[tallhappy]

Feel free to prove me wrong, though -- go right ahead and show us that the actual odds of getting two of the same retroviral fragments inserted into two genomes at the same locus is actually high enough to invalidate the ERV argument for common ancestry, along with supporting citations or evidence, contrary to everyone else's findings on this process, *AND* reconcile your claim with the observation that most shared ERVs *are* found at the same site. We'll wait.

I have twice now cited for you the recent gene therapy trials where retrovirally mediated insertion of a gene confering a serious immunogical condition called X-Scid was done. Of 11 children afflicted who received the therpay, nine had their symptoms alleviated by expression of the gene mutated in their disease.

But unfortunately, 2 of these nine came down with a side ffect where they came down with leukemia. 2 of 9 is a very high frequency. The trial was put on hold and the patients examined. In three cases (the two with leukemia and another without) the retrovirus had inserted such as to flank LMO2, a gene important in hematopoietic proliferation, and a leukemic oncogene.

Given that this insertion in to the same site happen not in two genomes, as you asked for, but in three out of only nine integrations, the targetted nature of integration, which is not understood, is apparent. Addressing this targetting is an active area of current research.

See my previous post which I posted just subsequent to this post of yours that I am responding to now for more discussion on the roles of retroviruses in evolution and for the functionality of their remnants in mammalian genomes.

I'd like to point out also that Eugene Sverdlov' group, who did the phylogram you posted from the Theobald article, discuss the non-random integration of the elements extensivley in their follow up articles, for eamples this one, Full-sized HERV-K (HML-2) human endogenous retroviral LTR sequences on human chromosome 21: map locations and evolutionary history, published in Gene 2001.

[narby]

I'm not an expert on ERV insertions. And Ichneumon certainly can defend himself. But assuming that ERVs always insert at an identical location you've still got a long way to go to demonstrate that the pattern of ERVs in primate and human DNA is not the result of a common ancestor.

1) The distribution of ERVs matches a common ancestor, in that older species diversions have less in common than newer species.

2) I also understand that mutations within the ERVs themselves match the age of the infection, as predicted from the age species divergence.

3) If your hypothesis was true that all these ERVs are recent infections, that would predict that insertions would be random across species (or present in ALL species), yet they are not.

You're obviously well schooled in this issue tallhappy. Well enough that you actually understand Ichneumon's argument and can research it on your own. In my layman's opinion, you appear to operate like a defense attorney who knows his client is guilty, but they have to make the best case they can.

You've made a case that ERVs are not completely random (implying 1/3 odds) that counters Ichneumon's evidence that the highest probability of insertion in his study was 280x random. Yet the case for common ancestry for ERV insertions does not stand or fall on randomness alone.

If I were a layman on the jury of this trial, I'd conclude that you lost the case. You've done a bit of damage to one element of Ichneumon's case. But his case rests on much more than whether ERVs are totally random.

Don't bother criticizing this post. I'm not in your league and I'll play the victim if you try. I'm just expressing my opinion that you lost.