Hey do you guys remember Michael Behe? Massive douche, wrote books about how EVILUTION IS IMPOSSI-BLEH! Gave school boards/teachers an excuse to teach Creationism in public school classrooms and pretend they were teaching science? He was like, the cock-of-the-walk when ‘Darwins Black Box’ came out, but then he made a total ass of himself testifying in Dover, and then he wrote that massive abortion, ‘Edge of Evolution’, and now dude has pretty much disappeared off Planet Earth?
Well, while Michael ‘Lilo’ Behe might be gone, he has not been forgotten!
Three years ago, Behe wrote ‘Edge’. It contained the dumbest comments I have ever read on HIV-1, just short of the crap I read from HIV-1 Deniers:
And exactly what has all that evolution of HIV wrought? Very little. Although news stories rightly emphasize the ability of HIV to quickly develop drug resistance, and although massive publicity makes HIV seem to the public to be an evolutionary powerhouse, on a functional biochemical level the virus has been a complete stick-in-the-mud. Over the years its DNA sequence has certainly changed. HIV has killed millions of people, fended off the human immune system, and become resistant to whatever drug humanity could throw at it. Yet through all that, there have been no significant basic biochemical changes in the virus at all.
Neither has much else happened at a molecular level. No new gizmos or basic machinery. There have been no reports of new viral protein-protein interactions developing in an infected cell due to mutations in HIV proteins. No gene duplication has occurred leading to a new function. None of the fancy tricks that routinely figure in Darwinian speculations has apparently been of much use to HIV.
These statements were hysterically wrong three years ago, and they just keep getting funnier as time passes.
Gene duplication and divergence has played an important role in HIV/SIV evolution. HIV-1 has new genes with new functions with new protein-protein interactions in humans vs SIV in chimpanzees.
Viral Protein U, in SIV in chimpanzees, downregulates CD4 (a viruses way of pissing on the fire hydrant, so to speak). Nef, in SIV in chimpanzees, does lots of stuff, including degrading a host anti-viral, tetherin.
Human tetherin does not look like chimpanzee tetherin. We have a small deletion in the cytoplasmic tail region… exactly where SIV chimpanzee Nef interacts with it. This might be due to selection pressure in humans long long ago, or it could be a side-effect of drift and severe population bottlenecks in human history. Doesnt matter– SIV Nef cannot get rid of human tetherin.
So what the hell was SIV supposed to do when it became ‘HIV’?
Well, Vpu in HIV-1 figured out a completely different way to get around human tetherin. Vpu in HIV-1 and Nef in SIVcpz get around the problem of tetherin in fundamentally different ways. Requires TONS of brand spanking new, never before seen on earth, protein-protein interactions. Has nothing to do with ‘gumming up the works‘, but a series of elegantly evolved mutations came together to accomplish a complex task. And when I say ‘never seen before on Earth’, I mean, ‘never seen before on Earth’. Unlike Nef and Nef-like factors, which have left their evolutionary-pressure-footprint on primate tetherins, Vpu and Vpu-like proteins that we maybe havent discovered yet have not been around long enough to have shaped tetherin, in any primate, including humans:
Vpu and Vpu-like factors (i.e. factors with the same specificity as modern Vpu proteins) are too recent to have had an effect on tetherin evolution.
Which brings me to more Behe lulz– Behe was obsessed in ‘Edge’ with how TOTALLY IMPOSSI-BLEH it was for random mutations and natural selection to ‘make’ anything. He even happily trots out the tired ‘monkeys at a typewriter’ cliche.
So, how ‘impossible’, exactly, was it for SIV from chimpanzees to turn into HIV-1 Vpu to gain a brand new function at no cost to its previous function? Seven amino acids.
Although none of the strains of SIVcpz Vpu were identical to the consensus Vpu of HIV-1 Group M, among several strains of SIVcpz Vpu (LB7, CAM5, EK505 and MB66) which include the closest relatives of HIV-1 group M (18), the SIVcpz LB7 strain would be predicted to require seven minimal adaptations within the two regions (amino acids 1-8 and 14-22) to gain the ability to antagonize human Tetherin.
OMFG! SEVEN AMINO ACIDS! All at the right place and the right time… THATS SO IMPOSSI-BLEH!