==Evolution deals with what will happen when I subject a population to selective pressure NOW.
Well seeing how we have never witnessed inanimate matter become a simple cell, or a simple cell turn into a more complex cell, or a more complex cell turn into a multicellular organism, or a multicellular organism turn into another kind of multicellular organism, perhaps you should just concede the debate right here and now. Or did you mean that scientists observe how selective pressure causes organisms to change from within the boundaries of their various kinds, assume that said changes are caused by random mutation plus survival, and then extrapolate the same ad infinitum without any present day confirmation whatsoever?
==Why would some ERV’s be unique to only some human populations? Do those ERV’s perform a function in only those human populations do you suppose?
Yes, think of the transposable elements of a genome like an environmentally sensitive Rubik’s Cube. Under certain environmental conditions all the colors match up on all sides, but when the environmental conditions change, certain squares begin to take on the color of a different side, and it is necessary for the frontloaded program that controls the genome to get all those colors to match again. Thus, it would be necessary to borrow bits and pieces from the changing colors of various sides of the Rubik’s Cube and move them to different sides to once again sync the Rubik’s Cube with it environment (this would easily fool your evo co-religionists into believing that the recombined ERVs were evidence of recent infections, or, conversely that they are evidence of ancient infection sequences that have since degraded). In the same way, the frontloaded organizing program of the cells borrows from the extensive repertoire of ERVs (and other repetative transposable elements, or RTE for short) that are capable of being mixed and matched with the existing ERV/RTE setup, and move them around until the organism is able to reestablish equilibrium with its environment. And lest you think there is no empirical support for the analogy above, there is...refs available upon request :o)
==We can see the incorporation of new ERV’s into a genome when reproductive cells are infected with RNA virus; do these newly incorporated ERV’s serve a function as soon as they enter the new genome? At what point and by what criteria would you say they became “functional”?
Actually, from what I have read, this is extremely rare. Do you have any evidence to suggest that this is common? Having said that, there is a growing body of indirect evidence that a soma to germ cell feedback loop exists that crosses the so-called Weisman Barrier. And wouldn’t you know it, the proposed mechanism for the final step (crossing the Weisman Barrier) are the transposable ERVs! Under this scenario, it make far more sense that successful adaptive strategies are developed in the soma/body cells, and then communicated via ERVs and possibly other transposable elements to the germ cells.
==And if you say ERV’s serve to increase genetic diversity in order to help “adapt” a population to changing environments; is this an example of de-evolution or degradation of the genome? Is becoming more adapted to your environment de-evolution?
We must distinguish between different types of mutations. I have always maintained that random mutations will result in genetic degeneration. However, directed, controlled mutations are a totally different ball game. We see directed mutation in bacteria, we see it in our immune systems, and we most certainly see a similar principle at work with respect to numerous epigenetic changes.
Evolution: genetic change of a population in response to environmental pressure.
By suggesting that ERV’s act to increase genetic diversity and act to adapt a population to its environment you are signing on to them being an agent of evolution.
So is a population becoming better adapted to its environment evolution or de-evolution GGG? Is becoming better adapted to your environment “genomic degeneration”?
No, incorporation of an ERV is not extremely rare and it can be studied and even induced by infecting cells with an RNA virus.
Despite your assertion that ERV insertion is all somehow preprogrammed and deterministic; if I study the insertion of an ERV into a DNA chromosome I can do a thousand insertion events and get a thousand DIFFERENT insertion points. If only Creationists were right on this one little thing it would be a boon to biology as if we could actually DIRECT ERV insertion and gene therapy wouldn't be such a problem.
So when a new ERV incorporates into a genome, does it immediately have a function? When would a newly incorporated ERV be said to have a function, and what function would it serve.
Still no explanation for why an ERV would look either “young” or “old” depending upon how widely shared it is among the species or between species.