Monday, 11 January 2016

YECs and OECs show why special creationists cannot answer the ERV evidence for evolution

I make no secret of the fact that I regard the presence of identical endogenous retroviral elements at the same place in human and ape genomes as the most powerful evidence for human-ape common ancestry.

The evidence for this is unassailable; they are unarguable evidence for large numbers of ancient retroviral infections which integrated into the host DNA ages ago, and as the odds of the same retroviruses integrating into exactly the same places in both human and ape genomes is billions to one against, the only rational explanation for these are infections of human-ape common ancestors by retroviruses which became integrated into the genome, and were subsequently inherited by both humans and apes.

Special creationists are desperate to explain away this evidence but have failed miserably. This however does not stop them trying to hand-wave away the facts, with Reasons to Believe for the OECs, and both Todd Wood and Answers in Genesis attempting to offer special creationist explanations. However, as Barry Desborough shows, their explanations are at best unconvincing, and at worst intellectually dishonest.

The YEC argument is laughably bad as it is shows why fundamentalist presuppositions poison science. A 2009 AiG paper that claims ERVs were created as part of the genome, and assisted in regulation, coding, and repair, with retroviruses deriving from ERV elements, rather than the other way round, with the Fall resulting in ERV degradation by mutation. The YEC Todd Wood, who has previously shown himself to be one of the few intellectually honest YECs takes exception with this:
"Since the human and chimp genomes are very similar, the majority of ERVs are the same and have the same apparent "disabling mutations." Given the separate origins of humans and chimps (Genesis 2:7), we've either experienced thousands and thousands of mutations that are exactly the same as chimps or those "mutations" were created that way in the beginning. Since creation is the simpler hypothesis, that means the apparent degeneration of human and chimp ERVs is precisely that: apparent. Like ERVs themselves, the "disabling mutations" were also put there for a reason."
AiG assert that the mutations in the ERV elements are real, whereas Wood claims that the degeneration of human and chimpanzee ERV elements is apparent. In both cases, their dogmatic rejection of the possibility of human-ape common ancestry because of their hyper-literal fundamentalist distortion of the creation narratives has forced them to ignore the obvious conclusion, and postulate ludicrous explanations to explain away the obvious. As Desborough points out:
So - either chimps and humans are unrelated, their ERVs are degraded, and the common mutations are a colossal coincidence (Liu and Soper) or chimps and humans are unrelated, and their ERVs are not degraded. (Wood). Yet there is massive evidence that ERVs are degraded - evidence that Liu and Soper themselves go into in detail. Perhaps the error that both parties make is the assumption that they both take. What was it now? Yes, that was it: "Chimps and humans are unrelated."
This is not science. One follows evidence to where the conclusion leads. Here, the YECs have assumed a priori that humans and apes simply cannot share common ancestry, and even when the evidence positively shouts common descent, they disallow this conclusion, and postulate ludicrous explanations to explain away this fact

While YECs are fond of claiming that the problem comes from competing world views through which the evidence is viewed, a far more accurate analogy comes from Greek mythology, namely the bed of Procrustes, a bandit who captured and tortured people by forcing them to fit an iron bed, either by stretching or amputation. In this case, the YECs are torturing the data either by ignoring or distorting them in order to make them comply to a predetermined conclusion, namely separate creation. As Desborough ably points out, the distortion required to avoid the obvious can be profound.

Moving on to the OECs, Desborough comments on  a Reasons to Believe article critiquing a 2006 lecture by the respected cell biologist and cancer researcher Graeme Finlay which made much of the 'presupposition / assumption' argument. However, as Desborough notes, the RtB author ended up hand-waving away solid inference as 'assumption' while making a number of egregiously bad assumptions herself.
Dr. Finlay took this well-established fact of clonal expansion and applied it to comparative analyses of chromosomal sequences of humans and NHPs. The chromosomes of all hominids are riddled with sequences known as endogenous retroviral (ERV) elements. About 8 percent of the human chromosome is composed of ERV sequences of unknown etiology (origin). ERVs are so named because they share sequence homology and other characteristics with known retroviruses.
However, as Desborough points out, the RtB author has made a completely outrageous assertion by claiming that ERVs are of unknown origin. This is false. ERVs are the remnants of ancient retroviral infection - structural similarity between ERVs and retroviruses,   codon bias of ERVs and the fact that real-time endogenisation of retroviruses has been observed are enough to make the case.  A mistake of this magnitude is enough to sink the credibility of the RtB  article. 

The RtB article in fact is factually inaccurate at points - which given that the author is a molecular biologist who has had experience in virology shows just how dogma can trump scientific training:
Virus replication is known to be restricted on one level by the types of cells any given virus can infect. This restriction is often mediated at the level of viral entry into the cell by protein receptors on the cell surface. Human retroviruses are known to infect somatic cells, primarily of hematopoietic origin, not gametes or gametic precursors. Gametic cell-types apparently lack the appropriate receptors for viral entry. 
Desborough is justifiably scathing in his response to this comment:
Retroviral replication is known to be highly error-prone. Mutations are not subject to any correction processes. The hugely parallel replication process will throw up large numbers of mutants - mutants that can cross over to different species, let alone different cell types within a species. The assertion that "gametic cell-types apparently lack the appropriate receptors for viral entry" is, I am sorry to say a *cough* presupposition. In fact, we know it is a false presupposition. It takes just one observation to falsify it. KoRV. Not only is there evidence that it has crossed over from another species, but there are exogenous and endogenous versions of it. How is it supposed to have entered the germ-line other than by endogenization?
How is it justifiable to call conclusions based on this sort of evidence and reasoning "presuppositions"?
Things only get worse with the RtB article, where the author gives two examples where the pattern of distribution of ERVs in great apes is apparently not consistent with common descent, and claims that divergences between LTR sequences at a site shared by multiple species can vary, implying different insertion times. In the first case, the author ignores the fact that incomplete lineage sorting readily explains this phenomenon, while the second case is an example of independent insertion events, so is irrelevant to the discussion of common descent. As for her third case, as Desborough notes:
Re. differing LTR divergence between orthologous pairs of LTRs, Roberts does not provide a reference, but differing fitness contributions and therefore differing purifying selection levels could well account for it. Age estimates are based on surveys of large numbers of data. Cherry picking individual outliers is inaccurate, and if it is done deliberately, it is dishonest.
Besides, as the seminal paper by Johnson and Coffin that examined the utility of using LTRs as a means of constructing robust primate phylogenies points out, "[e]xcept where noted, these sequences gave trees that were consistent with the well established phylogeny of the old world primates, including OWMs, apes, and humans." [1] It is very much cherry picking to focus on one example and extrapolate from it. Given that the LTR data allows us to construct phylogenetic trees consistent with the consensus tree, at most, the example cited by RtB is an anomaly, rather than a devastating refutation of the utility of ERV elements to demonstrate common descent.

It is surprising that the RtB author did not provide a link to the article providing the basis for her claims given the ease with which a simple search found the source, a 2015 Retrovirology article by Macfarlane and Badge. Interestingly, the authors have a view of ERVs which differs considerably fro that of the RtB author, Anjeanette Roberts. She claimed that ERVs are of unknown origin. Macfarlane and Badge however point out that:
Endogenous retroviruses (ERVs) are relics of exogenous retroviral infections of germ cells that result in integration of proviral DNA into the host genome. Throughout primate evolution HERV families have integrated into germline DNA and subsequently been vertically transmitted as Mendelian traits. Proviral insertions may be subject to host selection or be selectively neutral; in either case they will ultimately be fixed or lost from the population, such that presence/absence polymorphism is usually transient. 
This is of course the mainstream scientific position on the origin of ERVs, so Roberts is simply wrong to imply that ERV origin is unknown.

When one looks at her specific claim, it appears that the authors do not appear to share the RtB spin on their article:
The solo LTRs for the species specific loci K106, K109, 12q13 and Pan2Ap all grouped with their respective 5′ and 3′ proviral LTRs (Figure 4). This observation is consistent with the model that solo LTR formation, via homologous recombination between the LTRs of a provirus, occurs quickly after insertion. In striking contrast the ancient 1p31.1a insertion integrated into the common ancestor of human, chimpanzee and gorilla, but is dimorphic for a solo LTR and provirus within human (Figures 2 and 3) despite 8.5-12 million years of evolution. In addition the 1p31.1a solo LTR also grouped with the human 1p31.1a proviral LTRs, implying that it was recently generated, but the human 1p31.1a proviral LTRs cluster together instead of with their orthologs in chimpanzee (Figure 4). This pattern of similarity is suggestive of intra-LTR sequence exchange in one or both of the orthologous proviruses following species divergence. Similarly, the estimated divergence of the chimpanzee 1p31.1a proviral LTRs is 6.5 times greater than observed in human (Table 1), suggestive of sequence homogenisation between 1p31.1a proviral LTRs in the human lineage. (Emphasis mine)
It gets worse for RtB:
"Using LTR divergence as a measure of the relative provirus age we estimate that the chimpanzee ortholog inserted 7.87 (±2.78) mya. Due to LTR sequence homogenisation in recent human history, the human counterpart provided a much lower age estimate of 1.205 (±0.425) mya, showing that LTR divergence is not always a reliable indictor of proviral age." (Emphasis mine)
So we have the hypothesis of sequence homogenisation to explain the difference, and a reminder that at times LTR divergence will not be a slam-dunk means of estimating proviral integration age. This is reminiscent of the YEC approach of focusing on anomalous radiometric dates to damn the entire science of isotope geochemistry, ignoring the fact that the vast bulk of radiometric ages are reliable, and that anomalies serve to show limitations of specific radiometric dating methods in certain areas, rather than a blanket condemnation of the entire process. Furthermore, as the authors note: 
However, using LTR subgroup-specific variants, the human solo LTR of 1p31.1a (HML-2.LTR36) was calculated to have inserted 7.83 (±1.66) mya, congruent with our age estimate using LTR divergence in the chimpanzee provirus orthologue. Nevertheless, this age is slightly less than is expected based on molecular estimates of primate speciation dates. (Emphasis mine)
Interestingly, Roberts never referred to this fact which undermines the point she is making about the use of LTRs to date ERV integration events. Yet again, this shows that special creationists tend to misuse or misunderstand scientific papers when attempting to refute evolution. [3]


Despite what YECs and OECs assert, the evidence for common descent from the ERV data is overwhelming. To use a Biblical metaphor, they are a broken reed that will pierce the hand of those that lean on them for support.

Barry Desborough's website is definitely one that anyone seriously interested in evolution and creation should bookmark, just for its magisterial ERV section.


1. Johnson W.E., Coffin J.M. "Constructing primate phylogenies from ancient retrovirus sequences" Proc. Natl. Acad. Sci. USA (1999) 96:10254-10260 
2. Macfarlane C.M., Badge R.M. "Genome-wide amplification of proviral sequences reveals new polymorphic HERV-K(HML-2) proviruses in humans and chimpanzees that are absent from genome assemblies." Retrovirology 2015, 12:35 
3. Reasons to Believe has form not just on this point, but on endogenous retroviruses. Catherine Dunn notes how RtB misused one of her papers to provide evidence for their 'Creation Model' despite the fact that it provides evidence for common descent. RtB to their credit removed the reference to her paper after she contacted them, but if RtB so completely misunderstood a paper that provided evidence for common descent as one that provided support for their creation model, it suggests strongly that their ability to competently and honestly handle the biological evidence is vestigial at best.