I understand, I am just providing a different look at the gene data. Here is another paper frequently discussed here that shows a more compact but similar cut.
Go to figure 3
https://doi.org/10.1038/nature12111
This is very off topic, was there some point you wanted to make about these papers that is related to either ERVs or ancestral convergence?
It is about evidence for the general thesis of common descent. No need to discuss further.
No, it’s just the two things that Bill likes to bring up when he can’t think of anything else.
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I’ve discussed the ERV evidence here and elsewhere, so I thought I would add some information that has helped me discuss the topic in the past. I will probably break this up into several posts to make it a bit more manageable.
First, the human and chimp genome papers have the best info for the overall tally of ERV’s in each genome.
From the 2001 human genome paper:
https://www.nature.com/articles/35057062/tables/11
From the 2005 chimp genome paper:
https://www.nature.com/articles/nature04072/tables/2
For the human genome, there foiund ~203,000 ERV’s (ERV classes I-III) that take up about 5% of the human genome. MaLR’s are viral LTR’s that have become part of transposons (if memory serves), so they are listed in the same category. In the chimp genome paper, they only listed the species specific ERV’s. In that paper they saw 82 human specific ERV’s and 279 chimp specific ERV’s, that is ERV’s that reached fixation (or at least a common presence) in each lineage after the lineages split. This means humans and chimps share more than 99% of their ERV’s.
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Do retroviruses insert randomly? We can test this two different ways. First, we have direct observation of retroviruses in the lab, and this includes a resurrected virus whose sequence was derived from human ERV’s.
For modern retroviruses, we have this paper using HIV, ASLV, and MLV:
“The human chromosomes are shown numbered. HIV integration sites from all datasets in Table 1 are shown as blue “lollipops”; MLV integration sites are shown in lavender; and ASLV integration sites are shown in green. Transcriptional activity is shown by the red shading on each of the chromosomes (derived from quantification of nonnormalized EST libraries, see text). Centromeres, which are mostly unsequenced, are shown as grey rectangles.”
As you can see, the viruses inserted into all chromosomes and down their entire length. They insert all over the place.
The only bias they were able to find is that HIV likes to insert in regions with higher transcription activity, but these regions comprise nearly 50% of the genome, so it isn’t going to create an insertion at the same base 99% of the time which would be needed to explain the data. From the paper:
"For HIV the frequency of integration in transcription units ranged from 75% to 80%, while the frequency for MLV was 61% and for ASLV was 57%. For comparison, about 45% of the human genome is composed of transcription units (using the Acembly gene definition). "
Next, we have a paper detailing the reconstruction of HERV-K insertions into a infectious retrovirus.
So we can even go back into the past and observe how these ancient retroviruses acted, and wouldn’t you know it, they randomly insert just like modern viruses.
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Next, we have yet another test for random insertion of retroviruses that result in ERV’s, as well as a test of common ancestry.
As it turns out, the gorilla and chimp genomes contain a class of retroviruses called PTERV1. However, insertions from this virus are not found in the human genome. This offers us a great way of testing our hypotheses.
Special creation hypothesis: ERV’s are found at the same position because they have a common designer. Therefore, PTERV1 should be found at the same position in the chimp and gorilla genomes.
Common ancestry hypothesis: The gorilla lineage split off from chimp/human lineage first, and then the chimp and human lineages split. Since we don’t see PTERV1 in the human lineage this would indicate that the creation of PTERV1 insertions occurred after all three lineages were separate from one another. Therefore, PTERV1 insertions should be found at different places in the chimp and gorilla genomes.
We have two different hypotheses from each approach. So which is right? Wouldn’t you know it, the hypothesis from common ancestry is the one supported.
Right away, more than 95% weren’t even close to each other (the BAC-based method has a resolution of 10’s to 100’s of thousands of base pairs). Of the ones that were possibly within 100,000 base pairs of one another they were able to use known sequences to rule out even more of these insertions as being orthologous (i.e. at the same base). There are still a handful that are unknown, but they authors expect them to be non-orthologous just like the rest.
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And finally, we have the comparison of the sequences themselves.
Phylogenies of LTR sequences produce the trees we would expect to see from common ancestry and evolution. Yet another test for this data.
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Hey @T_aquaticus, thanks so much for sharing. Since you’ve done so much research on human and chimp ERVs, do you know how many are actually shared between the two? I’m aware of the one study which found that we share 205 out of 211 ERVs (that’s the one I used in the OP), but has anyone gone through all 200,000 of the human ERVs and looked at which ones are in the same places in chimps and other great apes?
It’s interesting to note that, according to binomial distribution calculations, even if we only share 205 out of all 200,000 ERVs with chimps, there’s still only an infinitesimal (<10^-500) chance of this happening without common ancestry.
Oops, I just saw that you already answered my question the first time around. So we apparently share all but 82 of our 203,000 ERVs with chimpanzees. That’s pretty amazing evidence for common ancestry.
Are you sure that that’s the total amount, though? They only looked at the aligned parts of the genome, what about the indels between humans and chimps which account for like 3% of the differences, so maybe there are more that are hidden? Even if that’s the case, there’s literally zero chance of separate ancestry given this huge amount of shared ERVs.
Edit: Just as an interesting aside, if we input 203000 total ERVs, 202918 (203000 - 82) shared ERVs, and a 0.0000001 chance of two ERVs randomly inserting in the same place, the binomial distribution calculator here gives a probability of… drumroll please… 1.691 * 10^-1,419,228. Yes, you read that correctly. The chance of this many shared ERVs, if common ancestry is false, is less than 1 in 10^1 million.
This assumes, well, I’m not quite sure what the assumption is, but something about how many possible insertion sites there are and how probabilities are distributed among them. But there is a small amount of observed homoplasy in similar insertions, as discussed here:
Han, K.-L., E.L. Braun, R.T. Kimball, S. Reddy, R.C.K. Bowie, M.J. Braun, J.L. Chojnowski, S.J. Hackett, J. Harshman, C.J. Huddleston, B.D. Marks, K.J. Miglia, W.S. Moore, F.H. Sheldon, D.W. Steadman, C.C. Witt, and T. Yuri. 2011. Are transposable element insertions homoplasy free?: An examination using the avian tree of life. Systematic Biology , 60: 375-386.
As you probably know, when a question is asked in a title, the answer is usually “no”, and that’s true in this case too.
Hi @John_Harshman, I’m aware of the fact that ERVs tend to insert themselves in the same locations, which is why I’m using the data from the HIV study that @T_aquaticus linked. The data in that study indicates that there are ~10 million sites in the human genome where retroviruses prefer to insert. For my binomial distribution analysis, I’m estimating that the probability of two viruses randomly inserting in the same location is 0.0000001. And that’s fairly generous to the creationist position, since those are only the sites that retroviruses prefer to insert at, and it’s surely possible for them to insert elsewhere.
I’m pretty confident. Below is another great resource for the ERV evidence. I can’t remember the name of the person who wrote it (Ellesbury or something?), but I remember the author as being a reliable source. The impression I got is that the author of the website asked on the authors the very same question you are asking, and it was confirmed that they compared ERV’s 1 to 1, or at least that’s the impression I get from the paragraph quoted below.
Added in edit: Thinking back on this, there is always going to be a threshold for ERV detection because they are slowly accumulating mutations. At some point they won’t be recognizable as ERV’s anymore. Also, we don’t have a complete sequence for the chimp genome, so there could be a few hidden away somewhere, especially given the fact that LTR’s are repetitive in nature. However, I don’t expect a massive change in the numbers.
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How do you eliminate that this shared DNA is not the result of special creation? Again how did 200k random insertions ever get fixed in any population?
Those who got it passed it on to their children, and they had children of their own.
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Do you have any suggestions?
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You can’t, because it predicts and therefore explains nothing. You can always just make up some story about why a creator would make it that way.
However, them being actual retroviral insertions and retrotransposons does both predict and explain what we see.
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It Does not explain the observation to any level of detail. You may accept the story that x happens so then x explains y. This is building theory on untested hypotheses which is a house of cards.
What needs to be tested is how random retroviral insertions can get fixed in a population rapidly enough to explain the observation. What also needs to be explained is the variation of “retroviral insertions” among primates and other vertebrates.
You mean the retroviral genes GAG, POL, and ENV, flanked by long terminal repeats, and the tell-tale signs of insertion flanking these, are not explained by them actually being retroviruses (which consists of the genes GAG, POL, and ENV, flanked by LTRs)?
That’s like saying the craters on the moon are not explained “in any detail” by them actually being craters produced by asteroid impacts.
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Your comparing craters to long organized sequences 
What’s the origin of a highly organized LTR? This is the result of a randomly formed sequence?