Feedback archive → Feedback 2008

An information-gaining mutation in HIV?

Wikipedia

A friend of CMI, Philip R of Victoria, Australia wrote:

An incorrect assertion. I could see nothing on the Amazon blog that remotely fitted the description that Dr Behe ‘admitted, to be wrong’.

This is a bit of ‘elephant hurling’, providing a list of references that would ‘snow’ many into just accepting the assertion without further question. Most would reason that no one would provide references that don’t actually back up the claim made. It’s a bluff, basically.

Reference 9, a 2005 paper, actually shows that the supposedly novel Vpu activity in HIV-1 (based on the title (?!) of Reference 1, which dates from 1988) is not confined to HIV-1, but is present in SIV (the ape / monkey form of the virus):

‘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.’ [Abstract]

All four different isolates of SIV that were investigated expressed a version of the Vpu protein. So where is the evidence that this is even a new protein, peculiar to HIV-1 (see later)?

I can’t see where anyone has demonstrated that this is a truly novel trait of HIV-1. Indeed the importance of Vpu to efficient HIV replication (Ref. 1) suggests that Vpu has been a necessary part of HIV and SIV all along. The claim seems to rest on an interpretation of the wording of a 1988 paper and subsequent research has certainly shown that the trait is not novel at all. As is so often the case, creationists are vindicated by further research that inevitably overturns evolutionary claims that are based on incomplete knowledge—see, for example, the story of ‘junk DNA’.

Ref. 9 compares the Vpu proteins from the different SIV viral strains and they are quite different from each other and from HIV-1 subtype B, but all of them successfully wreck the expression of CD4 (an important antigen expressed on the surface of various cells, including T-helper lymphocytes), which is now known to be a major action of the protein:

‘Taken together, these results show for the first time that Vpu proteins from SIV(cpz) isolates, although quite diverse in sequence and predicted secondary structure from the HIV-1 subtype B protein, are capable of down-regulating CD4, which is one of the major functions of the HIV-1 protein.’ [abstract; emphasis added]

Wikipedia

This suggests that Vpu does not have much specificity, which is not needed to wreck something (it would appear that Behe’s chewing gum analogy is not far wrong, i.e. something to ‘gum up the works’ doesn’t have to be very specific; proteins are naturally sticky molecules). That is, Vpu gums up the expression of CD4, ultimately resulting in the death of T-helper lymphocytes. This messes up the immune system, which then enables HIV to multiply and cause AIDS. But it is a very complex interplay of different factors, because of the extreme complexity of the human immune system. It also involves enhanced inflammation resulting from the imbalance in the immune system.¹ Interestingly, apoptosis (programmed cell death), a vital feature connected with normal T-lymphocyte action, involves a very complex sequence of events that shouts ‘design’.²

Reference 1 shows that the HIV-1 Vpu protein is 81 amino acids, which is hardly ‘pretty substantial due to the complexity associated with the proteins involved’. It is only one protein, and a relatively small one at that. And some of the SIV Vpu’s are much smaller, but still work (Ref. 9)—the piece of chewing gum does not have to have a very specific size! Vpu’s effectiveness seems to depend on a handful of negatively-charged amino acids, that’s all (Ref. 9). Such is not beyond the ‘edge of evolution’ that Behe identified anyway.

So even if Vpu did arise de novo, by mutations, which has not been demonstrated, it is not a very significant achievement for ‘evolution’.

Even if this was a truly novel HIV gene, it would not support the notion that mutations have created all the complexity of life on earth. If this is all that HIV could achieve with its astronomical populations, rapid generation times and high mutation rates, it argues against mutations creating the bacterial flagellum, the cilium, the Krebs cycle, the photosynthetic apparatus, the DNA replication, transcription and translation systems, or a host of other biochemical marvels that are part of life.³ This is a major point of Behe’s book The Edge of Evolution: even with its vast capacity for ‘evolution’ HIV hasn’t achieved anything significant. And if HIV can’t do it, organisms like worms, jellyfish and humans certainly can’t do it, even given eons of evolutionary time.

This sounds very condescending. It would appear that the protagonist himself has not understood the papers! And the question is not whether Vpu is beneficial to the virus (creationists do not deny that beneficial mutations occur). The question is rather, is it actually new and is it an addition of significant specified complexity that bolsters the belief that purely natural processes could create the ATP synthase complex (the world’s tiniest motor), for example? The leap of faith required is akin to believing, as John Woodmorappe says:

‘since a cow can jump, and we might not agree exactly how high it can jump under favorable circumstances, therefore we are free to believe that a cow can jump all the way around the moon.’

Summary: It seems that the skeptic (most of whom strangely refuse to be skeptical of evolution!) has misunderstood the basis of the use of ‘novel’ in Ref. 1, which is used in the sense of ‘newly discovered’, not ‘newly arisen’. Subsequent sequencing (e.g. see Ref. 9, 2005) certainly showed that Vpu is not unique to HIV-1, so it is not ‘novel’ in the sense that believers in evolution would like. So the argument evaporates.

Correct!

Correct again. See above.

I hope this helps.

Don Batten