Science, E. coli, and the Edge of Evolution: Part 2Originally published at Michael Behe's Amazon Blog
This is the second in a series of responses I’m posting this week, this one regarding the Darwinian website The Panda’s Thumb, where a woman named Abbie Smith 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.
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. I’ll pass over all that and try to stick to the substance.
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. 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.
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:
This chapter makes some important distinctions and addresses potential objections. It considers counter-arguments to my attempt to define the edge of evolution — not philosophical ones, about the “other side” of that boundary, but technical and logical ones about the line itself….
Another, more important point to note is that 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. [emphasis added here] The foreign proteins of pathogens almost always are intended to cripple a cell in any way possible. 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.
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. Yet The Edge of Evolution is concerned with how molecular machinery is constructed, not destroyed. One can’t ignore such critical distinctions and make progress. But, in my experience, many Darwinists overlook important differences.
She goes on to list several other properties of Vpu, but, while interesting, none at all are what one should call “fundamental” changes. For example, she notes, the HIV Vpu has several sites that are negatively charged by virtue of being phosphorylated. She continues, “Yet some SIVcpz Vpus have only one [phosphorylation] site, and instead utilize a simple string of negatively charged amino acids in place of the second site. Different ways of performing similar tricks with totally different amino acids. I think that’s biochemically significant as well.”
Well, I disagree. I don’t think that’s biochemically fundamental at all. In each case one has a blob of negative charge. Since the mutation rate of HIV is so extremely high, kinase sites are likely replaced every day in some virus with multiple glutamates or aspartates and vice versa. She also points out that some virus Vpu subtypes have altered the location of modification sites or acquired signals to localize protein in particular subcellular compartments. But again, because of the virus’s extremely high mutation rate, such sites would be expected to come and go frequently. As I emphasized in The Edge of Evolution, HIV’s enormous numbers and very high mutation rate cause immense variation. The question, however, is to what extent the immense variation has produced novel virus systems or machinery? And, as I indicated, the answer is very little. Butler at al (HIV Genetic Diversity: Biological and Public Health Consequences, Current HIV Research, 2007, 23-45) remark under the subheading “Biological Consquences of HIV Diversity”:
With such breadth of genetic diversity among HIVs, one might expect significant biological differences between the clades. Although interesting variations can be seen, much of the data concerning biological implications of HIV diversity is contradictory.
Plenty of differences do exist, and some are “interesting”, but not all that great.
Darwinists overlook the considerable power of the example of the relatively minor changes in HIV: there have been a truly astronomical number of copies produced in just the past fifty years or so. 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. 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.
Read Michael Behe’s first and third responses in this series.