whether zero, one, or even a few, protein/protein binding sites developed.

It does not follow logic at all for evolutionists to claim proof of principle when they have done no such thing at all.

Until evolutionists can come up with far better proof than what they are currently crowing about (one overlooked binding site), they are merely stating a conjecture of their imagination with no solid foundation in reality.

There aren’t any new protein to protein binding sites made by those 9- that is protein to protein binding sites within the virus.

Dr. Behe begs to differ:

Yes, I’m perfectly willing to concede that this does appear to be the development of a new viral protein-viral protein binding site, one which I overlooked when writing about HIV.

In Musgrave’s attempt to get around Dr. Behe’s hard number of 10^10 for HIV he tries to use the smoke and mirrors of effective population size used in population Genetics. Yet I looked at Behe’ sources in His book and they do in fact take into account the effective population size that is used in population genetics to arrive at there number. So Behe’s number is thoroughly thought out and firm as a rock.

Here are Dr. Behe’s sources on page 290 of EDge of Evolution”

15. Geritti, A.M.2006. HIV-1 sub-types: epidemiology and significance for HIV management.

http://www.co-infectiousdiseas.....28!8091!-1

Curr. Opin. Infect. Dis. 19:1-7. Rodrigo, A. G. 1999. HIV evolutionary genetics. Proc.Natl. Acad. Sci. USA 96:10559-61. Total body burden of the number of copies of HIV RNA is estimated to be much higher, about 10^11 (Haase, A. T., Henry, K., Zupancic, M., Sedgewick, G., Faust, R. A., Melroe, H., Cavert, W., Gebhard, K., Staskus, K., Zhang, Z. O., Dailey, P. J., Balfour, H. H. Jr., Erice, A., and Perelson, A. As. 1996. Quantitative image analysis of HIV-1 infection in lymphoid tissue. Science 274:985-89).

The effective population size is estimated at 500 to 10^5 (Althaus, C.L., and Bonhoeffer, S. 2005. Stochastic interplay between mutation and recombination during the acquisition of resistance mutations in human immunodeficiency virus type 1.J. Virol. 79:13572-78).

http://www-binf.bio.uu.nl/alth.....jvirol.pdf

16 Rodrigo, A. G., Shpaer, E. G., Delwart, E. L., Iverson, A.K., Gallo, M.V., Brojatsch, J., Hirsch, M. S., Walker, B. D., and Mullins, J. I. 1999. Coalescent estimates of HIV-1 generation time in vivo. Proc. Natl. Acad. Sci. USA 96:2187-91.

http://www.pnas.org/cgi/content/full/96/5/2187

You may want to take a real close look at this study Dr. Musgrave:

One of the major problems facing HIV molecular evolutionary biologists is sampling: with 10^10 virions produced daily in an infected individual, and 10^6-10^7 infected cells present,

Thus, since each virus is considered a chance for evolution to strut its almighty stuff the 10^10 replication number stands solid!

17. Coffin, J. M. 1995. HIV population dynamics in vivo. Proc. Natl. Acad. Sci. USA 96:2187-91.

http://www.sciencemag.org/cgi/.....7/5197/483

another note for you Dr. Musgrave:

These results lead to a simple steady-state in which infection, cell , and cell replacement are in balance, and imply that the unique feature of HIV is the extraordinarily large number of replication cycles that occur during infection of a single individual.

I just don’t understand your logic at all Dr. Musgrave. Your argument for limit to population size has no merit, whatsoever, since the entire HIV population of 10^10 is being replaced every day or two and each virus replication is in fact a search of variation for HIV. So the search area and population size of the HIV stands firm and is not limited as you are vainly trying to do.
In my opinion this was a desperate attempt at distortion on your part and you should be ashamed to call yourself a scientist, since apparently finding the truth has no meaning for you!

HIV has 9 genes. It has never had more than 9.

There aren’t any new protein to protein binding sites made by those 9- that is protein to protein binding sites within the virus. Dr Behe explained he is not talking about foreign proteins.

IOW it is obvious that Abbie disregards what Dr Behe is saying and then sets out to refute something he didn’t say.

Also Dr Behe is talking about constructive protein to protein binding sites. If the theory of evolution were indicative of reality there should be a muriad of such events. Yet we are still waiting for ONE!

http://www.amazon.com/gp/pdp/p.....38-2939066

Larry, thanks for the reference. Now you might want to look up what “received as exhibits” means.

Re:
“If admitted, the statements may be read into evidence but may not be received as exhibits.”
– from Federal Rules of Evidence Rule 803(18)http://www.law.cornell.edu/rul.....tm#Rule803

Why should I look it up? Why don’t you tell me what it means or what you think it means?

There is no applicable legal definition of the word “receive,” so I just used the normal definitions of the word that are appropriate in this context, e.g., “accept,” “take,” “approve,” etc.. And I did give you legal definitions of “exhibit,” e.g., “a document or object shown to the court as evidence in a trial.”

Also, with no basis whatsover, the Kitzmiller opinion said that this literature “refuted” irreducible complexity: “We therefore find that Professor Behe’s claim for irreducible complexity has been refuted in peer-reviewed research papers and has been rejected by the scientific community at large.”

You can’t always assume that what you read in the law may be taken absolutely literally.

Why not?

It doesn’t appear that Behe has responded to Musgrave on that topic yet. However, the population of HIV in an infected individual is about 10^10.

http://mbe.oxfordjournals.org/.....21/10/1902

The generation time is a day or two, so your infected person produces 10^13 per year. There are 40 – 50 million HIV positive people in the world, so in any given year the population of HIV virus in humans is about 4 x 10^20.

Behe is right about that.

I already posted the link to where Smith visited and dodged the issues:

http://www.uncommondescent.com.....4864%20rel=

It conveniently logs the back and forth responses that occurred elsewhere.