Answers to "ftacky's" questions are to be found in my FAQ, which is why I wrote it. However, I will respond to the questions as they have been put.
Q1) How could humans and other animals survive at all without the genetic materials essential for life BEFORE they became infected by ERVs?
A1) ERVs are not essential for life. Some elements of some ERVs have BECOME essential.
Q2) Why don't we see ERV insertions into germ cells today?
A2) We do. A good example is the Koala retrovirus, KoRV.
Q3) Why would such infections be preserved, even through apoptosis and unfavorable selection of infected organisms?
A3) 1) Apoptosis doesn't always occur in infected cells. 2) Reverse transcriptase is error-prone. The ERVs that survive in our genomes are not normally replication competent, and don't trigger apoptosis. 3) Retroviruses are known to have genes that inhibit apoptosis. 4) Many ERVs that do induce disease cause late-stage conditions, typically cancer. These are invisible to natural selection, because the carrier will have already passed reproductive age.
Q4) 4) What made ERVs change from viral activities and acquire transcriptional abilities to create essential genes?
A4) As I said above, reverse transcription is error-prone. Many of the retroviral genes created by it will be already mutated. If not, they will often be neutral changes WRT the host organism. Consider that modifying a gene by an error mutation is much more likely to produce a gene that does something, as opposed to gened being created from scratch purely by random mutations. Again, natural selection will select those mutated genes that benefit the carrier.
Q5) What made ERVs immediately turn into essential gene regulators upon insertion?
A5) Not immediately essential. See above. All retroviral proviruses include transcription promoters. Otherwise, the retrovirus would not be replicated by the host cell. Now, drop a promoter into a genome in a random location, and it is quite likely that it will promote the transcription of some native genes downstream of it. Again, selection will sort out which of these side-effects will be preserved because they provide some relative advantage, and which will be deselected.
Q6) Why have ERVs - initially pathological - NEVER been proven to cause disease but have been proven to be favorable for life instead?
A7) ERVs have been proven to cause disease. KoRV, mentioned above, is a clear example. ERVs are also implicated in late-stage cancers, and hereditary genetic diseases. Those that are favourable to life have been selected, naturally.
Q7) What made the identical ERV transcribe differently in humans and chimps?
A7) Do they? Where is the evidence? If they do indeed transcribe differently, remember that humans and chimps are different species, with differences in their DNA. The effect of any genetic element depends on its environment, and that environment includes the rest of the genome it is located in.
BTW, the poster "ftacky" in the link you provided makes a couple of errors.
1) The common ERVs that prove common descent are not found in "similar locations", but in precisely corresponding locations, down to single base-pair resolution. Endogenization in common ancestors is the only viable explanation.
2) HERVs are _Human_ Endogenous RetroViruses. The proof of common descent is the common ERVs in related species.
3) ERVs are found in unrelated species, but never in precisely corresponding locations. These are the result of separate endogenization events. Gibbons and the poor koalas, again, provide an example.
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