Roller

I would say "yes" to both questions. At least my understanding is such.

I think your 499th was "lower" on the forum meaning this was your most recent post. Your "501" was under the topic named Upstart religions: learn from Christianity!
Not that I care about such things as to who posted how much...

RufusAtticus

And I must mention that the pseudogene that they found a function for was produced from incomplete duplication of the parent gene. It's function relied on the pseudogene's transcript interfereing with the parent gene's transcript. However, unary pseduogenes like GLUO or UO can't possibly have this function.

Doubting Didymus

I actually havent come across any of the common responses people here have listed, except for having the fall involved in some way. The one that I get most often is when they pounce on the (generally accurate) fact that the insertions are more likely to occur in certain sites in the genome than others. Somehow, this is supposed to outweigh the incredible improbability of having all the right retroviruses in exactly the patern predicted by standard phylogenetic trees. I can only imagine that they are looking for an excuse to dismiss it, and when they find something, however flimsy, to dismiss something with, dismiss it they do.

Jayjay

I'm having trouble understanding how a particular ERV could possibly show up in different loci in different species. I'm not sure how easy it is for virii to cross between species, but it sounds like an unlikely thing to occur (and if it does, I'd expect the species in question to be closely related at least). More importantly, how do we know that it's the same ERV, if they are in different locations? How do we know to compare the two?

(For the record, I'm a layman on this topic.)

Actually, I managed to squeeze the 500th post in the Contracting Sun = Young Earth? thread. (Yup, having been notified on my post count I just had to check it out... vanity, my favourite sin!)

Roller

I'm not an expert on this. Actually I just started studying viruses but here's what I think. Retroviruses insert themselves randomly in the chromosomes. Perhaps not totally randomly, I think some parts are infected more often than others. Still, my guess is that the probability of their insertion by random chance in same loci, as in case with human and chimp chromosome, is pretty huge. So a particular virus can show on different loci in different species because he's randomly inserted.

From my understanding, human and chimp ancestor probably battled some virus that left his insertion in germ line cells, which then became heritable. And that’s how chimps and we share them, because we inherited them from our ancestor. Actually, there's a whole phylogenetic tree based on this research. Check this site: http://www.pnas.org/cgi/content/full/96/18/10254 for more information (although a bit technical). For less technical (and more straightforward), check good ole' talkorigins: http://www.talkorigins.org/faqs/comd...l#retroviruses

Viruses can and do cross. HIV virus arose with chimpanzees. Influenza is practically a bird virus, and that one killed 20.000.000 people in 18 months in 1918-1919. If I remember correctly, hantavirus originated in rodents.

How do we know they are the same viruses if they are on different locations? My guess is that we know the gene sequence of a particular virus. Then when we find such sequence in a genome, we know it’s the virus (and which one).

(edit: spelling... damned spelling...)

Baloo

Forgive me as I play Devil's Advocate for awhile.

IMO there is rational (albeit extremely ad hoc) ground on which creationists can stand in regards to the existance of ERV's: namely, the hypothesis that ERVs function as genetically encoded (read: intelligently designed) "vaccines" which protect organisms from infection.

I believe there is some backing for this in the form of an experiment by which scientists were able to attribute an increase in resistance to viral infection to an existent ERV: The envelope glycoprotein of human endogenous retrovirus HERV-W induces cellular resistance to spleen necrosis virus.
To cut to the chase: God put ERV's in humans (and all other organisms) to make them immune to certain viral infections. We share many such ERV's with chimps, because they're most physiologically like us and thus susceptible to infection from the same viruses; and we share far fewer with monkeys, because they're physiologically less like us, and less susceptible to the same strains of virus. This was a pre-Fall maneuver, where God knew Man might Fall, and that if Man did Fall, they'd need ERV's to survive all of "Fall fall-outs" (e.g. viruses). Shared ERV's are in the same place between species because common designer = common design.

Even though it hits a 9.8 out of 10 on the ad hoc scale, as far as I can see, the explanation does provide grounds which do not require a willful suspension of logic or absolute denial to incorporate ERVs into the creationist framework.

WinAce

Guess again. Under this hypothesis, humans and, say, pigs/chickens could reasonably be expected to share insertions chimps don't. (Bird influenza ring a bell?)

MortalWombat

But this ignores what is known about retroviral insertions, which are for the most part random (excluding for instance slight biases for insertions into transcriptionally active chromatin for some, but not all, types of retroviruses) throughout the genome.

This is applicable across the spectrum of retroviruses, from the lowly yeast Ty retroelements, to avian sarcoma virus, mouse mammary tumor virus, and to HIV. So for instance, in no two AIDS patients have there ever been shown to be insertions of HIV at two identical positions. So I don't see why this particular class of retrovirus would behave any differently.

Jayjay

MortalWombat: If particular ERVs are put in place by an intelligent designer, we'd not expect it to follow the random pattern of observed retroviral insertions. Right?

In essence, the common designer explanation requires that the shared ERVs (between species, kinds or other units of special creation) are always put in by a designer, but unique ERVs may or may not have been (with the obvious exception of those insertions we directly observe taking place).

Roller

If the designer intended for those viral insertions to protect us, then why against just some viruses? And wouldn't it be easier just not to create those viruses in a first place? Then there's no need for insertions. Problems with parsimony?