Friday, August 31, 2007

*squint* No one reads Uncommon Descent.

*weird look*

Ive learned something from The UD Adventure.

Type however moves you. Want to call someone a Creotard, but your holding youre tongue? Go for it! Want to get in a big fight with another Evolution defender on here, but dont want to give Creationists ammo? Do it!!! Because you are only talking to Sal and Dave.

Sally has linked to me several times the past few days. I was like "SWEET! Send all the IDers here! YES YES EXPOSE THEM TO SCIENCE! WHOOOOOOO!!! HAHAHA SILLY SAL!"

Then I checked my sitemeter and googleanalytics. *gives readers a weird look again* Like, 80 hits from UD per day. My stats are up, as we're all checking the comments... But 80 hits? A link from one of my blog brothers and sisters gets at least 100 more direct hits for a few days. Blake pops you up at least 500 hits. PZ or PandasThumb put me in the stratosphere (3K isnt big for PZ, but its friggen HUUUUUUUGE for me!).

Major drama on one ScienceBlog (**COUGH!**) can also send the hits through the roof.

But major drama and multiple links from UD, THE ID Creationism blog... 80? And some of those are from my regular readers clicking in from UD. 80?

Really?

Sally, got a link to your sitemeter?

I found their technorati-- Authority of 368. Thats good! But then I realized they dont contribute to anyone elses Authority (none of Sals links are on my technorati) and all of their points come from OUR links to them. Thousands and thousands of points from SciBloggers. SciBlog posts, feeding UD traffic, which trickled down to 80 hits on ERV.

*squint*

Nobody reads UD.

Except us.

Thursday, August 30, 2007

Sal buys 'Wheres Waldo' book, never seen again

Im a deceitful little thing-- hiding scientific facts in plain sight.

ERV blog, 8/2/07-- Vpu, is in fact, a new gene1. Of the five major phylogenetic groups of SIV, Vpu is only found in one group-- Chimpanzee SIV (SIVcpz) and its descendants—including HIV-1. It is absent in all of the other major lineages (Sooty Mangabey, African Green Monkey, Sykes Monkey, and L'Hoest Monkey). This means that Vpu is in HIV-1 but not HIV-2. 2

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. "Sure it's new in chimpanzees, but its not *new* in HIV-1!" Sorry, you'll find no escape with that limp-wristed, ad hoc parry. SIVcpz Vpu and HIV-1 Vpu act in different ways, biochemically , which is predictable enough when you do something as simple as comparing amino acid sequences. For instance, if you compare a laboratory strain gag to SIVcpz gag, you get a similarity of ~75%3. Not too shabby. On the other hand, if you compare the subunit portion of env (the gene I use to create phylogenetic trees because it's the most variable between viruses) you get an AA similarity of only ~59.5%.

The amino acid similarity between HIV-1 Subtype B Vpu and SIVcpz Vpu is ~37%.

ERV blog, 8/12/07-- A picture I thought was good enough for a child to understand.
UD, 8/28/07-- 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.

* 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.

UD, 8/29/07-- 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.

But as I said in my essay and here-- HIV-1 Vpu and SIVcpz Vpu are totally different genetically, biochemically, and functionally.

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.

ERV comments, TODAY-- The Factician said...

Mr. Cordova,

Let me point you to the relevant portion of ERV's post--->

""Sure it's new in chimpanzees, but its not *new* in HIV-1!" Sorry, you'll find no escape with that limp-wristed, ad hoc parry. SIVcpz Vpu and HIV-1 Vpu act in different ways, biochemically , which is predictable enough when you do something as simple as comparing amino acid sequences. For instance, if you compare a laboratory strain gag to SIVcpz gag, you get a similarity of ~75%3. Not too shabby. On the other hand, if you compare the subunit portion of env (the gene I use to create phylogenetic trees because it's the most variable between viruses) you get an AA similarity of only ~59.5%."

For the more tentacally inclined

Lest we forget the other critters being abused by Creationists:

Anemone's Raise a Tentacle in Support of Evolution


Different organism, same punchline:

It is clear that the people contributing to this forum did not indeed read the actual article. Else they might have been surprised themselves to learn about the genetic evidence for the common descent of all animal phyla from the eumetazoan ancestor.
Bonus-- Pretty pictures!!

Bonus #2-- Kevin also picked the BEST BLOGGER TEMPLATE EVER!

SHIV vs HIV vs SIV: Creationists know everything

... Except how to read.

Towards the end of The Great UD Adventure, Sally decided he knew more about HIV and the HIV research world than me. Granted, lots of people do know a hellovalot more about HIV research than me.

But Sal is not one of those people.

So like I did before, lets use Creationist Behavior as a learning opportunity!

I’m having problems accepting that viropoin capability was novel after emergence in humans in light of this paper:

Scrambling of the amino acids within the transmembrane domain of Vpu results in a simian-human immunodeficiency virus (SHIVTM) that is less pathogenic for pig-tailed macaques.

To date, no studies have been performed to assess the role of this domain in virus pathogenesis in a macaque model of disease. Using a pathogenic molecular clone of simian human immunodeficiency virus (SHIVKU-1bMC33), we have generated a novel virus in which the transmembrane domain of the Vpu protein was scrambled but maintained hydrophobic in nature (SHIVTM), which presumably would disrupt any ion channel TM properties of this protein

Thus, these results show for the first time that the TM domain of Vpu contributes to the pathogenicity of SHIVKU-1bMC33 in pig-tailed macaques.

This paper would appear to weaken the claim that even if “Viroporin capabilities have not been found with SIVcpz Vpu”, that they emerged brand spanking new in humans.

Thus, this would appear not to be an appropriate counter example to Behe’s claims. The fact that one may not see a function in one strain does not imply that it emerged brand new in another strain. It is entirely possible this was a loss of fucntion, and with respect to the issue of this viroporin capability, it was a loss of function (if at all).

Speaking of which, were there even studies done on SIVcpz regarding scrambling of the TM domain? Can’t very well find them if one doesn’t even look for them.

Now, dont laugh at him. Reading is really hard for some people. Maybe he didnt notice the title of the paper he cited:

Scrambling of the amino acids within the transmembrane domain of Vpu results in a simian-human immunodeficiency virus (SHIVTM) that is less pathogenic for pig-tailed macaques.

Thats less pathogenic, folks. Screwing with Vpu makes SHIVs less pathogenic.

Maybe Sal doesnt know what a SHIV is. Hmm... That cant be possible, because the authors of that cited paper define their SHIV right in the intro:
The simian-human immunodeficiency virus (SHIV) is a chimeric virus that contains the tat, rev, vpu, and env genes in a genetic background of SIVmac239.
The tat, rev, VPU, and env genes are from HIV-1. The remaining proteins come from SIVmac. Creating these chimeras is one way we can study AIDS in non-human primates. For instance, pig-tailed macaques cannot be infected with HIV-1, but if you exchange a few HIV genes with SIVmac genes, you can infect them and study AIDS at an organismal level!

And lo and behold, thats exactly what the authors did.
Our laboratory has been using a pathogenic simian-human immunodeficiency virus (SHIV)/macaque model to examine the role of Vpu in disease. Using the pathogenic molecular clone SHIVKU1bMC33, we previously showed that an intact Vpu contributed to the CD4+ T cell loss that occurs during infection with the pathogenic SHIV and that disease in macaques only occurred if compensating amino acid substitutions occurred in the Env and Nef proteins. In order to study the role the TM plays in vivo to enhance pathogenesis, we constructed a mutant SHIV virus (SHIVTM) in which the TM domain of the Vpu protein was scrambled but kept hydrophobic as previously described. In this study, we have analyzed the in vitro replication of this virus and its ability to cause CD4+ T cell loss and disease in macaques. Our results indicate that SHIVTM was not as pathogenic to pig–tailed macaques as the parental SHIVKU1bMC33, indicating that the TM domain contributes in part to the rapid CD4+ T cell loss and disease onset caused by SHIVKU1bMC33.
If you screw up the transmembrane region of HIV-1 Vpu, you get a less pathogenic virus that cant kill CD4 cells as efficiently. Thats what I said. So in addition to no experimental evidence for viroporin formation (see my essay references), this group found no genetic or biochemical reason to expect viroporin capabilities in SIVcpz. Thats also what I said.

*shrug*

You could have read my essay 100 times in the amount of time it took you to find that paper, Sal. Read. Read slowly. And then think reaaaal hard about whether you want to ask an HIV researcher a question, or whether you want to tell that HIV researcher you know more about her specialty than her. Save you some embarrassment in the future.

Another savage blow to my Behe critique

ERV, banned at UD for being *sarcastic*, aka repeatedly anticipating and demolishing Sallys attempts to move goal posts, and answering Davies attempts at being *mean* with cheer.

Have fun scissoring each other, pussies.

ROFL!

Poor Tweedle-Dee and Tweedle-Dumb, too stupid to know Behe was trying to let my post blow over. Trying sooooooo hard to ignore my post, hoping others would forget I wrote it... And then Dee and Dumb plaster it on the front page of UD and let me smash their Creationist Claims on their own damn blog!

AAAAAAAAHAHAHAHAHAHAHA! IDiots! AAAAAAAAHAHAHAHAHAHA!!!!

Tuesday, August 28, 2007

Homework first, play with Creationists later

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)

Monday, August 27, 2007

And on the 5th day, Creationism was killed

hehehehe Day 5 of grad school. Spent 3 hours talking about things that Creationists say cant happen. Gene duplications, domain mixing/shuffling, evolution of immune systems, convergent evolution, evolution of globins...

It was a bloodbath.

Poor persecuted Creationists. Wouldnt make it past the first test.

I know Ive joked about Behe not paying attention in class, but Jesus... Day 5. Days 1-4 were basically administrative, intro to amino acids, and protein purification. Day 5 we're talking about stuff that Behe claims is impossible. Yeah, Im calling him 'Dr. Behe'. **VOMIT**

How not to impress your peers: Crappy gels

I was all excited last week because I thought I found an awesome paper to review for you guys:

Suppression of viral gene expression in bovine leukemia virus-associated B-cell malignancy: interplay of epigenetic modifications leading to chromatin with a repressive histone code.

Sweet, huh? Retroviruses, epigenetics, cancer, WHOOO!!!!

Alas. Theres a really fast way to get people to question your work before they read one word of your paper: publish crappy gels.
I thought I might just be biased, as Im good at running gels, and I like it, but a PI commented "You know, gels are like keeping your shoes tied. If you cant do it, you look sloppy. Its embarrassing."

The authors inability to run nice gels effected their paper. They used P32 to label their nucleotides-- They should have been able to quantify exactly how their transcript levels changed under different epigenetic conditions. Like on my gel I linked to, you should be able to draw a box around each of those bands and say "There is X-fold more Band 4 in lane 2 than there is in Band 4 in lane 3."

But they couldnt because of their sloppy lab work.

But that was the whole point of several figures in the paper-- they tried to show a dose-->response curve with a chemical that effects epigenetics... and the gel just looked like a damn mess. Yeah, you add drug and you got more viral transcripts, but thats a yes/no answer. Running a gel on
P32 labeled nucleotides should and could have given a descriptive answer.

Run a large gel instead of a mini. Skip wells. But for the love of Bowie, dont ruin your experiment, ruin your discussion, and ruin your reputation by publishing a crappy gel. Blech.

Saturday, August 25, 2007

Mother Teresa-- Oh whatever.

If you want to read this article without throwing up, I suggest ignoring the parts that claim atheists are always dumpster diving to expose poor, poor defenseless theists, or writing 'manifestos'.

It is worth it-- Even covered in a thick layer of theistic frosting, MT comes off as a world-class nut bar who hid serious psychological and neurological issues behind a drywall of 'religion.'

She wrote in 1951 that the Passion was the only aspect of Jesus' life that she was interested in sharing: "I want to ... drink ONLY [her emphasis] from His chalice of pain."
Gottlieb also suggests that starting her ministry "may have marked a turning point in her relationship with Jesus," whose urgent claims she was finally in a position to fulfill. Being the active party, he speculates, might have scared her, and in the end, the only way to accomplish great things might have been in the permanent and less risky role of the spurned yet faithful lover.
"If I ever become a Saint — I will surely be one of 'darkness.' I will continually be absent from Heaven — to [light] the light of those in darkness on earth," she wrote in 1962.
Creepy chick. *Kinda* emo.

Oh! But theres hope for us evil atheists! Turns out that we're all well on our way to becoming 'spiritual masters!'
The church anticipates spiritually fallow periods. Indeed, the Spanish mystic St. John of the Cross in the 16th century coined the term the "dark night" of the soul to describe a characteristic stage in the growth of some spiritual masters.
Masters of the Universe? Sweet!

Friday, August 24, 2007

If I hadnt already given my soul to David Bowie,

... I would seriously consider giving it to Muse.

Weve all had a nutty week-- I have some science posts lined up, but school + work + puppy = insane ERV this week. But my week was not nearly as nutty as poor PZ. Lets just kick back, relax, and enjoy some good 'ol atheist sci-fi music. (in the second one, I think its electrical cords, but pretend theyre tentacles :P)



Thursday, August 23, 2007

Did you ever see that "Twilight Zone" where the guy signed a contract...

...and they cut out his tongue and put it in a jar and it wouldn't die, it just grew and pulsated and gave birth to baby tongues? Pretty cool, huh?

At least PZ didnt sign that contract! Or this one, like the poor "Kid Nation" kids:

...were required to do whatever they were told by the show’s producers, 24 hours a day, 7 days a week, or risk expulsion from the show, according to a copy of the contract signed by the children and their parents.

The 22-page agreement leaves little room for parents to argue that they did not know what their children might encounter. As is standard in such agreements, the parents and the children agreed not to hold the producers and CBS responsible if their children died or were injured, if they received inadequate medical care, or if their housing was unsafe and caused injury.

CBS and the production companies, Good TV Inc. and Magic Molehill Productions, retained the rights to the children’s life stories “in perpetuity and throughout the universe.”
See, PZ! Could have been worse! Creationists just have a few clips of you. If they were clever, they could have owned your soul in this life... AND THE NEXT!

hehehehehehehehe!!

Tuesday, August 21, 2007

HIV Denial in the Internet Era

Tara and Steven Novella have a PLoS paper up called 'HIV Denial in the Internet Era.' Wonderful introduction to HIV Denial!

My only complaint: Doesnt mention my most favorite person in the universe. Ah well, Tara and Novella ignoring her makes me feel good too.

Bonus that makes up for my complaint: Steves got a cool blog!

Monday, August 20, 2007

Cost of ERVs soul: 2 cookies

I officially became a student today. I had a couple of classes last week, but class didnt officially start until today. Considering my day usually consists of multitasking about 5 different experiments in three different buildings, calling my behavior in class today "ADHD" is an understatement. THREE hours I was sitting in lecture. And by sitting, I mean 'fidgeting, messing with my pens/paper/phone/etc, and changing positions every 2.5 seconds'. Holy crap I cannot handle this 'sitting still and listening' thing anymore!

However, one really funny thing happened today. I am pleased to report to you all that Biblos treat grad/medical/dental/pharm/nursing students exactly like four year olds. Today I was accosted in the union by Baptists.

Baptist: "HAVE YOU GOTTEN A SACK YET??"
Me: ........ "What is it?"
Baptist: "JUST SOME TREATS FROM BLAHBLAHBLAH BAPTIST CHURCH!!!"
Me, peering in the bag: (Goddammit. Cookies. White chocolate Macadamia.) "AW THANK YOUUUU SOOOO MUUUUUCH!!"

I also got a free dinner, should I choose to accept it, at their Bible Study. And a bottle of bubbles that says "DONT BLOW OFF CHURCH!" HAHAHAHAHA! Oh, I dont blow off church, but church can blow... hehehe never mind.

But I did learn a valuable lesson from these baking Baptists: dont just hand out cookies to promote your ideology or message. Even people who violently disagree with you will take your cookies. And then theyll make fun of you on their blog. Save the cookies for your real friends.

:P

Kook Sues PZ-- NOT a Joke

Remember a while back, when PZ reviewed some crappy book by a no-name author, and you were like "Why the hell did PZ write about this guy? Weird." and then you went about your day?

Well, that wasnt just any no-name author. It was a high level grade A screwball that has decided to take on the entire blogodome.
SciAm
LippardBlog

This scum-covered-quacker has put everyone in the blagosphere at risk. Hes trying to ruin the fun for everyone. Wanna review Behe? He can hold his finger on a temper-tantrum trigger. Wanna quote-mine a respected scientist, Creationists? Wait patiently for a phone call from her lawyer.

Luckily, the 'legal' folks that have read the review say its crap and wont make it past a judge, and (secret) Neil de Grasse Tyson told no-name last November to take his name off the book, well before PZs review, but still-- waste of time, worry for PZ, worry for SciBlogs, worry for all of us... I hope this guy never works again.

Edited to add-- HOLY CRAP! No-name put some comments on PZs blog-- What a friggen KOOK! I DO "see why rominent scientists have endorsed the model as plausible, ublishable, and worthy of investigation."

Sunday, August 19, 2007

Evangelical Pisses Everyone Off: Atheism=Autism

LOL! Complete with VOX quotes and comments about PZ!

Despite his half-hearted disclaimer at the end, this guy pissed everyone off-- theists, atheists, parents of autistic kids, great schadenfreude!

Money shot is in the comments:

About 95% of the atheists I have met seem to be "quarrelsome, socially challenged men." If there is a correlation, and the problem is a type of "mind-blindness" then it should not be surprising to find that reason-based arguments are ineffective when trying to change their opinion of God. We Christians tend to treat atheism as if it was some form of Enlightenment-era rationalism and provide arguments that appeal to their reason.

But as Dawkins and Co. have shown, their views on God have little to do with reason and rationality. In fact, they are almost pathologically unable to recognize just how weak their arguments are – and therefore find it hard to understand why "bright" people don’t accept them too.

HAHAHAHA! Im always a man. Im a 'man' in research. Im a 'man' in classes. Im a 'man' in the gym. Im a 'man' in religion. Im a 'man' with the best boobs in town *thumbs up* ROFL!

ID Creationists confused, frightened by the Google Machine

Add this to the list of things Deniers and Creationists have in common.

This morning Google News popped up the newest critique of 'Edge of Evolution' for me when I turned on the computer at ~7 am. Its a positive review, but it was from a layman, so I was going to give him the benefit of the doubt and send him a nice email pointing him towards reviews from SciBlogs and PandasThumb (which Blake Stacey cataloged for us!) where actual scientists working in the fields Behe molested universally dismissed 'Edge'.

Alas, before I got around to sending it, Denyse tipped Camerons hand:

Cameron Wybrow wrote me a while back wanting to know why most legacy Canadian mainstream media will not publish anything about the intelligent design controversy beyond the often incompetent or politically motivated stuff that the New York Times would put out.
Oops! So... the only way ID can get a positive review of 'Edge' out is to get a non-scientist with an ax to grind, who inflates his credentials as a 'science' journalist, and cant use Google to write one?

Niiiice!

Poor D cant even figure out how to use Google to link the review.

The Google Machine. So confusing. They should put up directions or something...

Saturday, August 18, 2007

A powerful refutation of my Behe post

The best refutation of my post (to date) came from a poster on Amazons "Edge of Evolution" page:

Ms. Smith,

Read your post-quite impressive in some respects.

You are obviously enjoying the fruits of an excellent scientific education. No telling how far you can go if you acquire the requisite taste, professionalism, good judgment and manners to go with it.

Perhaps you should consider emulating Professor Behe in those areas.
WHOOOO! I got the Dawkins Defense: "I think youre mean. That means Im right. Next time, dont be so mean."

Guess this means Im officially Hurting The Cause now, ROFL!!

ERVs do not exist.

Index to Common Creationist Claims about ERVs

Courtesy of a new source of blogfodder: ERVs do not exist.

Endogenous retroviruses (ERVs) are segments of DNA which, due in part to some similarities and their seemingly haphazard distribution, are thought to have resulted from past viral infections.
Even if this idea were correct, it does little to support evolution in the microbes-to-man sense.
... and so on.

This is part of a larger Creationist scheme-- put words like 'purportedly' and 'supposedly' in front of basic scientific facts. Create confusion in followers by making facts relative. "We look at a sequence and see GOD! Scientists look at a sequence and see MUTATION! Same data, different interpretations... You arent a MUTATION, are you?"

The LTRs of ERVs are distinctive enough that we can sometimes determine what kind of retrovirus the ERV used to be (alpha, beta, etc). We can even find families of related ERVs and reconstruct an infectious retrovirus from their leftover bits. There is no other way to 'interpret' this data, other than stating that ERVs are ERVs.

Thursday, August 16, 2007

PLOSs Evil Twin

Soon to be freely available online for our mocking pleasure, Journal of Creation.

I wonder if this means Bora has a Creationist doppelganger... **cue Twilight Zone music**

Creationist Perversions

No, not their ubiquitous physical perversions, their ubiquitous mental perversions. Wanderin Weeta pointed me towards this gem from a poster at IIDB:

Example: let's begin with the hypothesis that viruses are not our enemies. Let's hypothesize that in the beginning, they were all "good" as Genesis implies. Then we work within the framework of that hypothesis and study viruses. I suspect we will soon learn that viruses are only pathogenic when they are out of their proper context or when they are in their proper context but they have mutated, etc. If we adopt this type of thinking, then I suspect we could harness the originally designed purpose of viruses, and put them to good use for the benefit of humanity as is already being done on a limited basis.
Reality: Some viruses are 'good'. Some viruses are 'bad'. Some viruses are just there.
Creationist Perversion: All viruses used to be Good. The Fall made viruses Bad.

Reality: Some viruses are only 'bad' is the 'wrong' organism, eg Nipah Virus in fruit bats, SIV in African Green Monkeys. Some viruses are pathogenic in everyone it can infect (influenza).
Creationist Perversion: Everything was in its proper place after Creation. Pathogenicity is a result of The Fall.

Reality: Sometimes viruses mutate, and things are worse for us (Red Queen). Sometimes viruses mutate, and things are better for us (co-evolution, domestication, etc).
Creationist Perversion: Things used to be perfect. All mutations are bad.

Reality: Evolution helps us design vaccines, weak points to extort with drugs, ways to limit outbreaks, etc
Creationist Perversion: Creationism could help us too...

Wednesday, August 15, 2007

Summer Virus Fun

As youre enjoying the last few days of summer vacation, playing in the ocean, remember this:
There are 1 million-1 billion viruses in every cm3 of seawater.

Just so you know.

:P

Tuesday, August 14, 2007

My advice to undergrads: Post Bac!

And Science agrees with me! If you think you *might* want to go to graduate school, dont go straight into grad school!! Do a post bac! Taking a year or two 'off' from school to:

  1. See if you really really really want to do grad school
  2. Get you ready for grad school (learn a ton of protocols, how to present papers, how to interact with lab members, etc)
  3. Learn what a life of research really means (you have NO IDEA as an undergrad, I dont care how many summer internships you did)
  4. Make connections
  5. Get an idea of what you want to do long term (PI? Liberal Arts Professor? Drug R&D? Clinical? Molecular? Animal work?)
Grad school isnt going anywhere. Theyre still going to be there in two years if you take time off, no harm, no foul. Plus... what if you hate it? What if you read ERV religiously and have a romanticized view of virology... but you do NOT want to deal with grad school? Its better to find that out as a tech than after youve wasted your research mentors time and money for one or two years. If you realize you dont want a PhD while youre a tech, you can still have a great career as a professional tech. You dont have to write grants. You dont have to worry about neurotic grad students. You dont have to hire post docs. You can work 9-5. Hell, at this point in my career, I could probably make more money by staying a tech than getting a Masters or PhD, I just really want a PhD. Good techs and research assistants are worth their weight in gold.

Taking time off to do a post bac is one of the best career decisions Ive made-- Undergrads, think about it ;)

Monday, August 13, 2007

College Deconversions

hehehe PZ and Jason have posts up about kids deconverting when they go to college. This is just a fantastically funny personal joke for me.

  1. As regular readers know, I didn't know 'Creationists' and 'Fundies' were real until I got to college. hehehe I was as sheltered as a Fundy kid LOL!
  2. My welcome party to Oklahoma was attending a radical Christian hate rally (against science, atheists, education, everybody) lead by Creationist Brad Harrub. He made a BIG deal about only letting kids go to *special* colleges, otherwise they'll deconvert. I laughed.
I knew a couple kids in biology at Truman that made it through Fundie-fied (went to dental school, I believe), but I learned about Creationism from a girl who deconverted from Fundy to sane theist. By the time we got to upper level biology classes, we were making jokes at Creationists expense regularly.

hehehe Poor Fundies. Cant catch a break. But one thing that really irritated me was PotF insistence that EVIL ATHEIST PROFESSORS were foisting their RELIGION on poor, defenseless good Christian kids. No. Religion was never brought up in any of my classes. Not even in philosophy. My philo prof went to Notre Dame, but he played Devils Advocate and sided with me so many times, I could have sworn he was an atheist-- But Ill never know. Dont know the religion of any of my biology professors (though I heard one was an atheist- I never had him, and one was a Mennonite).

Again, poor Fundies. Cant stand the thought that kids are deconverting because Fundies are NUTS... It must be because of Evil Atheist professors. HA!

True Dog Lovers(TM)

Yeah, Im doing it. Im playing the 'True Scotsman' card. Wanna fight about it? :P

So I was looking for this story I saw a few weeks ago on Dateline. Nice little 2 minute story at the end of the show on a dog that saved a little girl from a sexual predator. The whole segment was "The dog alerted..." "The dogs owner..." "The dog..." "The dog..." "The dog..."

The breed of "the dog..."? Pit. Textbook white and tan American Pit Bull Terrier. But even in the shadow of the Vick case, they wouldnt say the word. They wouldnt say "Pit saves little girl from sexual predator."

But boy howdy, if that pup had bitten that little girl, Dateline wouldnt have had any trouble reporting "PIT BULL EATZ BAYBAY!"

Link to the story.

Anyway, as I was searching for that link, cause Ive been just a *little pissed* of late, and I found lots of wonderful sites by individuals that are True Dog Lovers(TM). This one is awesome: Happy Pit Bull! Kinda restored my faith in society after the recent train-wreck from individuals I have never met, but trusted, and expected more of.

Who would have thought that people who proclaim to be rational Dog Lovers would have the exact same position as one of the most insane women in this country. Sorry-- You can call yourself a Dog Lover, a Martian, an 18th Century Concert Violinist-- But reality prevents me from accepting your claims.

Have an irrational fear of pits? Convinced that they are going to kill you while you sit in their living room? See pit bull shadows around every corner as you walk down the street? Dodging questions about your Final Solution for pits, because you know its inhumane? You are NOT a True Dog Lover(TM).

Sunday, August 12, 2007

An Illustrated Guide to Vpu

For Casey, care of Ian Musgrave (click for larger image)

Green = New Gene + New Molecular Machinery + New Protein-Protein Interactions
Blue = HIV Originates
Pink = New Molecular Machinery + Gene 'Working in a Different Way' + New Protein-Protein Interactions
Red = Gene 'Working in a Different Way' + New Protein-Protein Interactions
Thank you so much, Ian! hehehe Terrible professor. 'Teaching' things. Bah!

Send in the pawns! Part Deux!

A well meaning Creationist poster at Pandas Thumb bravely attempted to defend Behe (once again, Behe prefers to let other people defend his incompetency). He cited a paper that proclaims:

Both Vpr- and Vpu-induced apoptosis involve the activation of the caspase pathway (references 48 and 49, and this study). Although the precise mechanism for Vpr-induced apoptosis is still unclear, recent observations suggest that it might be caused by a Vpr-induced permeabilization of mitochondrial membranes resulting in the release of apoptogenic proteins such as cytochrome c or apoptosis inducing factor and the subsequent activation of caspase (50). While it was suggested that Vpu itself might have poreforming properties (51, 52) making a mechanism for induction of apoptosis similar to that of Vpr conceivable, our data suggest that Vpu instead functions by inhibiting the NF-{kappa}B–dependent expression of antiapoptotic genes.
There is a lot wrong with this, and I want to make it clear I do not blame Collin for not understanding why his quote does not save Behe. Behe hasnt even attempted to defend himself-- kudos to Collin for trying. We can at least use Collins attempt as a learning opportunity.

The referenced paper addresses one question and one question only: Does Vpu effect apoptosis?

Thats it.

Not whether Vpu forms ion channels, but if Vpu sets off some kind of cell suicide pathway. Viroporins are more of a side comment in the discussion section, not the foundation of the papers hypothesis.

This paper does not support Behe-- It makes things worse. Vpu might have yet another trick up its sleeve. It might interact with a cell death pathway.

Or it might not:
It has also been shown that HIV-1 particle adsorption, even of defective particles, can induce efficient activation-dependent apoptosis in bystander CD4+ and CD8+ T cells. In addition, secreted HIV-1-encoded proteins, such as Tat, Nef, or Vpr, and apoptosis-inducing factors released from HIV-1-infected cells, such as Fas ligand, tumor necrosis factor alpha, or tumor necrosis factor-related apoptosis-inducing ligand, have all been shown to trigger apoptosis in uninfected bystander cells. On the contrary, several hypotheses derived from in vitro studies have investigated possible mechanisms for the direct killing of infected cells, as follows. Apoptosis induction by recombinantly expressed Env, Tat, Nef, Vpr, and Vpu has been demonstrated. However, much of the evidence on mediators of HIV-1-induced cell death is contradictory. For example, Tat has been associated with apoptosis induction in some studies, while other studies have shown its protective role against apoptosis. The wide variability of these findings may be due, at least in part, to the fact that most of these studies have examined the effects of large amounts of recombinant HIV-1 proteins artificially expressed in various kinds of cell lines.
Translation: Vpu might kill infected cells directly, but the studies that have demonstrated that werent exactly carried out in a realistic manner. Think of the artificial sweetener studies-- If you give a mouse 50 pounds of fake sugar to eat, hes gonna get a tumor. Pump a cell full of Vpu, the cell is going to die. This paper cites Collins paper directly, as one of those 'not-exactly-realistic' studies.

But Klaus Strebel was the first author on one of the papers reporting the discovery of Vpu-- Im going to listen to him when he talks about Vpu. We will just have to see where research leads Vpu.

But this doesnt effect the fact that Vpu whomps Behes claims about HIV in 'Edge of Evolution.'

So good try, Collin. Im still waiting for Behe.

Thursday, August 09, 2007

Pit Bull Denialism Denialism

I know you all are wanting a resolution to Luskins post, but Im not interested in IDs attack Chinese Crested tonight. Once again, I have to defend pits from fear mongerers.

This attack came from an unexpected source-- A contributor on a ScienceBlog. ScienceBlogs has taken a rational stance on pits in the past, with wonderful posts by both Kevin Beck and Chad Orzel (I almost gave Chad a heart attack with my sarcasm, and I still feel bad about it).

Im disappointed Keven turned around and made the decision to call my dog a 'fucker' in the above referenced post. I didnt see it at first, but I caught it just as Arnie was begging for a cherry PopTart.

Kevins co-blogger, Jim, doesnt seem to think Vicks actions were all bad. Pit bulls are evil, vicious dogs, and there is nothing their owners can do about it.

It would be naive to assume that a dog's behavior (or that of pretty much any animal) is entirely or even largely dependent on training and environment. To discount inherent biological factors is specious. The reality is that pit bulls have the "biological equipment" to inflict damage that other breeds, say basset hounds, do not. This statement simply reflects the obvious facts of biology; and it does not condemn all members of any given breed to a given behavior.
Jim is an expert on dog breeds (much better qualified than the AKC, which opposes BSL), being a "dog lover" who not only doesnt own a dog, but has evidently never owned a bull breed, or evidently met one (though he assures us that he doesnt want his first pit meeting to be on a country road. No problems with meeting rabid beagles on country roads, though.) And he clearly knows more than silly people like me and my rescue friends who rescue and rehabilitate abused and neglected bull breeds into wonderful family members-- Our opinions dont count, because its, um, um... He doesnt say why our opinions dont count.

He also doesnt give all the 'details' of the CDCs dog bite/mortality stats.

He also doesnt say what his Final Solution is for pit bulls.

Best I dont know.

Add 'Dr. Joan' to the list of SciBlogs I will never read again.

Wednesday, August 08, 2007

Finally! A new lab member!

Its just been me and Bossman for a while now. Almost had an undergrad (... or two...), but I scared them off. Today we finally got a postdoc (whom we've both worked with before). Great guy-- works hard, but still has a fun personality. Hes a co-postdoc with the PI next door. A joint immunology/virology project, which will be very cool... in 2 years. hehe!

Were also looking for a tech to take my spot when I start school. The hiring process has been kinda fun! Research isnt like a cult! Its like 'Big Love'! Hiring another research tech is like finding a third wife :P

Oh gawd, please dont let Zuska see this post... hehehe!

With 'pyro-something' AND 'epigenetics' in the title, you know its gonna be cool

Just found a paper discussing where HIV likes to integrate. Hmm-- Not too particularly interesting, as weve already kinda looked at that.

Whats interesting is the technology these folks used to do something that would have been inconceivable just a few years ago.

Pyrosequencing.

Pyroseqencing takes sequencing to the next level. A process like sequencing the human genome, which took many years and billions of dollars, only takes a few days and a few thousand dollars with pyrosequencing. Yeah. I do NOT want to look through the data that comes out of one of these sequencing assays LOL (though Ive heard the software is good)

So these folks infected some cells with HIV with the hope of characterizing the DNA around integration sites. Then they found ~40,500 different integration sites. *blink* We used to have to find them one at a time. Not 40,500 at a time. Awesome. But again, what could this paper tell us that we didnt already know?

They used various databases and models to figure out HIV integrates:

None of that is experimental (except for the initial sequencing)! Its all technology! 40,500 damn integrations! Awesome!!!

Tuesday, August 07, 2007

Send in the pawns!

Michael Behe, Michael Behe, Michael Behe. What are we going to do with you? I put the odds at about 90% you would ignore me, 5% you would respond as a Creationist, and 5% chance you would respond as a biochemist (Im optimistic!). But for you to make the decision to allow poor little Casey Luskin make a fool of himself defending you? Throwing a friend under the bus? That was not something I expected from you. How cruel. I mean whens the last time he took a biology class? High school? Eighth grade? Poor fellow doesnt even know the difference between biochemistry and genetics. Look, I would never make fun of his education, as theres no shame in not understanding what I wrote. I know the jargon is gobbledy-gook to sane people. But for you to shove advanced, extraordinarily specific papers and terminology in his face and yawn 'Defend me, pawn'...

There isnt one sentence in poor little Caseys post that I feel its necessary to respond to*, and Im sure he worked his little knuckles to the bone on it. He even tried to reference a LANL paper (so cute, little guy doesnt understand that THAT paper refutes you too), and I bet it took him hours to find it, and several more to read it. But biochemistry isnt the responsibility of non-biochemists.
Biochemistry is biochemists business.

Thats you, right, Michael Behe?


Oh, but wait-- Answering my point isnt The Point, is it? The Point is Average Joe Creationists know that we scored big. You messed up BAD. They need to read anything that says "Nothing to see here! All is well! Move along now!" The Pawn Casey can handle that job well enough for you, eh?

But you know you were pawned by a kid, Behe.


*smile*

Im not going anywhere.




* If you read my post and dont know how to refute something Casey said, please post your question here so we can talk about it! If you have questions, odds are other people do too!

Monday, August 06, 2007

Reason #87245619784 Im a lucky bastard:

I dont get BugGirls jokes about academia being a cult. I mean I get it, Ive heard story after story... But I have no personal experience with this stuff myself. (BugGirl-- this is in jest, I like your post!)

1. Authoritarian structure
Well, someone has to be in charge. I wouldnt call my boss authoritarian, though. He makes the calls, but he encourages me to think for myself and to speak my mind. Actually, Im fairly certain he would have fired me long ago if I didnt continually question him. And Ive never been any more frustrated with him than I have been with my best friends. Everyone is frustrating at times, but its not a core feature of his personality and our interactions.
Bleh, and an authoritarian PI is short-sighted-- Sure you will get some publications out if you tell everyone what to do all the time, but youre also known for the quality of PhDs you turn out. Maybe its just my martial arts background thinking, but the students are a reflection of the mentor.

2. Isolation from society and use of mind control techniques
*shrug* Im living in Oklahoma. My job is not the cause of my isolation from 'society' :P

Peer Group Pressure - Suppressing doubt and resistance to new ideas by exploiting the need to belong.
Confusing Doctrine - Encouraging blind acceptance through complex lectures on an incomprehensible doctrine.
Verbal Abuse, Sleep Deprivation and fatigue - Creating disorientation and vulnerability by prolonging mental and physical activity and withholding adequate rest and sleep.
Dress Codes - Removing individuality by demanding conformity to the group dress code.
Financial Committment - Achieving increased dependence on the group
Controlled Approval - Maintaining vulnerability and confusion by alternately rewarding and punishing similar actions.
I think grad school encourages the opposite of peer pressure! It encourages being contrary (which is why I love it so much)! I love going to journal club, where its like a contest of who can take the nicest little papers and rip them to sheds! LOVE IT! Youve got to learn that in grad school! If you cant critique your own work, someone else will do it for you, and its never pretty. And its better that a friend/classmate critiques your work before your adviser or committee does!
Bossman just locked me out of the lab for a week to go on vacation, and came close to calling my parents to force me to go to the doctor during my Spring Adventure. Its not profitable to him for me to be sick, tired, stressed-out, and disoriented.
And my lab... We're the bums of the department. 'Dressing-up' days means wearing jeans without holes in them (relatively clean). Ive recently discovered Old Navy polo shirts, $10 each, that allow me to dress cheaply and not be so bum-ish (normally its tye-dye or free company T-shirts). Im working with radiation and biohazardous materials every day! Spill some P32 on a $200 pair of jeans, and theyre gone forever... not that you dont have other things to worry about if youve spilled P32 on your jeans...

3. Control of the environment
Another reason my boss rocks-- He has always made it perfectly clear that whatever I want to do is what I want to do. Look, we all appreciate a PhD on the other end of the phone when the damn AutoMACS screws up. I dont care if you want to work 9-5 with an R&D company. But I want to rule the world have my own lab and rule the world do research forever, and my boss supports that. I didnt go to med school just because my parents wanted me to*, Im certainly not going to try to get a PI position just because my boss might want me to. Silly.

Geeze with all the stories I hear about sexual harassment and impossible/invisible research mentors and cult research clubs... Im a lucky bastard.

(Hat tip to Ian)


* My parents didnt *want me to go to med school* I wanted to go to med school, and they supported that.

Friday, August 03, 2007

Quick Translation For Laymen!

Sorry, folks! I should have added this as a short note on the end-- I knew a lot of what I wrote would be gobbledy-gook to sane persons, but I wanted to put enough detail in to close off any of Behes escape routes. Thank you to the commenters that suggested this!

Quick summary:

Behe says over and over and over and OVER in 'Edge of Evolution' that HIV:

  1. Has no new genes (specifically says something about no new genes through duplication).
  2. Has no new protein-protein interactions.
If you dont believe me, check out a copy at your local library, or brows one at Borders-- page 137-ish he really gets going.

The problem is, HIV-1 and HIV-2 both have new genes. HIV-1 has a gene called Vpu, and HIV-2 has one called Vpx. Vpx is the result of a gene duplication-- a second Vpr.

Vpu has evolved a multitude of 'new' protein-protein interactions. Its even done something particularly cool-- turned itself into an ion channel! Thats kinda weird for a virus.

HIV-1 and HIV-2 have done these things in modern times. Its not magic. Its science.

Ill be home tomorrow! More posts then!

Thursday, August 02, 2007

Michael Behe, please allow me to introduce myself...

Note: WHOO! Up on Pandas Thumb! Thanks, guys!

Im ERV. This is my dog, Arnold Schwarzenegger. And this is my friend, Vpu . I presume you and Vpu haven't met, as you recently repeated in an interview with World magazine the same sentiment you gurgled ad nauseum in 'Edge of Evolution':

"Like malaria, HIV is a microbe that occurs in astronomical numbers. What's more, its mutation rate is 10,000 times greater than that of most other organisms. So 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. Yet all 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. If we see that Darwin's mechanism can only do so little even when given its best opportunities, we can decisively conclude that random mutation did not build the machinery of life."

I find it rather difficult to believe that you two haven't crossed paths, as Vpu turns up in a simple Google search. And as a matter of fact, Vpu is sitting right there in the totally unnecessary and worthless diagram in 'Edge of Evolution'. See? Right there:

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If you had taken the time to label this pointless diagram, you might have noticed your error, and we wouldn't need to have this conversation. Alas, Vpu is a tiny molecule, and he's easy to overlook if you don't want to see him.

Vpu, is in fact, a new gene1. Of the five major phylogenetic groups of SIV, Vpu is only found in one group-- Chimpanzee SIV (SIVcpz) and its descendants—including HIV-1. It is absent in all of the other major lineages (Sooty Mangabey, African Green Monkey, Sykes Monkey, and L'Hoest Monkey). This means that Vpu is in HIV-1 but not HIV-2. 2

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. "Sure it's new in chimpanzees, but its not *new* in HIV-1!" Sorry, you'll find no escape with that limp-wristed, ad hoc parry. SIVcpz Vpu and HIV-1 Vpu act in different ways, biochemically , which is predictable enough when you do something as simple as comparing amino acid sequences. For instance, if you compare a laboratory strain gag to SIVcpz gag, you get a similarity of ~75%3. Not too shabby. On the other hand, if you compare the subunit portion of env (the gene I use to create phylogenetic trees because it's the most variable between viruses) you get an AA similarity of only ~59.5%.

The amino acid similarity between HIV-1 Subtype B Vpu and SIVcpz Vpu is ~37%. Ah but that study was published in 1990. Perhaps things are different now? I found the AA sequence of NL4-3 (lab standard Subtype B) and several recently entered SIV cpz sequences at the Los Alamos National Laboratory HIV Sequence Database4-- I got the same numbers. Highest was ~39% AA sequence similarity.

Turns out a LOT of evolution has been going on in HIV-1 since it was transferred to humans 50-60 years ago. What are the biochemical implications of these differences?

In humans, there are two functions of Vpu5-- One is inducing the degradation of CD4 molecules. CD4 is the host cell receptor HIV needs for infection. Removing CD4 from the cell surface prevents superinfection (more than one virus infecting the same cell) and helps prevent newly released viruses from turning around and infecting the same cell (also prevented by an HIV maturation step involving protease). To put this the simplest way possible, Vpu involves the evolution of at least two protein-protein interaction sites—one to interact with CD4, one to interact with the pathway that degrades the CD4.

The second function is to act as an ion channel in the host cell plasma membrane6. Five Vpu proteins come together to form a Na+K+ viroporin 7. This has been shown to assist in particle release, making the cell charge more conducive to the release of new particles. This involves the evolution of more protein-protein interactions—the individual Vpu proteins must interact to form the pentamer, plus an action site that can be used to block ion flow 8.

Viroporin capabilities have not been found with SIVcpz Vpu. Knowing what we know about Vpu, this is not surprising. If you scramble the transmembrane region of HIV-1 Vpu (the portion responsible for the ion channel formation), viral release is crippled9. And when you compare AA homology between SIVcpz and HIV-1 Vpu in the transmembrane region is unremarkable (roughly two)—that's as good as a 'scramble'. So theoretically, ion channel formation evolved in HIV-1 when it infected humans to overcome a species specific and cell specific host factor 10. Though the list of viroporins discovered is continually growing, the evolution of a viroporin de novo is not menial task.

This seems like a pretty significant biochemical change in HIV-1, to me.

But the 'pathetic' evolution doesn't stop there. The feature both Vpus have in common, CD4 degradation, is carried out in completely different ways. HIV-1 Vpu requires two casein kinase II sites. You could almost call it irreducibly complex-- If you dont have both CKII sites, CD4 isn't degraded. Yet some SIVcpz Vpus have only one CKII site, and instead utilize a simple string of negatively charged amino acids in place of the second site 11. Different ways of performing similar tricks with totally different amino acids. I think that's biochemically significant as well.

Ah, Michael Behe, you might try to talk your way around Vpu NOW by saying, "Vpu might be *new* new in HIV-1, but its not *NEW* *new* new. It hasnt changed in HIV-1 since humans acquired it!"

Alas, 'same number of genes that work in the same way' goes beyond the differences between HIV-1 Vpu and SIVcpz Vpu. HIV-1 is divided into three groups, M, N, O. Group M is the one making a mess of the world right now, and is further divided into Subtype A, B, C, etc, and circulating recombinant forms of the subtypes (Subtype AG, for instance). Two relatively well characterized subtypes are Subtype B and C. Subtype C HIV can be defined by its Vpu, as it is so different from the other subtypes12

For instance, Subtype C Vpus are characteristically longer than the others, have key phosphorylation sites shifted, have an extra CKII site, and its tertiary structure is totally different (Subtype B Vpus have an Mr of 43,000 in an SDS-PAGE gel, while Subtype C is 34,000). But what does this mean, biochemically?

It turns out that one of the biochemical differences is that Subtype B Vps have a Golgi retention signal in the second alpha-helix of the cytoplasmic domain 13. This means that Subtypes B Vpu prefers (if you will excuse me personifying a virus) 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. Michael Behe, if you don't understand the epidemiological and clinical significance of this 'pathetic' evolution, well, that might explain why you aren't doing HIV research.

So heres a quick time-line for the evolution of impossible genes and impossible protein-protein interactions, courtesy of Ian Musgrave (one of those dreadful PhDs/Professors that has something to teach this pre-grad student):

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Michael Behe, as a courtesy to you, this essay isn't even going to touch Vpx, a gene specific to the HIV-2 and SIV sm lineage. Vpx is one of those pesky gene duplications you say don't exist in HIV (Vpr x2). I also won't point out how silly it is of you to claim HIV has not evolved biochemically, when the HIV research community has barely scratched the surface of HIV's biochemical evolution (for the love of Pete, we don't even know what HIV-1 Subtype Cs gp120-gp41 look like!).

Look, the fact of the matter is, all of this information on Vpu is publicly available. No one was hiding this information. This wasn't a 'trick.' Vpu was not discovered yesterday—it was discovered in 1988. There is no excuse for you to write an entire book on the premise of HIV not being able to do something, when it is clear that these impossible feats did happen. This is just one of a billion plus examples of lazy Creationists taking advantage of the ignorance of their followers. I'm just a friggen pre-grad student who knew what the HIV-1 genome looked like and had a few minutes to do a PubMed search. I haven't even taken a course in biochemistry.

*sigh* So lets hear it, Behe, what's your excuse for missing this? Go ahead—run off to PubMed and find a paper to pubjack. I'm not going anywhere.

Reference:
1. A novel gene of HIV-1, vpu, and its 16-kilodalton product
2. Diversity and Evolution of Primate Lentiviruses
3. Genetic organization of a chimpanzee lentivirus related to HIV-1
4. LANL HIV Sequence Database
5. The HIV-1 Vpu protein: a multifunctional enhancer of viral particle release
6. The human immunodeficiency virus type 1-specific protein vpu is required for efficient virus maturation and release
7. The Vpu protein of human immunodeficiency virus type 1 forms cation-selective ion channels
8. Drug-protein interaction with Vpu from HIV-1: proposing binding sites for amiloride and one of its derivatives
9. Identification of an ion channel activity of the Vpu transmembrane domain and its involvement in the regulation of virus release from HIV-1-infected cells
10. HIV-1 Vpu Promotes Release and Prevents Endocytosis of Nascent Retrovirus Particles from the Plasma Membrane
11. Vpu-mediated CD4 down-regulation and degradation is conserved among highly divergent SIV(cpz) strains
12. Molecular characterization of the HIV type 1 subtype C accessory genes vif, vpr, and vpu
13. Identification of a region within the cytoplasmic domain of the subtype B Vpu protein of human immunodeficiency virus type 1 (HIV-1) that is responsible for retention in the golgi complex and its absence in the Vpu protein from a subtype C HIV-1