Pandas Thumb Fails to Refute Michael Behe on HIV Evolution
Pandas Thumb guest contributor Abbie Smith has posted an alleged refutation of Michael Behe. Behe stated in The Edge of Evolution that "in just the past few decades HIV has actually undergone more of certain kinds of mutations than all cells have endured since the beginning of the world." However, Behe then observed that "those mutations, while medically important, have changed the functioning virus very little. It still has the same number of genes that work in the same way. There is no new molecular machinery." Smith claims that Behe's statement is refuted, but her evidence is nothing more than the fact that Human HIV-1 has a gene called Vpu which was present in HIV when it first infected humans, and that this gene can perform 2 functions. In fact, the only basis of evidence for the "evolution" of Vpu that Smith provides entails sequence comparison between human HIV 1's copy of Vpu and Chimpanzee SIV's copy of Vpu. Behe provides a lucid rebuttal to this assumption-based argument in The Edge of Evolution: "modern Darwinists point to evidence of common descent and erroneously assume it to be evidence of the power of random mutation." (pg. 95) Since Vpu apparently existed when HIV infected humans, it's not clear how this evidence refutes anything Behe said.
The best argument Smith makes for the power of Darwinian evolution is the observation that the Vpu proteins found in different strands of HIV can reside in different parts of the cell (she observes, "Subtypes [sic] B Vpu prefers ... to be in the Golgi, helping degrade CD4, while Subtype C Vpu prefers to be in the plasma membrane, assisting with the release of new viruses"). Does this imply that Vpu recently evolved a new function? Hardly. As this paper from Klaus Strebel, a researcher at the National Institutes of Health, explains, Vpu generally performs both functions Smith cites: "Vpu has two primary biological activities. These include the degradation of CD4 in the endoplasmic reticulum and the augmentation of virus secretion from the plasma membrane." Strebel's paper continues:
Vpu consists of an N-terminal hydrophobic domain, that functions as membrane anchor, and a hydrophilic cytoplasmic domain. ... The cytoplasmic domain contains sequences critical for CD4 degradation while the membrane anchor domain has a critical function in regulating virus release and plays an important role in the formation of cation selective ion channels.In other words, Vpu has two different protein domains, each of which performs one of the functions cited by Smith. Thus, neither Vpu protein in the two strains of HIV acquired any new function, for as far as we can tell, both Vpus in both strains of HIV generally perform both tasks.
There appears to be no hard evidence that Vpu acquired any new functions since it infected humans. Since all Behe stated is that since HIV has infected humans, it has "changed ... very little. It still has the same number of genes that work in the same way. There is no new molecular machinery," it appears that Behe was refuted in no way, shape, or form by Abbie Smith. Smith provides no evidence for any type of HIV evolution beyond what Behe already acknowledges has taken place.
Finally, Smith claims that Behe says that "HIV has not evolved biochemically." But this is not true. As noted, Behe actually stated, "HIV has actually undergone more of certain kinds of mutations than all cells have endured since the beginning of the world." But Behe observes that all these random mutations have resulted in no new genes or functions since HIV infected humans. And Smith provides no evidence to show Behe is wrong. Apparently Smith considers insignificant changes that do not generate new genes or new biological functions to be impressive examples of biochemical evolution. Such examples of evolution will never explain the full complexity of the cell or answer the arguments made by Behe.