Why Aren't the Twin Locations of >100k+ ERV's (human vs. chimp) Discussed More?

God could plant fingerprints at crime scenes, but I don’t see anyone asking to have fingerprint evidence thrown out of court because of this possibility.

We can observe live retroviruses creating new ERVs in host genomes. As shown above, you can even revive ERVs so that they become viable retroviruses. The only reason you would doubt that ERVs are the product of retroviral insertion is if you don’t like the conclusions it leads to. If YEC’s do use the argument you are describing then they have tacitly admitted that the evidence, as it stands, points to common ancestry.


To put it another way, no one is saying that ERVs evidence common ancestry because they lack evidence for function. If every ERV did provide function of some sort in the human genome they would still be evidence for common ancestry.



I could use your opinion on this matter:

In the study above, we find this in the abstract:

“Retroviral infections of the germline have the potential to episodically alter gene function and genome structure during the course of evolution. Horizontal transmissions between species have been proposed, but little evidence exists for such events in the human/great ape lineage of evolution.”

"Based on analysis of finished BAC chimpanzee genome sequence, we characterize a retroviral element (Pan troglodytes endogenous retrovirus 1 [PTERV1]) that has become integrated in the germline of African great ape and Old World monkey species but is absent from humans and Asian ape genomes."

“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.”

Did this writer just say what I think he said? While we here, on this thread, are discussing the more than 100,000 ERV fingerprints shared by both Chimps and Humans - - is this writer saying he found a bunch of ERVs that are not shared?

Isn’t that like saying: “Humans can speak English, but Chimpanzees cannot; so they must not share a common ancestry!”

The writer is saying that after the chimp and human lineages split there was a retrovirus that created insertions in both the gorilla and chimp lineages but did not infect any human ancestors. This is further supported by the fact that the authors were unable to find any unambiguous orthologous PtERV insertions between the chimp and gorilla genomes which is what you would expect if those insertions happened after the human/chimp split.

I have actually ran into creationists who make those sorts of argument. They claim that since we are using a homology argument to evidence common ancestry you can falsify evolution by finding differences between species. I guess they forgot that evolution means “change over time”, so pointing at changes isn’t going to falsify the theory. Common ancestry is actually based on a phylogenetic argument which few creationists seem to grasp.



Hahaha! So, is the writer SHOCKED by this finding? Maybe he got valuable practice in the lab…
That’s gotta be some kind of low-value conclusion for the history books…

I don’t think that any geneticist would be shocked by the observation that genomes continue to evolve after a speciation event.


I suppose the equivalent to the “rabbit in the pre-cambrian” finding that YECs would really want to hope for in this context would be if they could find matching ERVs in both the gorilla and the human genomes but that were missing in the Chimp genomes. This would throw a real wrench in the whole ERV thing, not by solving it with some better solution, but by blatantly not fitting the accepted picture: since anything that passed from gorillas on through humans would have to have also been passed to Chimps since they branched off later than gorillas. In short it would make it look as if gorillas were more closely related to us than Chimps, which presumably contradicts a mass of evidence that shows the opposite.

Did I get all that correct, @T_aquaticus?

Hi Mervin,

Don’t forget about incomplete lineage sorting. Because of ILS predict a certain amount of noise in the phylogeny. An ERV that is homologous in great apes and H Sapiens but not in Pan Troglodytes is an example of that noise.

Biologists, please correct or elucidate further as necessary.

Ahhh - and that shows that I’m out of my league in even trying to tease that out! I tried.

I’ll have to spend some time back on Venema’s ILS explanation again to even understand your reminder. I know that further evolution could change some of these alleles after the speciation event, but I thought that the ERVs would survive in big enough numbers to still leave their tell-tale evidence despite some small percentage of them being altered. Thanks for interjecting.

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I think that although your example makes sense at first glance, it assumes a single unified line of descent, when actually we are dealing with populations which have multiple versions of the genome in play at any given point in time. So if not all the ERVs became fixed in the population between the divergence of gorillas and the divergence of chimps/humans, the situation you describe could indeed arise. But we wouldn’t expect it to be common—with a lot of ERVs matching in gorillas and humans but not chimps.

Correct me if I’m wrong!

hi T. this paper actually found at least 6 ervs that dont fit with the primates phylogeny (and these ervs are in the same location so we cant claim that they happened after the split). this is why they try to solve it by a convergent loss:

" If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely"

so both scenarios are unlikely since we need here at least 6 convergent cases: 6 ervs insertions at the same site or 6 ervs deletions at the same site. a real contradiction to the common descent prediction. but there are more problems with the ervs argument. another problem is the fact that some creatures cant survive without some ervs. so how they survived before they get these ervs? these two problems can be explain easily by a common designer and not by a common descent.

we actually know that a retrovirus can get host parts and add it to its genome. so basically its possible that all retroviruses created from host genome and not the opposite. it can also explain why they are in the same locations among many species.

That’s why the entire paper is about why it seems most likely that these represent invasions via an exogenous source, i.e. a “bombardment” of chimp and gorilla genomes by retroviruses. Not ERVs, but retroviruses. The Discussion walks through the multiple lines of evidence explained by that hypothesis.

The Yohn et. al. 2005 paper reveals that you can easily tell if populations were infected independently or whether the viral infection was passed on to offspring. This particular virus infected only the chimpanzee and gorilla lineages, but not the human and orangutan lineages. In other words, you can easily tell if they were transmitted in an endogenous vs. exogenous way (see Human Retroviruses - Medical Microbiology - NCBI Bookshelf) as @sfmatheson just pointed out.

The discussion of the main parts above was concerning endogenous virus fragments- close to 200,000 that do fit in photogenic trees and do show the tell tale signature of endogenous viral transmission and are very clearly not exogenous insertions - if we want to talk about impossible odds, then that is what we are talking about. We are talking about hundreds of thousands of ERVs (and yes some have become functional which says nothing of how they were transmitted) inserting themselves and sorting themselves in a phylogentic way which is nothing short of what the young earth creationist model requires of animal sorting during the flood all over the world perfectly.

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I don’t think that ILS explains the data in Yohn et al. They make a very strong case for concurrent and extensive retroviral infection of two of the lineages.

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Ooops… @pevaquark… you lost me here. Are you saying they’ve sorted themselves per nested
Hierarchies? Or in some other ways?

hi pevaquark. first: how many of them are shared among chimp and human? how many of human\chimp shared with creatures like cat or dog? how many of the 200,000 ervs are full ervs and not just chunks of ervs? (as a general note: english isnt my natiive so i dont understand some words here and there in general).

Very true. It is entirely possible for an ERV to be polymorphic or heterozygous in a population just prior to a speciation event. After the speciation event the heterozygous ERV can disappear from one population but stay heterozygous in the other lineage where it eventually becomes fixed. There could have been an ERV that was heterozygous in the common ancestor of humans, chimps, and gorillas which remained heterozygous through the later split between chimps and humans. After the split between chimps and humans it became fixed in both the gorilla and chimp lineages while disappearing from the human lineage. This is incomplete lineage sorting.

This is an expected outcome of speciation and heredity, but it should be limited to a few ERV’s and couldn’t explain why 200,000 ERV’s don’t show the expected pattern of species distribution.


The number of ERVs shared between chimps and humans is about 203,000 which is nearly all of them (>99%). As to sharing ERVs with more distantly related species, I’m not sure if anyone has looked. The problem is that ERVs often recombine to produce solo LTRs which accumulate mutations to the point that they are difficult to detect using standard algorithms. Think of it like fingerprints which slowly degrade over time to the point they are no longer detectable.

Also, many ERVs are chunks of retroviral genomes. As mentioned earlier, they like to recombine, especially at the LTRs. When you have very similar DNA sequences at two points in the genome they like to stick together because of matching complementary bases. Since LTRs are identical in sequence at the time of insertion this makes them vulnerable to looping around and sticking together which results in the DNA between the LTRs being excised. What you are left with is a single LTR.

it should be interesting. what about a scenario wich these ervs in the genome are a part of the original design and not a viral infection?