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

I finally reviewed a tempting video on the somewhat intimidating category of Evolutionary proof referred to as topic of Endogenous Retroviruses (ERV’s). I have deliberately avoided this topic for a year … but the video below does a brilliant job of explaining the major elements in just 10 minutes!

Totally impressed!

So why isn’t this topic more widely used whenever we end up in a loop-the-loop on the issue of the broken Vitamin C gene?

What do y’all know that I don’t know yet about this category of evidence?

[ Disclosure: Funny chimp images with notations not in the original video! ]



I’m glad you liked my thread kickoff…

But do you have any thoughts why this 16 EVR analysis isn’t a mainstay of every exhibit or communication about the massive evidence for COMMON DESCENT?

This beats the BROKEN VITAMIN C gene all to pieces … and would have loved to have understand this position a year ago …

16 EVR’s in identical location between Chimps and Humans?

What evidence do you think tops this analysis?

Because if you know one that is more compelling, I’ll start using it immediately!


I agree that it is a great argument, and the video explains it well. Unfortunately, the level of scientific literacy makes it difficult for the general population to follow and appreciate it. The vitamin C illustration while not as powerful, is simpler and easier to follow for those not science literate.
Of course, that does not explain why the science literate YEC professionals do not accept it. I’ll let them answer that.

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@JPM, Agreed!

Perhaps the solution is to emphasize the “visually obvious” aspect of ERV’s … rather than go into complex discussions of what Endogenous Retro Viruses “means” or “is”.

All that talk about the RNA converting itself into DNA is probably something saved when questions are asked… IF they are asked.

If we just described the virus attack and the virus inserting its genetic code into the host genetic string … that’s as technical as we need to get.

16 virus attacks… on identical locations of Chimp and Human chromosomes … that’s the PUNCHLINE!

Let’s start using it!

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Thanks for sharing George. I hadn’t come across the ERV evidence for common ancestry before @T_aquaticus posted back in August of last year: ERV evidence for pastor with a lawyer's mind - #18 by T_aquaticus

Just from ERVs you can construct phylogenies that mirror just that of other methods of organizing ‘species.’ I think the probability estimates in the video are a little high (but the overall probability is much higher) because ERVs can have selective site preferences, which as @T_aquaticus notes in the post just above moves the probability from 1 in 3 billion to about 1 in 10 million per ERV insertion location. However, instead of just 16 ERVs, we are looking at much much more than this in reality…

Humans have approximately 200,000 ERVs and we share 99.9%+ of all of them with chimps so now our probability goes to:
1 in (10,000,000)^200,000 or 1 in 10^1,600,000 making even the most irreducibly complex system/protein folding look like a cakewalk!!



Lo and behold… it is more complex than I hoped it would be. But based on your input … it’s not terribly so. As soon as you mentioned ERV exhibiting site preferences, I understood what you meant. That’s certainly relevant. But then you trumped everything by pointing out that there is evidence of 200,000 ERV sites, rather than just 16.

Did @T_aquaticus mention a good source for this kind of investigation?

My goal would be to use the video above as a template, but replace the questionable probabilities with something more precise.

And it’s not just in identical locations, it’s identical viruses with the same base pairs in those locations.

The GULO point deletion in Vitamin C is nice because it highlights the ancestry at the single base pair level. You can very easily look at the same gene in various mammals and just demonstrate the point with 90 base pairs.

ERVs make up some 6-8% of the human genome and thus we are talking tens of millions of base pairs scattered throughout the genome. It’s definitely harder to visualize and see as quickly. The video you posted did a nice job of showing specifics of some of the more we’ll studied ERVs in identical places.


The actual number of orthologous ERVs (orthologous = same place in genome) is closer to 200,000. Of the 200,000+ ERVs in the human genome, less than 100 are not found at the same spot in the chimp genome. I can go into more detail on where this info can be found if anyone is interested.

I can’t think of any other pieces of evidence that are as easily explainable to the general public. You can get into the weeds with LTR divergence, but the placement of these ERVs in the genomes is a concept that seems to be easily grasped by newcomers.


The best analogy I have come up with is a dictionary. Take two people and give them each a copy of the OED. Send them to different rooms. Ask them to randomly pick 500 words out of the dictionary and mark their location in the OED. Bring them back to the same room and compare the results.

First, you will notice that each person picked words towards the center of the dictionary. They also tend to pick words away from the edges and more towards the center of the page. You may also find that left handed people may pick words from the left side more often than the right, and the opposite for right handed people. However, even with these slight biases you still observe that they never picked the same word out of the 500 total that they randomly picked.

The same for retroviruses. They have slight biases towards certain large sections of the genome, but it isn’t nearly enough to account for 99.9+% of the ERVs matching between humans and chimps. The only explanation is that these ERVs were already present in a common ancestor and were inherited by both the chimp and human lineages.


@T_aquaticus, me me me me! Back here… behind the football quarterback! Where can I find a workably concise discussion of the findings?

By the way, “less than 100” are NOT found at the same spot… you mean like 85? Or do you mean like 4 (which is also less than 100).

To what do geneticists owe the difference in locations? At first glance, if it is not in the same location, might we conclude that the ERV’s in question infected the primate population a long long long time ago? … thus making them more prone to transposition through the normal workings of “imperfect replication”?

If we have 199,900 ERVs that are in the same place, I think that would be sufficient!

First, we go to Table 11 in the human genome paper:

human genome paper (2001)

The elements we are after are the LTR elements in the ERV-class I-III. Those total 203,000 insertions (don’t miss the x1000 at the top of the table) in the human genome, making up about 4.5% of the human genome. If memory serves, MaLRs are bits of retroviruses that found themselves in transposons and get moved about the genome through transposon activity which is a bit different than retroviral insertion.

Next, we go to the chimp genome paper which was published 4 years after the human genome paper. We will look at Table 2.

chimp genome paper (2005)

This table only lists the lineage specific insertions. This is another way of saying these are the insertions that don’t have a twin in the other genome. There are a total of 82 lineage specific human ERVs and 279 lineage specific chimp ERVs. This means that out of all 203,000 human ERVs only 82 are not found in the chimp genome. This would mean that chimps also have about 203,000 ERVs shared with humans as well as 279 ERV insertions specific to their lineage, most of which are PtERV insertions that infected chimp and gorilla ancestors but not human ancestors.


This diagram may help:

There are certain viral genes that are easy to pick out, and the genome is flanked by long terminal repeats (LTRs) that are also easy to pick out. We see this genome structure in modern retroviruses, and we see them in ERVs. Given the life cycle of retroviruses it is pretty obvious that the ERVs are the result of retroviruses inserting into the host genome.


There are two good references for probabilities. First, you have a paper that looked at three different retroviruses: HIV, MLV, and ASLV. Of the three, only HIV showed any real bias, but it certainly isn’t enough to explain 99.9% of insertions occurring at the same base.

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

80% of the time HIV will insert into areas that have genes in them, but about half of the genome is comprised of these areas. There are 3 billion bases in the haploid human genome, so that is an 80% chance of inserting somewhere in a set of 1.5 billion bases and a 20% chance of inserting into the other 1.5 billion. Still random enough to be used as a test of common ancestry.

The other reference is often used by ID/creationists.

" But although this concept of retrovirus selectivity is currently prevailing [37], practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified `hot spots’ containing integration sites used up to 280 times more frequently than predicted mathematically [41, 43]."
Perpetually mobile footprints of ancient infections in human genome

That paper was referencing a separate paper that actually contained the results we are interested in.

“In all experiments, estimates of the m.o.i. ranged from two to three integrated proviruses per cell. A pool of 10 ug of infected TEF DNA (from -5x l0^6 cells) would therefore contain 1-1.5 x 10^7 integration events. If integration occurred at random throughout the genome (size 2x 10^9 bp) we would expect to see about two to three integrations, in each orientation, within the 500-bp stretch of DNA analyzed in each reaction.”
Distribution of targets for avian retrovirus DNA integration in vivo.

What they did was add a small bit of DNA (their DNA target) to a big pool of human DNA and then added retrovirus. They designed the DNA target so that they could detect when an insertion occurred within it, and then did the math to figure out the preference for that DNA target. Think of it like a single detector in a big field where planes randomly drop bombs. By calculating the number of bombs dropped and the area of the field you can predict how many bombs will hit your detector if it is a completely random process.

Let’s unpack the math. For purely random insertions they would have expected 2-3 retroviral insertions in their target DNA out of 10 to 15 million total integrations in the entire pool of DNA. For some DNA targets they saw almost 900 insertions, about 300 times what they would expect from random insertions. This means that out of 10 to 15 million insertions there were 900 insertions in the 500 base pair DNA target they were testing. Obviously, that type of bias is not enough to produce matches 99.9% of the time for 200,000+ independent insertions in two different genomes.

Added in edit:
Completing the math . . . even in the case of the strongest bias, that is 900 insertions out of 10 million in the same spot. This means that if every single human and chimp insertion occurred at a hotspot, only 0.009% should occur at the same position if all the ERVs in each genome were acquired independently and not through common descent. Therefore, ID/creationism would predict that 200,000*0.00009 = 18 insertions should be shared, and that is in the best of cases. That doesn’t match observations.


Just in case I haven’t tripped the information overload sensor . . .

We can observe retroviruses creating new insertions in the host genome, but scientists have also demonstrated that ERVs can give rise to functional retroviruses.

“Human Endogenous Retroviruses are expected to be the remnants of ancestral infections of primates by active retroviruses that have thereafter been transmitted in a Mendelian fashion. Here, we derived in silico the sequence of the putative ancestral “progenitor” element of one of the most recently amplified family—the HERV-K family—and constructed it. This element, Phoenix, produces viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny.”
Identification of an infectious progenitor for the multiple-copy HERV-K human endogenous retroelements

What they did was line up multiple HERV-K insertions from the human genome in order to find the consensus sequence which is the most common sequence between the different insertions. This is a simple concept where you take the most common base at each position:


In effect, you are taking a lot of the mutations out of the sequence that have accumulated since the virus inserted into the genome. Once you have the consensus sequence figure out in your computer you can build the sequence in the lab, and then stick it into cells. When you do that you start seeing viral particles forming and infecting cells. Take the mutations out of ERVs and you get functional retroviruses, exactly what you would expect to see if ERVs were produced by retroviral insertions in the past.



Completely mind-boggling!

Now, see, if I were a YEC, I would just say:

“Yeah, you think these are some kind of evidence of a virus inserting itself in the DNA, but there is so much to the functioning of DNA that we don’t yet understand. Just because it looks like a virus doesn’t mean it was a virus. God could have put a virus-like strand of DNA in both human and chimp genomes at the same location for some as-yet-undiscovered purpose that has nothing to do with past interactions with viruses. I mean, you weren’t there, right? And there’s no corroborating evidence of these viruses outside genetics, is there?”

Are any prominent YEC folks taking this approach? And if so, how does one respond?

I thought prominent YEC folks when presented something like this just change the subject and ask another vague technical question, (But how do you explain the fact that there is only 6 inches of dust on the moon?)

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If I had just shown that all that a mathematical process just turned “garbage DNA” into the blueprint for a working virus, I would be able to confidently say to a YEC denier:

“If God goes through all this effort to create persuasive evidence of Evolution and Common Descent, who are you to oppose His zeal to teach these things - - all because of your simplistic interpretation of a few chapters of Genesis?”

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They have ‘functionality’ listed under the ‘red herring’ section:

there are no “functional ERVs;” only a small percentage of ERVs with functional components…any functional components are necessarily post-insertion exaptations, and the fact that they are necessarily insertion means that they can not be part of any ‘original design.’ The issue of functionality is simply a red herring, when discussing how ERVs necessitate common ancestry.


Wow… I’d never seen that site before! Thanks!