No, I'm suggesting the possibility of an enzymatic mechanism for the insertion locations as opposed to nonfunctional products of retroviral infection that have inserted randomly into the host. The whole proof of the common descent explanation lies in the vast improbability of mostly random viral insertions occurring in the same location in two different mammalian species because the DNA chain is too long for coincidence.
Cordially,
I am not confident that I understand what you are saying.
Let me try to restate it.
The evidence shows that artifacts, presumed to be caused by retroviruses, occur in the same genomic location of species which are presumed to share common ancestors. The presence of such artifacts is consistent with whether the artifact could have been present or absent in the presumed common ancestor.
I think that you are saying that there may be some enzymatic bias to "where" a retrovirus artifact occurs and thus the occurrences seen today are not descendant from a single infection event but instead just look like a single event.
If that is what you are saying and if that is what occurred, and given the very large commonality of genetic content for all primates, then wouldn't a great number of such artifacts have random frequencies? Wouldn't there be a majority of cases which would violate the presumed common ancestor appearance?
For example, humans share a majority of their genetic information with dogs, I believe. This would mean that at least half of the retrovirus artifacts which might appear in dogs could also appear in humans. This means that there would be a high frequency for artifacts found in humans and dogs, but not found in any other higher primates. Any enzymatic mechanisms would exist in both species with a frequency which matches the common genetic makeup.
If I understand the retrovirus evidence, it is the lack of artifacts in places where they could occur with a frequency dictated by common mechanisms but the presence of artifacts where they are consistent with common descent.