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

That will indeed be “the question” (or at least “a question”) when and if such ERVs are discovered. Those ERVs, like all interesting genomic elements and mutations, will be studied carefully, with attention paid to what is known about their behavior. To date, I know of zero examples of ERVs in “same location, but more distant species” that defy explanation via testable and even well-known mechanisms of molecular biology and population genetics.

Like the unsupported claims of Ewert about gene families missing from intervening lineages (see my comment here), ERVs in distant lineages in the same genomic location are phenomena that will require specific and robust explanation. First, of course, someone has to show that the phenomena are real. My hunch is that this will be difficult, because the phenomena are fictional.

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Well an orthologous HERV-K was found in chimps, bonobos and gorillas, but not humans:


Another one was found absent in chimps and gorillas:


Another problem is that humans do not have endemic infectious retroviruses:

There are explanations for these (which I think was Stephen Matheson’s point in his post below). So it is not as though these defy explanation. But they can get complicated and questionable (by questionable, I merely mean vague, or not well supported), I don’t mean impossible.

So yes, aside from cases that do not fit, the retroviruses do provide supports for CD. You brought these data up in the spirit of taking a larger view. That is, in response to the DG model, what about ERVs?

That’s a good point, but you know that works both ways, as there are many more problems with evolution and CD. There are a great many specific examples you can look at. I also like this meta study (Klassen, 1991) of 49 studies. Figure 6 shows how the empirical data consistently do not fit CD:

Again, one can always come up with explanations for the empirical data, and that’s fine, but it is important that we’re not talking about anomalies. The data, on the whole, do not fit CD, so you have an enormous parsimony cost with CD (like geocentrism, it works, but you need a lot of extra mechanisms). That’s why it is difficult to answer Ewert’s paper merely by saying, “well, we add more mechanisms,” as I mentioned above.

Also, in the spirit of stepping back and taking a larger view, in addition to the patterns, there are also process problems with evolution. With your ERV question you brought up primate evolution, so I’ll stick with that.

One interesting problem here is the chimp-human DNA similarity or ~99%. As you know this often is taken as powerful evidence for evolution and CD. It also presents a challenge, because what we know from biology indicates this isn’t going to work. What I mean is, you can make all kinds of changes to a genome, and get little or no phenotype change. The mapping is pretty robust. But a 1% change to get you from a primitive, rudimentary primate to a human being? That really seems far out.

It does not seem very credible, given the science, to expect such a tiny genetic change to produce such enormous quantum leaps in phenotypic improvement.

But I appreciate your ERV point, it is a good one.

Well this is not particularly controversial. For example:

Yeah, it is. Ewert’s claim is much bigger than anything in that review article you posted. See my comment. It’s about whole gene families.

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Not sure that qualifies for ‘uncooperative homologous ERVs (e.g., same location, but more distant species)’ but it is very interesting- I wish it were more common but I think this is a lone case of a nested ERV that is homologous in 3 primates but not homo sapiens! That still seems to support CD, with plenty of reasons why it is not in a homologous spot in humans. I don’t see why any ERV ever should be in a homologous spot without CD, let alone hundreds of thousands of them for chimps/humans.

Good eye. I wasn’t aware of such. So there isn’t even the option for the hundreds of thousands in humans to be inserted after the human lineage began but rather inherited through ancestry.

That’s what I would say with ERV evidence.

So the figure is interesting, but it in itself is not particularly helpful or earth shattering as the paper is moreso about highlighting the flaws of the CI vs. anything else- it is certainly not a knockout of any sort against CD! Seeing how the community interacted with this paper was useful for me (just looking at the papers that have cited this work) as the paper helped improve statistical analysis of cladograms.

Here is a recently accepted paper that outlines many potential methods to assess tree support:


Ouch. It’s bad enough to be misrepresented. But then the touche at the end.

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Thanks Chris. The warning was somewhat appropriate as my stomach started to do that one thing it does when I check my stock investments every morning.

@Cornelius_Hunter its going to make me grumpier than usual I think for you to keep bringing up this Klaussen paper as evidence against CD as it seems the paper isn’t quite all that you’re making it out to be. I do appreciate your ERV engagement earlier though it seems you consider it an ‘anomaly’ in light of massive evidence against CD like the Klaussen paper which is not massive evidence at all. Perhaps we can keep this thread focused on ERVs and if you find a really good topic that CD fails on, you can start another thread. I would still be curious to hear some non-CD engagement with ERVs.


Well it is unfortunate that problematic evidence is thrown out on the basis of an erroneous, misrepresentation, and no defense is allowed. Chris Falter apparently did not read, or does not understand. But I got it–stick to ERVs here.

You defended yourself in multiple posts in the thread I linked to. Interested readers may follow the link.

Cornelius, go defend your interpretation of the Klassen paper in the other thread that you posted several times in. Is the Klassen paper problematic for CD? No it’s not and stop this persecution complex nonsense: you can correct any erroneous misrepresentations and make a defense.

He read it, many others read it, I read it. And the conclusion I’ve come to unfortunately (as I really take what you say seriously: I was reading a paper in my pajamas late at night when my kids are sleeping- that is precious time for me :sweat_smile:) is well something like this:

Appreciate it!


That’s a non sequitur. No one is saying that ERVs are evidence for common ancestry and evolution because they are non-functional. Also, you need to show that the cost incurred by ERVs in the regions they are found would have been too high. You also need to show that there is a known mechanism for specifically removing ERVs. If there are no mechanisms for removing ERVs from the genome then you are left with the standard selection of alleles, substitutions and indels that reduce any cost incurred by ERVs. There are currently human ERVs that are heterozygous in the human population, and there doesn’t appear to be any strong selection against them.


ILS is a known and observed mechanism. If there were ERVs which were heterozygous in the common ancestor of gorillas, chimps, and humans then it is possible that ILS will fix the ERV in some lineages while they disappear in others which would create small incongruencies in the expected pattern. However, these should be exceedingly rare, and they are. Out of the 200,000+ ERVs that fit the expected pattern only a handful don’t, and this is what we would expect to see from common ancestry where ILS is possible.

You are projecting. More than 99.9% of the ERVs fit the expected pattern, and that pattern is consistent with common ancestry. You reject the evidence and stick to a lack of common ancestry. You are projecting your own unwillingness to dump a failed model onto others.

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We do have retroviruses that infect us: HIV-1, HIV-2, HTLV-1, and HTLV-2.

“Four types of HTLV, type 1 to 4, have been described in humans and for 3 of them simian counterparts (STLV-1, STLV-2, STLV-3) have been identified in multiple NHP species. The majority of human infections are with HTLV-1 which is present throughout the world as clusters of high endemicity.”
[url=The origin and diversity of human retroviruses - PMC]Peeters, et al. (2014)

Arguments from incredulity don’t get far in science.


What we have is an observed mechanism that produces orthologous ERVs in different organisms. That mechanism is common descent. We observe that human relatives share the same ERVs because they inherited those ERVs from a common ancestor. We also have the observed mechanism of retroviral insertion, and we know from those observations that retroviral insertion is random enough that only very rarely should two insertions happen at the same base in the genome.

We have directly observed retroviruses inserting into genomes, and we have the data demonstrating that only a tiny, tiny percentage of insertions should occur at the same base in independent insertions.

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again? see my comments above. we also observed the opposite (ervs parts can be created from host parts). so both options are possible. combine it with the fact that some creatures cant survive without some ervs and the best explanation is that these ervs are actually in the same spots because of common design.

Outrigger, did you understand the paper we’ve discussed extensively that demonstrates how one can potentially identify the difference between ERVs that are passed along to offspring vs. ERVs that separately bombarded different lineages? They produce extremely different signatures in the genome as the rest of @T_aquaticus 's quote that you left out for some reason demonstrates:

The normal life cycle of a retrovirus includes transcription of the inserted viral genome, so I’m not sure what you are getting at. That doesn’t put the origin of the insertion in doubt. We can directly observe the origin of new ERVs in the lab and in the wild.

You just reinforced my point. Of course we have modern endemic infectious retroviruses. The point was in regards to natural history. The fact that we have modern endemic infectious retroviruses simply demonstrates that host restriction systems are not a viable explanatory mechanism. This evidence flatly contradicts common descent. Quoting from the paper which I posted, which I recommend reading:

Actually, it is an argument from the current state of the art in biology.

To reiterate, the chimp-human DNA similarity is somethign like ~99%. What we know from biology indicates that 1% changes in the genome don’t even come close to traversing the enormous distance in phenotype space to get you from a primitive ape to a human. You can make all kinds of changes to a genome, and get little or no phenotype change. The mapping is robust. The science indicates that a 1% change will not go from a primitive, rudimentary primate to a human being.

Now can we prove this is the case? Of course not. One can always hypothesize that higher order (e.g., regulatory) changes will work this magic. But it really is, at this point, a complete unknown. You are arguing for an unknown–somehow a 1% genetic change brings on this enormous change. This is not indicated, and requires an unknown mechanism.

And when I point this out, you defend yourself by claiming I am making an argument from incredulity.

Unless it’s those pesky tool using kind:

It’s only a matter of time until they become BioLogos forum moderators :nerd_face: