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.
Not well schooled *enough*, it seems. See below.
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 noticed that too, eh?
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.
Oops, you fell for his mistake/propaganda.
He falsely tries to imply that if 3 subjects out of 9 in a gene-therapy study had retroviruses integrate at the same locus, that this means that 3-out-of-9 retroviral integrations somehow "homed in" on the same location.
WRONG!
Hint: How *MANY* retroviruses (and thus retroviral integrations) are induced in *each* patient in a gene-therapy treatment?
This wasn't "3 out of 9", it was "3 out of a mind-bogglingly large number". Those critical three only got noticed because they caused the individual cells which had the "fatal" location disrupted triggered leukemia in their unfortunate recipients, but there were *VAST* numbers of *other* random integration events in *each* patient which caused no problems at all.
Hey, tallhappy, do your own homework for a change, and tell us how many unique integration events there are, in total, in 9 patients in a gene-therapy study?
So what are the *actual* odds of overlapping events, out of *all* integration events, in a study like that, eh?
Randomness has little to do with the conclusion. All that is needed is a distribution of insertion loci. Were the same virus DNA inserted in different places in closely related species, that would suffice.
That was my case.
His argument pivotted on it and was inacurate and anachronistic. Interestingly if he'd read the article or understood it if he read it he would have seen that the non-randomness of integration is well discussed in the article from where the phylogram was borrowed. (he erred as well on its description, but that is for later to elucidate).
Also he has admitted my long time contention "or case" that his interest in not in discussing science but in what can be considered evangelizing or prosylitizing -- as he put it writing for the lay people.
Thanks for your comments, I appreciate them.