Bob, I'd like you to consider the state of some HERVs, while none are known to be active as inherited in humans, there are many full-length retroviral genomes. (In the case of HERV-K111 we are still sorting out just how many have been overlooked.)
The most common way in which full-length retroviral genes in HERVs are inactivated is by misplaced stop codons, frame shifts are also prevalent. If you were to design a "patch" to correct this it would only need to contain a few base pairs, though you would want a longer sequence to see that it matched up correctly with surrounding sequences. It is apparent there are many ways to cause transcription of HERVs, so that is not a problem. All you need to do is fix those small errors. Similar errors do not prevent diseases in animal models as with MMTV or JSRV. A helper virus supplies the missing base pairs or gene functions. The virus can be described as both an ERV and an exogenous virus. This is much easier to observe in animals with short life cycles, where viral replication is rapid, than it is in humans.
I would be far more surprised if nature overlooked the option of supplying just enough information to transcribe and reactivate these proviruses than I would be to learn that this also takes place in humans. Those cells are behaving as if they are fighting viral infection. Why not treat it as if this were a viral infection? The fact that a process does not satisfy academic definitions of viral infection means much less to nature than to academic researchers.