In one of his books (The Edge of Evolution), Michael Behe proposed the idea that evolution has limited capabilities; it predominantely breakes existing genes but it rarely (if ever) comes up with something new. For example, Behe said that evolving a protein-protein binding interaction is exceedingly difficult.
Ian Musgrave objected against this, claiming that the HIV-1 viral protein U (Vpu) evolved a new binding site. More specifically, Vpu allegedly gained viroporin activity: it forms an ion channel and increases the permeability of infected host cells.
I don’t believe that this is a good example for protein evolution. Channel activity of Vpu seems to be conserved among primates. This means that viroporin function is not a special attribute of HIV-1 Vpu and thus, recent evolution cannot be demonstrated. See here:
You wrote “conserved among primates” but the topic is a viral protein in a specific lineage of retroviruses, namely the SIV/HIV-1 lineage. The article you link provides evidence that the viroporin activity arose early in that lineage. It does not refute, or address, whether that change involved new binding sites or whether it is an example of recent evolution of elaborate protein functions.
So, I don’t think you understood the paper you linked. If you read it again, you’ll see that it is all about HIV-1 and its already-known relatives, that it’s not about primates at all, and that it is a clear example of protein evolution. Not that we need any more of those.
Now I’m confused. In his second reply to Behe, Musgrave wrote that Vpu gained channel activity only within the HIV-1 M Group:
SIV Vpu is not a viroporin, HIV-1 O Vpu is not a viroporin. This is a new activity that evolved in HIV after the split from SIV over a 10 year timeframe and is part of the reason that the HIV-1 M clade is the most common type of HIV in the world.
The paper I cited seems to directly refute this. Quote:
Already Vpugsn, the evolutionary oldest of the proteins tested here, generates channel function. Collectively, this implies that channel formation is an inherent and evolutionary old property of the Vpu protein.
I haven’t read his piece and don’t have time to do that today. My suggestion (not very helpful, I know) is to have a look at Musgrave’s citations and perhaps to look at the primary literature. I found this review article that suggests (as I thought before) that the viroporin activity is not exclusive to HIV-1. But if your quote of Musgrave is accurate then he seemed to think, a long time ago, that it was.
That would make the adaptive immune system impossible for the apparently intended meaning of the phrase “exceedingly difficult”(which I’m sure is supposed to mean “couldn’t be expected to evolve”).
Heck, one has to wonder how viruses manage to evolve to infect new hosts in different species?
