Another poor response to ERV evidence for common ancestry by a creationist.

Back in 2009, I posted an essay on my website that I had just finished on the three ways endogenous retroviruses provide evidence for common ancestry.

When we examine the collective genome of Homo sapiens, we find that a portion of it consists of ERVs (IHGS Consortium, 2001). We also find that humans share most of them with Chimpanzees, as well as the other members of Hominidae (great apes), the members of Hylobatidae (gibbons), and even the members of Cercopitheciodae (old world monkeys) (Kurdyukov et al., 2001; Lebedev et al., 2000; Medstrand and Mager, 1998; Anderssen et al., 1997; Steinhuber et al., 1995).

In 2005, the available sequence of the Chimpanzee genome was aligned with that of the human genome, and an extensive comparison analysis was performed. As part of this analysis, the researchers looked at every available solo LTR and full-length ERV in the chimpanzee genome, and checked to see if there was also one at each corresponding locus. Just as with the examination of indels, the results were that less than 100 ERVs are human-specific and less than 300 ERVs are chimpanzee-specific (Chimpanzee Sequencing and Analysis Consortium, 2005; R. Waterston, personal communication, April 22, 2010).

In summary, indel variation shows that most transposable elements, such as ERVs, cannot be lineage-specific; they must be orthologous. When the indels are examined, this is corroborated, and less than 0.1% of ERVs are found to be lineage-specific. Finally, definitive confirmation is obtained by genome-wide comparison, where virtually all ERVs are directly observed to be in orthologous loci

When we examine the collective genome of Homo sapiens, we find that a portion of it consists of ERVs (IHGS Consortium, 2001). We also find that humans share most of them with Chimpanzees

Back in 2009, I posted an essay on my website that I had just finished on the three ways endogenous retroviruses provide evidence for common ancestry. Since then, I have continually updated it—especially the section on common creationist responses. So when a creationist blogger, named Jonathan M, recently announced on the Evolution News & Views website that he intended on responding to my essay, I was intrigued.

But my intrigue turned to disappointment, once his two-part “response” was published (p1, p2):

1. It contained errors and misrepresentations, such as claiming that only a handful of the tens of thousands of ERVs shared between chimpanzees and humans are actually shared, presenting differences in expression between genes with and without intronic insertions as differences between genes with orthologous insertions, and classifying PtERV1 insertions as sources of deviation from the nested hierarchy of orthologues ERVs, rather than sources of deviation from the LTR-LTR discontinuity ratio patterns. It also contained what may be a functionality non sequitur, but what appeared to be the false claim that hominoid syncytin-1/2 and murid syncytin-A/B are in orthologous loci, respectively.
2. Jonathan M. routinely presented arguments verbatim that were addressed in the common creationist responses section of the essay he claimed to be responding to. For instance, he presented the HERV-K-GC1 argument, where he concluded that “the inserts in the chimpanzee and gorilla lineages must be independent events,” without even addressing my extensive explanation of homologous recombination of duplicate genomic segments and allelic segregation—both of which were the focus of the research publication he was quoting from. He also repeatedly made the PtERV1 argument (mostly via uninterpreted quotes), which I had also explained in detail.
3. Much of Jonathan M’s response was unoriginal, and the quotes were from abstracts of research publications he likely didn’t read. Of the 9 quotes he provided, two were copy/pasted from a 2006 article by Dan Reynolds, and three were copy/pasted from a 2001 article by Sean Pitman (he also copied Pitman’s misattribution of the quote to the wrong publication). Even the surrounding text he wrote sometimes read like a paraphrase. Yet despite all this, he never cited either of these articles as sources.

And to top it all off, even though Jonathan M. didn't even attempt to explain the hierarchical patterns, or why they corroborate one another (something I lamented the universality of in the essay itself), he nonetheless boldly concluded with; “Unfortunately for Darwinists, however, the evidence for common ancestry is paper thin on the ground.”

All this, and much more, is discussed in the thorough rebuttal I posted. And judging by the continuous revisions Jonathan M. has been making to his shrinking response, it is clear that he has taken notice. Thus far, he has removed his entire paragraph and his quote on syncytin, removed any mention of gene expression and its associated quote, and corrected the misattribution he copied from Pitman. A screen shot of Google Cache’s June 3rd archival record tells the tale.

The last sentence of my rebuttal conclusion should sum up my sentiments:

I can only hope that if anyone else responds to my formulation of the ERV argument for common ancestry, they do not provide non-responses, and do provide a "comprehensive working creationist model that is consistent with uncommon ancestry and incorporates the whole of ERV data."

Well, since your results didn't line up with an ancient understanding of our world and universe, you're automatically disqualified. Sorry.


Keep in mind, when modern medicine's research hits a brick wall on a particular project, the most reliable source to correct such errors is the Bible. There are no substitutes! People don't understand it, but, the Bible is the cornerstone of modern medicine, oil exploration, computer science, structural engineering, and a slew of other scientific disciplines.

If you don't understand what I said, don't worry about it.

Come back and see us, soon!

Notice the ERVs Class I and tell me something. How do you reconcile your statement that we share 'most of them' (ERVs) when the most abundant family of ERVs in Chimpanzees isn't even in our genome?

You have a very serious problem with the age of the ERVs you claim are not 'lineage specific'. ERVs are actually another problem for a common ancestor. In fact CERV 2 (Chimpanzee ERV) has an estimated age of 21.9 mya to 14.1 mya with no human orthologues. The CERV1/PtERV1 with 100 members is estimated between 5 mya and 7.8 mya. That means that the most abundant ERVs in the Chimpanzee Genome came about before or right around the split (See Genome Biol. 2006)That means in addition to the adaptive evolution of the human brain our ancestors would have had to adapt their immune system to push these ERVs to the brink of extinction.

[CERV1] can be found in African great apes but not in humans. What is more the ERV virus is nearly extinct in the human genome with only a couple that actually work.

What is more you are citing the HGP paper from 2001, I assume this is from the initial sequence of the human genome paper. The thing is that the chimpanzee genome would not be sequenced until 2005, how on earth do you figure we have most of the ERVs in common when no definitive comparison had been done at that time?

Would you like to revise this statement?

When we examine the collective genome of Homo sapiens, we find that a portion of it consists of ERVs (IHGS Consortium, 2001). We also find that humans share most of them with Chimpanzees.

It amazes me that this is still even being used as an argument when it's a pretty strong argument against chimpanzee/human common ancestry.

ERVs are sometimes distinguished from solo LTRs, rather than referring to both as ERVs. When the authors of Polavarapu et al. (2006) said that PtERV1 is "one of the most abundant families of endogenous retroviruses in the chimpanzee genome,

When we examine the collective genome of Homo sapiens, we find that a portion of it consists of ERVs (IHGS Consortium, 2001). We also find that humans share most of them with Chimpanzees

" they may have been talking specifically about full length ERVs. This is supported by the fact that they follow the statement in question with a description of full length ERVs:But regardless of what they meant, it remains true that there are tens of thousands of ERVs (or ERVs + solo LTRs, depending on terminology) in chimpanzee and human genomes. So, obviously, a family with only a couple hundred members cannot represent any significant portion of the total set of full length ERVs + solo LTRs. Regardless of who makes such a statement (I'm guessing the authors didn't intend to do so), the statement would still be obviously false. Given the confusion brought about by the authors' choice of words, I suggest emailing them for clarification. I will be doing so as well.

I addressed this in my essay:.
I addressed this in my essay (first quote) and in my response to Jonathan M. (second quote):These CERVs are non-orthologous, and as such, are not sources of deviation from the orthologous ERV pattern. They are not problematic for common ancestry.

I only cited the 2001 "Initial Sequencing and Analysis of the Human Genome" paper as a source for the stated number of ERVs in the human genome. I cited the 2005 "Initial Sequence of the Chimpanzee Genome and Comparison with the Human Genome" paper as a source for the explained direct observation that the majority of ERVs in the human genome are shared with chimpanzees: The "definitive comparison" was done with the CSA Consortium (2005). More on that below.

I would not. Either a given ERV in the human lineage is accompanied by a corresponding ERV in the same genomic location in the chimpanzee lineage (orthologous ERV), or that given ERV is not accompanied by such an ERV (non-orthologous ERV, i.e. specific to one or the other, i.e. lineage specific ERV). In CSAC (2005), table 2 lists the only lineage specific, i.e. non-orthologous ERVs the researchers could find in each lineage, of the tens of thousands present. To corroborate that this was the case, I emailed the authors, and they confirmed it. They aligned the available sequences and "looked at all the ERVs known to be in the human genome." They then "checked to see if [each] site was 'empty' or 'full' in the aligned chimp sequence (R. Waterston, personal communication, April 22, 2010)." All those found to be non-orthologous were included in table 2. Again, they represent only a handful of tens of thousands. The researchers directly observed that the majority of ERVs in the human genome are in orthologous loci in the chimpanzee genome.

I disagree. As I explain in my essay, it is not just the sharing of ERVs that provide evidence of common ancestry:

. The problem with homology arguments is that the necessarily allow for the inverse logic. If sequence identify being similar or identical argues for common ancestry then differences are proof against.

That makes no sense to me since they are included here as LTRs, notice it includes ERVs class I, II, III and others.

Retroelements and the human genome: New perspectives on an old relation

That is not what you said, this is what you said:

When we examine the collective genome of Homo sapiens, we find that a portion of it consists of ERVs (IHGS Consortium, 2001). We also find that humans share most of them with Chimpanzees

We find that we share 'most of them' and yet the most abundant ERVs in the Chimpanzee genome are absent in ours.

Feel free to email the authors and while your at it maybe you want to email the Chimpanzee Genome Consortium.

[The CSA consortium] also include Class I ERVs indicating the chimpanzee genome contains 234 (>1MB) while the human genome contains 5 (8 KB).

The findings of the Chimpanzee Genome Consortium are consistent with Polavarapu et al who wrote their paper a year later. What these findings are not consistent with is your statement that most of the human ERVs are found in the chimpanzee genome.

You made a statement that turns out to be fundamentally wrong, I would like some justification for not qualifying the statement and now dismissing the evidence.

That's not what they say, in fact, they don't mention the orthologous ERVS much at all.

What is more important is that ERVs represent something like 7% of the known divergence and they only occur in 1 live human birth out of a hundred. You are not just looking at an invasion of ERVs since the split, your are looking at major germline reconstruction and inundation. This is remarkably strange to me since we would have lived in the same geologic area (equatorial Africa) until about a million years ago, some estimates indicate a mass migration from that region about 40,000 years ago.

Here's the problem, ERVs are nearly extinct in the human genome with only a few that actually work. The problem with homology arguments is that the necessarily allow for the inverse logic. If sequence identify being similar or identical argues for common ancestry then differences are proof against.

Transposable elements in 'Retroelements and the human genome' make up 45% of the human genome, retroelements make up 42% and LTRs including ERVs primarily make up 8%. What I would like to know is as a ratio what percentage of those have been inserted since the split, not only human but chimpanzee sequences. I am constantly fielding statements like this that don't stand up to close scrutiny. What percentage do CERV1/PtERV1 represent as compared to HERVs? More importantly, how do you determine that?

You lost me, it is specifically the commonality of human and chimpanzee ERVs that you claim as proof of common ancestry. You have made some pretty impressive statements, now I am going to need to know where the direct comparisons are.

What is more the dating of the ERVs create a problem since it makes no sense.

In fact CERV 2 (Chimpanzee ERV) has an estimated age of 21.9 mya to 14.1 mya with no human orthologues. The CERV1/PtERV1 with 100 members is estimated between 5 mya and 7.8 mya. That means that the most abundant ERVs in the Chimpanzee Genome came about before or right around the split That means in addition to the adaptive evolution of the human brain our ancestors would have had to adapt their immune system to push these ERVs to the brink of extinction.

So ERVs make up 8% of the human genome, do you seriously expect me to believe that they resulted from germline invasions? If this were the case then ERVs would be the source of human diversity since they would have to be happening on a staggering scale and rapid pace.

I don't know why you don't see a problem here but one thing is clear to me, this is just another homology argument that can't stand up to close scrutiny.