I note, from a post in another thread, Frenegi appears to have conceded the case for ERVs being of viral origin

nygreenguy :How does the positioning of ERV's and their sequences fit the hypothesis you mention? ERV's vary greatly among species, all of which live under the same biosphere. I dont really understand what exactly this hypothesis is you are mentioning (at least in any actual descriptive detail)

ferengi: The hypothesis that the chimps and humans could have been exposed to the ERV's independantly and not inherited them vis a "common ancestor".

By "exposed to ERV's [sic] independantly [sic]", I presume he means exposed to retroviruses independently.

Well, no. I'm afraid this is way beyond the bounds of credibility, based on what we know about how and where retroviruses integrate into host DNA, and based on the huge number of ERVs in orthologous locations in species such as Homo and Pan.

The vast majority of the 200,000 odd ERVs found in both the chimp and human genomes are in orthologous locations. The Mitchell study linked to above was of a limited sample of integration sites for a selection of retroviruses. Nevertheless, the sample found no repetition of integration sites among the 400 to 500 odd sites for each retrovirus.

Even using the extremely modest figure of 400 possible sites, the probability of 200,000 instances of ERVs occurring in orthologous locations in both species by chance is 1/(400^200,000).

A slightly more likely scenario is that various ancestors acquired retroviral integrations into their germline cells and bequeathed them to their descendants. See ERVs - 'Watermarks of evolution' in our DNA.

Here are the implications of the Mitchell study spelled out.

Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences
  • Abstract

  • The completion of the human genome sequence has made possible genome-wide studies of retroviral DNA integration. Here we report an analysis of 3,127 integration site sequences from human cells. We compared retroviral vectors derived from human immunodeficiency virus (HIV), avian sarcoma-leukosis virus (ASLV), and murine leukemia virus (MLV). Effects of gene activity on integration targeting were assessed by transcriptional profiling of infected cells. Integration by HIV vectors, analyzed in two primary cell types and several cell lines, strongly favored active genes. An analysis of the effects of tissue-specific transcription showed that it resulted in tissue-specific integration targeting by HIV, though the effect was quantitatively modest. Chromosomal regions rich in expressed genes were favored for HIV integration, but these regions were found to be interleaved with unfavorable regions at CpG islands. MLV vectors showed a strong bias in favor of integration near transcription start sites, as reported previously. ASLV vectors showed only a weak preference for active genes and no preference for transcription start regions. Thus, each of the three retroviruses studied showed unique integration site preferences, suggesting that virus-specific binding of integration complexes to chromatin features likely guides site selection.

Integration site preferences or biases might just provide some useful information in countering retroviruses, so studies like this could be important.

Each of the six retroviruses/cell types studied in this sample of 3,127 DNA integration sites, however, was found at between 407 to 822 locations, depending on the retrovirus.

This means that the chances of a retrovirus integrating in the same location in the DNA of two different cells by coincidence, based on this survey, is at most 1/407.

Let's call it 1/400 for simplicity.

Remember that this probability is based on a limited sample of integration sites.

Analysis of a bigger sample would be bound to yield a smaller probability, because there are bound to be more integration sites.

But let's just say that the probability of two retroviral integrations appearing in the same place in two different cells, by coincidence, is at most 1/400.

That means that the probability of two retroviral integrations appearing in the same two places in two different cells, by coincidence, is at most 1/400x400 = 1/400^2 = 1/160,000.

That also means that the probability of three retroviral integrations appearing in the same three places in two different cells, by coincidence, is at most 1/400x400x400 = 1/400^3 = 1/64,000,000.

And so on.

All humans share around 200,000 retroviral integrations appearing in the same 200,000 places in every cell of their bodies.

Coincidence?

No.

The probability of coincidence is, at most, 1/400^200,000.

The only explanation is that they inherited them from integrations into germ line cells of common ancestors.

Chimpanzees also share, with humans, around 200,000 retroviral integrations, that appear in the same 200,000 places in every cell of their bodies.

The explanation is the same.

Humans and chimpanzees share ancestors.