To Peter Berean

A Peter Berean asked me a series of questions on a FaceBook discussion group.

https://www.facebook.com/groups/815524058785996/permalink/1046567909014942/

He had already been linked to my FAQ, but seemed to have problems navigating it and had additional questions. There follows my response. Peter's comments and questions are in quotes.

"The ERV argument is basically a probability argument... that common loci of alleged ERVs cannot occur by anything other than a common ancestor (viral infection thereof)."

"Do you have a calculation for that probability?"

Well, the studies documented at the link below show no repetition of integration sites within 400+ loci. The probability that two integration sites of the same virus, to the same target cell type, in two independent infections would be at most 1:400^1. The probability of 200,000 independent integrations at corresponding loci would be 1:400^200,000. You don't need to worry about the possibility that this is a coincidence. The only explanation is that they are inherited copies of the same integrations.

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

Table 1

"1. Functionality destroys the ERV argument."

This is always desperately clung to by science-deniers. Nobody argues that all ERV elements have no function beneficial to their hosts. (They do. They also have functions deleterious to their hosts.) I have seen many people claim that the proof from ERVs relies on none of this genetic material having any function (junk). This is a false, straw-man argument, and as such it is dishonest.

Here are my FAQ entries dealing directly with function.

ERVs do stuff. Doesn't that prove that they didn't originate from retroviruses, but were designed? https://barryhisblog.blogspot.com/p/ervs-do-stuff-doesnt-that-prove-that.html

ERVs promote the transcription of host DNA. Doesn't this prove they are designed? https://barryhisblog.blogspot.com/p/ervs-promote-transcription-of-host-dna.html

ERVs are essential in reproduction (syncytin and the formation of the placenta). How can this be? https://barryhisblog.blogspot.com/p/ervs-are-essential-in-reproduction.html

"2. Hot-spots REDUCE the areas for such insertion, and so lower the improabability threshold for the ERV argument... contradicts the low probability of the ERV arg claim."

See above. Here is more on target site preference, and why it doesn't help the denialist claim.

http://www.evolutionarymodel.com/ervs.htm#Target_site_preference

And this from my FAQ. https://barryhisblog.blogspot.com/p/relationship-between-integration-sites.html, Don't retroviruses target particular locations in the DNA? Doesn't this explain corresponding ERVs?

"3. Do you have a scientific reference that provides the total number of alleged ERVs in chimps and humans; and the total number of alleged ERVs that are in exactly the SAME base-pair location/locus?"

Yes. You will find them @ https://barryhisblog.blogspot.com/p/from-table-11-of-initial-sequencing-and.html, How many ERVs are shared, in common locations, in the genomes of humans and chimps? 

"4. What fraction of those alleged-ERVS actually have ALL of the elements
needed to prove that this is an ERV?"

You don't need all the elements to prove that something is an ERV, but you are welcome to try and figure out how many full-length ERVs there are from here. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1951428/, Rate of Recombinational Deletion among Human Endogenous Retroviruses.

"5. What fraction of those alleged-ERVs have NO function in the organism?"

Most ERV elements that have any effect (good or bad) for their hosts are promoters, not the retroviral genes themselves. Promoters are short genetic sequences in retroviruses that are necessary to get their own genes transcribed in the host. Other elements, such as env genes, have been exapted as syncytins, discussed above. I don't think any organism has multiple different syncytin genes. So the answer is that it is mostly promoters, and your question is studied here @ https://academic.oup.com/bioinformatics/article/24/14/1563/182042, Retroviral promoters in the human genome.

Peter, that is all the time I can spare on this at the moment. Please bear in mind that I am not your personal unpaid tutor. The scientific literature on ERVs is vast, and I can't be expected to answer all questions on the subject in precise detail. I suggest that if you are not satisfied with my answers, you study the subject yourself. There is much material that is free to access, and it is easily searched for. I suggest you use Google Scholar to ensure that the material you access is the most reliable.