Ive got two tests and a paper to worry about first tonight, but if you all are blissfully homework free: Go play!
So I woke up this morning, made some coffee, checked my e-mail, and did my usual Sitemeter/Technorati check. I had a ton of hits from UD. From a post on sea anemones. "Oh god" I thought "Theyre using my glowing viruses as Evidences for Intelligent Design(TM)."
Thankfully, that wasnt the case.
Someone just asked about my essay as a side comment (even Average Joe Creationists are uncomfortable with Behes silence). Sal was nice enough (silly enough?) to provide a link to my essay, happily removing all doubt that Behe is *unaware* of my post, and adding even more pressure on Behe to respond. LOL!
Anyway, I know 99% of you cant post at UD, so please feel free to leave comments here!
Response 1, 08-28-07:
Sal, thank you for providing me a forum where I can answer your questions. That makes you two steps ahead of Behe. To answer your questions—fine. Lets say all viruses in the lentivirus family related to HIV-1 lost their Vpu. It probably cropped up millions of years ago—long before we were there with Qiagen kits to watch what was happening, so I will happily entertain that possibility*.
HIV still does not have, quote, the ‘same number of genes.’ If we grant your premise, all branches of immunodeficiency viruses ‘lost’ a gene. ‘Same’ minus one. And, HIV-1 Vpu doesn’t look genetically or act biochemically like its ancestor, SIVcpz Vpu. They don’t ‘work in the same way.’ Behe is still wrong.
Additionally, what has happened while we were watching is the evolution of the Subtype B and Subtype C sequences. Not only are HIV-1 Vpu sequences vastly different from SIVcpz Vpus, but B and C Vpus each have their own specific biochemical markers and specialties. We’ve watched that happen. Thus, Behe is still wrong.
And we have barely scratched the surface of HIV evolution. Hes only going to get ‘more wrong’ from here on out.
* We know Vpu is new in HIV-1 because of the directionality of necessity. As I referenced in my original essay, Vpu evolved in a very specific way in HIV-1 to overcome a cell specific and human specific host factor. Please see reference 10- I tried very hard to find PLoS/PubMedCentral references for this very purpose.Response 2, 08-28-07:
I believe Mike was referring specfically to human strains after the introduction into humans…
You dont want to reinterpret what Behe said this way. HIV-1 and HIV-2 are entirely different creatures. Also, HIV-2 has a gene duplication– something Behe said ’specifically’ hadnt happened in HIV.
He preferred to us directly observed evolutions rather than using interpretations possibly biased by a preconception such as a phylogeny…
How, exactly, do you explain the apparent phylogeny of primate lentiviruses, then? And, this doesnt help your case. Again, lets grant your premise– HIV-1 is not related to SIVcpz. HIV-1 and HIV-2 are entirely different creatures. This makes things worse for Behe.
The Vpu protein did not emerge de novo after introduction into humans. Is that correct?
Absolutely right, which I addressed in my essay: “Ah, Michael Behe, you might try to talk your way around Vpu now (though you were evidently unaware of its existence moments ago) by insisting that it is not *new* new.”
By the way, I appreciate your candor regarding the possibility of Vpu gene loss in ancient strains of HIV rather than gene emergence.
Anything is a possibility with HIV. But experimental evidence is normally used to figure out which possibilities are viable, and which can be discarded. Vpu is a new gene, not a ‘lost in everyone else’ gene.
Response 3, 08-29-07: Davie has turned moderation on my comments so he can read them before everyone else. Im THAT exciting!
Sal-- *quip, sorry* HIV-1 is not AIDS. You progress to AIDS after being infected with HIV-1. :)
Again, I will grant your premise-- Behe meant nothing happened in HIV-1 AFTER it was introduced to humans.
Behe still has a de novo multiprotein complex to worry about, and several de novo protein-protein interactions. He says that hasnt happened. He even made a table to say it hasnt happened.
I have never typed that Vpu is novel in humans. Its new in a branch of primate lentiviruses, again, look at reference 10. Its the sequence, biochemistry, and functionality that are different in humans.
Michael-- The number of phylogeny papers for HIV-1, 2, and SIV is massive (go to PubMed/PLos and search 'HIV phylogeny'). The easiest thing would be to point you towards the Los Alamos National Laboratory HIV sequence database. There, you can get sequences to line up yourself, if you dont believe anyone!
Dave-- Yup! Thats the quote (I knew he said it at least once)! HIV-2 has a new gene with lots of fun functions.
Here is a recent (free) paper on the topic!
PaV-- Sure! HIV-1 could have gotten Vpu from the chimpanzee genome! The sequence is so divergent (not only in humans, but in SIVcpz) that we have no idea where it came from at this point. Its not an obvious gene duplication like Vpx.
But as I said in my essay and here-- HIV-1 Vpu and SIVcpz Vpu are totally different genetically, biochemically, and functionally. The main difference is that HIV-1 Vpus can form 'viroporins'. Thats pretty wild.
The function they both have in common (destroying CD4 markers) is irreducibly complex in HIV-1... But not in SIVcpz. And then theres the evolution of novel protein binding/localization sequences in at least two subtypes (we havent looked at them all yet).
But the virus is still no more than a virus...
*frown* There is a reason HIV-1 has taken over this planet while HIV-2 has not. Vpu is part of that reason.
The differential evolution of Vpu between the subtypes points towards a way of stopping the subtype that is out competing every other HIV-1 out there.
Youre free to believe Vpu evolution is 'insignificant', but I doubt HIV-1 would agree with you.
That is a very old Creationist Claim, btw.
Response 4, 8/29/07:
If we drive Ms. Smith away, others might think we had to resort to banning because we could not defend ourselves, or could not point out when her reading of Behe was inaccurate. This should be an easy thing to do, and no cause for getting rid of her.
Thank you, Sal. And your readers have brought up wonderful questions. However, answers will only be posted to questions on my blog if my comments are going to be ‘held in moderation’ here.
This is your blog– youre free to moderate as you see fit. But Im not wasting my time answering your readers questions if youre going to trash my responses.
Dave– Im looking at a copy of ‘Edge’ right now. Would you like to read it out loud together?
“Yet through all that, there have been no significant biochemical changes in the virus at all…”
Response #5, 8/29/07:Mike was referring to #1, and Ms. Smith to #2, therefore, because this is an equivocation, #2 cannot be used as a counter example to #1.
Fine. Lets grant your premise again. Behe really meant '1. protein-protein binding within the same organism upon which a critical function depends.'
Vpu proteins interact with other Vpu proteins to create a tetramer-- a viroporin. Its also integral for particle release in humans, requiring more HIV protein-protein interactions. Completely new function/molecular machine in HIV-1. It is NOT in SIVcpz. And, Subtype C evolved biochemically to form these viroporins better than other subtypes. References for all of this is in my original essay.
Are you ready to start listing to what I say, or are you going to keep squirming?
(correction, pentamers, not tetramers :P)