If indeed they are deleterious the fixation problem is worse. A purely neutral assumption is the easiest way to see if there is a reasonable chance what we are observing are random retroviral insertions.
O Ancient one 
.
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And still, not a blessed thing gets through to him.
In your last comment, you said there are too few fixed unique ERVs, assuming that:
assuming the average mutation is neutral and the rate of occurrence of retroviral infections in the germ line .
According to the paper you sent me, ERV mutations are deleterious and thus are rapidly selected against. That means unique ERV mutations will not persist in the population, explaining why there are few fixed unique ERVs.
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You might say he has a fixation with it.
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One of the first pieces of evidence I would point to is LTR divergence. When a retroviruses inserts into the host genome the two flanking LTR’s are identical in sequence due to the way in which viral replication works. As the ERV is passed vertically within a population the mutations that occur in each flanking LTR will cause the sequences to diverge. This allows us to make some predictions if the viral origin and common ancestry is true. The time since insertion for an ERV is determined by how widely dispersed the orthologous ERV is in a phylogeny. More time means more divergence. This is exactly what we see in ERV’s. As discussed in the following paper, with figures:
As with most of these discussions on genetics, it is the phylogenetic signal that creationists can not explain. As expected, the phylogeny built on LTR divergence recapitulates the consensus phylogeny, and the 5’ and 3’ LTR’s are the most divergent in the tree.
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The fact that they can doesn’t mean that they do. Emv-3, the provirus that I studied, is in an intron of the dilute, now Myo5a, gene. It is excised by homologous recombination between the LTRs at the rapid rate of one in 10^5. Those mice are revertants–their coat color is wild-type because the solo LTR doesn’t detectably disrupt the myosin gene, while the whole provirus does–but not completely, providing a pretty coat-color variant that was bred by mouse fanciers:
https://linkinghub.elsevier.com/retrieve/pii/0092-8674(83)90419-1
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And that divergence also makes it less likely that the ERV will be excised by homologous recombination.
If the paper is right would you expect randomly inserted ERV’s to get fixed in the same location in the genome across species?
If we see “ERV’s” in the same location across humans could the sequence be something other than random ERV insertions?
Okay, compared to “actually retrovirus insertions are not random” and “ERVs don’t actually form a nested hierarchy”, I think yes, this is in fact the worst ERV argument.
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They do think they can explain it, however, with the retort “If God wanted to make it that way, he could have.” So the issue is more with differing understandings of what constitutes an explanation.
And remember, @Andrew_Christianson , Bill has been saying stuff like this for years, thinking he is doing science. I kid you not.
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I should have clarified that. Got carried away 
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This is an entirely different argument than the fixation problem, but no, we would not expect ERVs to be fixed in the same location across multiple species without common ancestry. The paper explains that recombination rates and gene density vary between species:
“…within humans, the genomic distribution and persistence of ERVs is controlled by gene density and local recombination rate, respectively. This is consistent with certain TE classes in some species but not others. Thus, factors controlling the evolution, distribution, and persistence of TEs are likely to depend on a complex interplay between specific TE classes and particular host species.”
So even if the exact location of an ERV insertion was predicated on gene density and local recombination rate, ERV locations would still be inconsistent between species. Since ERV locations ARE consistent between different species, this is support for the insertions happening in common ancestral populations.
If we see “ERV’s” in the same location across humans
Fixation means near 100% allele frequency in a population. Within a population, natural selection, genetic drift, and bottlenecking/the founder effect all trend populations towards fixation.
Humans have low genetic diversity with 99.9% genetic similarity. If most ERVs are ancestral, they should also be 99.9% similar across humans; i.e. fixed.
could the sequence be something other than random ERV insertions?
Wouldn’t a better test of whether or not ERVs are viral be to demonstrate genetic identity as viruses and lab revived behavior as viruses?
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Mr. Romanes handled that argument 140 years ago.
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Common ancestry also predicts which ERV’s should not be orthologous. There are hundreds of PtERV insertions in the gorilla and chimp genomes, but no such insertions in the orangutan and human genome. Therefore, given the observed distribution of this type of retroviral insertion we would expect them to be lineage specific, hence non-orthologous. That is indeed what we observe.
Common ancestry explains both the pattern of orthologous AND non-orthologous ERV’s. IDcreationism doesn’t have a good explanation for either.
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