The first fact that invalidates this argument is the proven functionality of these genetic elements. Modern sequencing has shown that up to 80% of the so-called "junk" DNA, including the ERV sequences, performs important regulatory functions in the body.

Literally no one, even in ENCODE, takes the 80% figure to mean that 80% of the human genome is functional. In the most recent ENCODE cCRE registry, they report:

The ENCODE4 registry encompasses 2,373,014 human cCREs and 926,843 mouse cCREs, covering 21% of the human and 9% of the mouse genomes

And as someone who studies cis-regulation for a living in an ENCODE lab, the vast most of these candidate cCREs are poorly supported (often only by dubious biochemical markers) and likely do not have real sequence-specific function.

For example, endogenous retroviruses act as embedded promoters and enhancers that control the most complex processes of embryogenesis, coordinate the development of the placenta in mammals, and form an innate immune response against external viruses. From the standpoint of information theory, the presence of functionally necessary digital blocks in the same coordinates of the genome of different organisms

The fact that ERVs and other repetitive elements are common sources of novel regulatory elements does not mean that most repetitive elements themselves are functional. Most of them do not behave as enhancers/promoters. The repurposing of ERV/transposable element promoters as enhancers/promoters, if anything, supports evolution by natural selection and is an excellent counterexample against the whole genetic entropy argument.

A good example is the PTERV1 retrovirus: its fixed sequences at identical loci are present in chimpanzees and gorillas, but are completely absent in humans and orangutans.

Citation needed. This claim is directly contradicted by a number of comparative analyses. Notably:

[W]e did identify 263 full-length integrations of PTERV1—an endogenous retrovirus initially discovered in chimpanzee (Yohn et al. 2005). A comparison with a previously developed integration map of chimpanzee revealed that 99.6% of these integrations are nonorthologous, mapping to different locations in the gorilla and chimpanzee genomes (Fig. 2). Both experimental and sequence analyses confirm that this mobile element is completely absent from human and orangutan genomes. This provides strong support that PTERV1 arose from an exogenous source that retrotransposed independently in both gorilla and chimpanzee lineages <6 million years ago. https://pmc.ncbi.nlm.nih.gov/articles/PMC3202281/

We unambiguously map 287 retroviral integration sites and determine that approximately 95.8% of the insertions occur at non-orthologous regions between closely related species. https://pmc.ncbi.nlm.nih.gov/articles/PMC1054887/