If ERVs are designed, what are the design purposes of these features?

I asked a series of questions on various discussion groups, asking what, if endogenous retroviruses (ERVs) were designed by some intelligent or unnatural agent (or intelligent and unnatural agent), was the design purpose of various aspects of ERVs. An unidentified friend of a member of one of these groups endeavoured to respond to my questions when they were relayed to him. I reproduce my questions and the friend's responses here, and I reply to each of the friend's responses. My questions and replies in red. His responses to the original questions in black.

In general, the answers are either bizarre, miss the point, or cite odd isolated instances of function documented by mainstream science that have not caused anyone working in the field to question the conclusion that ERVs are derived, by inheritance, from retroviral integrations with ancestral germ-line DNA.

The questions were originally numbered, but the friend listed their references (1 - 6) numerically, so I have assigned a letter to each of the original questions. My references are numbered 7 - 10. We begin with question a).

Update. My correspondent, identifiable only as a friend of a Facebook acquaintance, and now the possessor of the Facebook account, "Flambeau Flambeaux" has published comebacks to my responses to his answers on Dropbox at ERV-Questions-and-Answers.pdf. I have copied the comebacks into the relevant sections here and I have added my comments. References he makes in this second round are given separately below. Flambeau also made some comments for the comments section. I shall include those when time allows. But we start with his second-round preamble and my reply to it.

Preamble: I worked in the field of bioinformatics and contributed to the field. The evidence makes me question many ERV’s being derived, by inheritance, from retroviral integrations with ancestral germ-line DNA. Therefore it is wrong to say anyone working in the field has not questioned this mechanism.


Reply to preamble: All good scientists question everything. But what I was saying is that I know of nobody working in the field who seriously doubts that ERVs are the result of endogenizaton. That is still the case, because I don't know who Flambeau is, and what his or her contributions were. However, many intelligent, qualified and experienced people also believe in very unusual things, so it's possible. By the way, there is no need to use scare quotes around my first name. I am who I say I am. Here is my Facebook page, where you can find a lot about me. I'm a retired teacher and software engineer - not a qualified in this field, but I have done my best to learn about it. To me, it is the clearest evidence for common descent, and if nothing else, discussing it with people who doubt evolution at least relieves scientists from having to do so so that they are free to concentrate on their proper work.

A note about the scientific method: In science, we create hypotheses as candidate explanations of our observations. In a sense, all the repeatable observations that we make are potential falsifiability tests of our hypotheses. "Does this new data fit with our explanation or not?" If the new data means that our hypothesis no longer makes sense, then the hypothesis needs replacement or fixing. But there is an insurmountable problem with a design hypothesis that claims that the data, whatever it is, can be "explained" by design, even if we don't always know what the design purpose was! This is why my questions are about design purpose, not mere functionality. I find the sentence below, "This is not how the repeatable, testable, scientific method works", deeply ironic, coming as it does from someone who apparently advocates design as a hypothesis.

a) What is reverse transcriptase designed to do?

It has been shown to be a prognostic breast cancer marker (1) It can also be used like an alarm system for viruses if ERVK reverse transcriptase genes are increased then most likely their need is increased and therefore a virus may be present.(2, 3) And lets not forget… this is awefully similar to well known non-viral cellular reverse transcriptase telomerase to help telomere repair. Its not as foreign as one might think.

Re. your reference (1): So HERV-K reverse transcriptase has been lying there, undiscovered up until 2008, just waiting to provide us with a signal of breast cancer? All reverse transcriptases, or just some? Different ones for different diseases, perhaps? Do they actually cause these cancers, or are they just correlates of oncogenic HERV components? From the abstract: "These results imply that HERV-K-T47D-RT might be expressed in early malignancy and might serve as a novel prognostic marker for breast cancer. Furthermore, these results provide evidence for the possible involvement of endogenous retrovirus in human breast carcinoma.”

(2, 3) Superinfection interference is a phenomenon known to occur with exogenous retroviruses (involving env genes, not RT). See (6). This is actually another item of evidence that ERVs descend from proviruses.

Regarding telomerase reverse transcriptase, it may not be as native as you might think. See (7).


'Barry’ appears to acknowledge reverse transcriptase could be a prognostic breast cancer marker and is wrong about RT and superinfection. He asks further questions about the prognostic marker, and yes, it could very well possibly be an onco or protoncogene, which most genes that are associated with growth and replication are. It being a possible cancer causing gene is not necessarily mutually exclusive from it being a marker, as we all know, it takes more than one mutation to cause cancer. 

If he saying superinfection interference does not involve RT(or pol genes), this is factually incorrect, see Moelling et. al. 2015.(1) Of course it would make sense for innate RT’s to play their part in viral defense, if the virus is converted to an inert silenced form (Silencing RNA and DNA molecules) this would potentially render the virus inactive. “We have noticed a surprising homology between the siRNA silencing system and the interferon response, as well as to siDNA... ERVs can serve in defense, in addition to having roles in gene regulation and cancer.”(1) They go on to further explain other possible mechanism that RT go about silencing viruses “The infidelity of the RT during reverse transcription, leading to one mutation per 1000 nucleotides, is a major driving force for change”(1) They further clarify it “RTs expressed from the many ERVs and shorter retrotranscribing TEs likely play a role in illegitimate reverse transcription of incoming viral RNAs.”(1) It is this illegitimate reverse transcription that may aid human defense. Even Gag genes have been identified in fighting off viruses.(1)

In the “evolutionary relationships” section of the article ‘Barry’posted, the evidence for why telomerase reverse transcriptase is not native is that they did a phylogenetic analysis, looked at it compared to something similar in drosophila,(2) another article says the telomerases in yeast “closely resemble the reverse transcriptases”,(3) another that suggests its widely conserved (4) etc etc. Basically the evidence in a nutshell is that they look similar to that of other species therefore they must be inherited. This is not how the repeatable, testable, scientific method works. The best someone could get away with is to hypothesise that theory. However, you cannot conclude this is a fact.

The use of a HERV-K reverse transcriptase as a prognostic marker for breast cancer is a perfect example for illustrating the distinction between something that just happens to have a useful function, and something that has been designed to perform a function.

Re superinfection interference, the paper referred to is behind a paywall, and some readers may not have access to it. It is best to quote the relevant section in full.

"Assuming that the RNA world preceded the DNA world, one may ask whether the abundant DNA phages or any other DNA viruses had RNA-or retro-precedents in ancient times. Only a few such transition-state viruses are known, such as a retrophage in Bordetella pertussis bacteria. This retrophage is a temperate phage that expresses an RT the infidelity of which has a mutagenic effect on a bacterial receptor gene that determines phage tropism. At least 36 types of such retro phages may exist. The infidelity of the RT during reverse transcription, leading to one mutation per 1000 nucleotides, is a major driving force for change of bacterial tropism. This example demonstrates the contribution of the mutagenic RT to genetic diversity and genomic variations. 

Apart from such a retrophage, there is an example of a retroviroid described in carnation plants. These flowers contain a small viroid-like RNA (CarSV) and its homologous DNA generated by an RT. Thus, this virus combines a viroid with an RT, presumably originating from a pararetrovirus of plants.25 Another interesting combination of a viroid with a retrovirus is known in a human disease caused by the hepatitis D virus (HDV), whereby HBV acts as helper virus for the ribozyme/viroid HDV RNA for packaging and infectivity.26 

RTs expressed from the many ERVs and shorter retrotranscribing TEs likely play a role in illegitimate reverse transcription of incoming viral RNAs. Indeed, integrated viruses from ten non-retroviral families have been described to be integrated as DNA in host genomes, including RNA viruses such as borna and Ebola-related viruses, and even tripartite circular RNA–containing bunyaviruses such as hantavirus.27 Endogenous bornavirus sequences may protect humans from infection. In contrast, horses, which lack endogenous bornaviruses, more frequently develop Borna disease, which includes symptoms of depression." (1)

(My emphases.)

So the RT being discussed is one, not from an endogenous retrovirus in an multicellular organism (the context of this discussion), but one of the few known retrophages, whose mutation rate drives the evolution of bacterial trophism. It is well known that reverse transcription by exogenous or endogenous RT is error-prone. Endogenization remains the parsimonious account. Endogenous RT is error prone because it's origin is in exogenous RT, which is also error-prone. This is not an answer to why all the RT-containing endogenous retroviruses in the likes of chimps and humans should have reverse transcriptase designed into them. 

I don't know what the design function of RT in hepatitis D would be. It seems the the design brief is both to cause disease, and protect from disease...

"Illegitimate reverse transcription" is undefined, (reverse transcription is reverse transcription is reverse transcription) and the speculation that (non retroviral) reverse transcriptase could play a role in protection from (non retroviral) diseases is just that - speculation. We must bear that in mind when my correspondent says, in his/her very next paragraph that, "This is not how the repeatable, testable,scientific method works. The best someone could get away with is to hypothesise that theory". And why design bornavirus in the first place, endowing humans with a degree of protection against it in their genomes, and not horses? What did horses do? Even if Moelling et. al.'s speculations are correct, that an endogenous variant of bornavirus RT protects against exogenous bornavirus, what is the point, the design aim, of inducing depression in horses? Far more parsimonious to propose that bornavirus just happened to endogenize in the human lineage, but not in the equine one.
Let us pause and think. There are two possibilities.

i) ERVs are designed, in part at least, to resist retroviral infection, using the very same genetic components that all retroviruses use, both for replication and for superinfection resistance themselves - components either designed, coincidentally, to be the same as retroviral ones, or being the same because the original sources of retroviruses were ERVs. 

ii) ERVs are endogenized retroviral proviruses, using exactly the same superinfection resistance mechanisms as proviruses integrated into somatic cells because they have the same source - exogenous retroviruses.

As to those who believe that ERVs were designed to generate retroviruses as a means of genetic engineering: retroviruses using integrase are an extremely poor choice of vector, integrase being pretty indiscriminate in choice of integration locus. And why should an intelligent designer design defences in ERVs to resist infection by the very things they were designed to produce?Regarding telomerase reverse transcriptase, it was Flambeau who first brought it up. I brought up the (strong) possibility that it has common origins with other reverse transcriptase. The data supports the idea. It is definitely inherited. Whether or not it is inherited in common is an interesting question, but it is beyond the scope of the current discussion. Certainly, the idea that it is designed is pure speculation. This is not how the repeatable, testable, scientific method works.

b) What is integrase designed to do? 

This can fix “double-stranded oligonucleotide as a substrate mimicking viral long terminal repeats (LTR)”(4) together with DNA. The study points out, viral integrases were only able to be used on themselves: “whereas Rous sarcoma virus and human immunodeficiency virus type 1 integrases were active only on their corresponding LTR substrates”. It goes on to say “The results strongly suggest that K1O encodes a functional integrase with relaxed substrate specificity.”(4) The part that says “relaxed substrate specificity” is very important, because unless the evolutionary biologist tries to argue that the relaxed specificity happened due to mutations, you have an integrase capable of fixing long terminal repeats, which is handy because the grandfather gene P53 is usually responsible for fixing the DNA, and it is good to have redundancy, especially if P53 gets mutated, which is what happens in cancer.

So an integrase extracted from HERV-K10 was shown to "fix" LTRs in highly artificial conditions, in vitro, so it can "fix" anything and therefore all endogenous integrases are there to fix things? References?

A by-product of the action of integrase is a repetition of a short section of original DNA at the integration site. I wonder what this little detail is for if ERVs were not themselves originally integrated by integrase?

In pharmacology, now my field of expertise, proof of concept experiments are used to test if the drug worked; in vitro; before 'phase 0 clinical trials’; before it is tested in humans. Even if there was no other evidence for it working in vivo, there is more evidence that it’s a possibility than not. I would say its strong evidence, and answers the question directly. Of course if you look through the literature yourself, you can find many other uses for integrase, whereby it may play a role with other proteins by possible physical interactions like that with RNA Polymerase III “Integrase interacts with RNA Polymerase III specific subcomplexes to promote insertion of Ty1 elements upstream”, in vivo and in vitro(5) RT “integrase interacted with RT ”(6) the list goes on, I recommend to look it up for yourselves.


(5) What is the design purpose of these TY1 element insertions?

(6) Characterizes the requirement of integrase for the reverse transcription of HIV-1 - not an endogenous retrovirus. It's function is clearly to enable the replication cycle of HIV-1.

There is no design hypothesis here for endogenous integrase.

c) Why were ERVs designed with a viral codon bias? 

As I have already pointed out in a previous answer a few weeks ago, when they tried to resurrect the phoenix virus the “viral codon bias” showed it could not have correctly folded proteins even when the researchers tried to fix all known DNA mutations. Instead the best they did was just replace large sequences with known functioning DNA. Therefore I would argue, it’s not actually viral codon bias. 

This is no explanation for the viral codon bias. There is no mention of protein folding or the replacement of "large sequences with known functioning DNA" in the "Phoenix" paper (8). The nearest to this is the replacement of the promoter. "As the HERV-K(HML2) LTRs are not functional in every cell line (Ruda et al. 2004; Lavie et al. 2005), we also replaced the U3 part of the 5′ LTR by the CMV promoter, with its start site positioned so as to conserve the expected nucleotide sequence of the native retroviral transcript." Given your wild speculation based on a highly artificial setup in your answer to b), I think I can claim double standards on your part.

The obvious explanation for the viral codon bias in ERVs is that they are inherited from proviruses.

The question itself assumes there is a viral codon bias. I think we can show there is not a viral codon bias by looking at the editing they did to form the phoenix virus. Let’s go through Barry’s paper’s methodology:(7)

The changes they made to the HERV-K sequence: the total assembled consensus, provirus copies, that were human specific was 9.4kb(7) (a difference of 62-1649nt to the source sequences [0.65-17.5% total change–see the length of the sequence: ‘AC025420’ compared to 9.4kb]), the researchers excluded the sequences with 292-nt human specific consensus copies deleted at the beginning of the env gene (3% of the whole sequence).(7) One of the most interesting changes is that they introduced a part of a functioning virus, the cytomegalovirus. Interestingly, the reason they did this was:“When assaying the different 5′ LTRs in the Tera-1 cell line, we found that all but one 5′ LTRs were transcriptionally active, with activities ranging from 18.34 to 4.25% relative to the activity of a luciferase control vector for which expression was driven by a strong CMV promoter.”(8) CMV promoter is 567nt.(9)(6% of the whole sequence) The “provirus” HERV-K isn’t separated by one frameshift in the genome... but they did that so it would make a functioning virus (which would include a number of unknown “indel” [frameshift insertions or deletions] changes, x% of the total sequence). Moreover, look at the wording of this part of the article, “Noteworthy, this consensus provirus is distinct from each of the sequences used to generate it, with at least 20 amino acid changes on the overall sequences.”(7) This means there were definitely more than 20 amino acid changes, (at least 20) how deceptive. And why talk in terms of amino acid changes when your figure is in nucleotides/RNA? Well..the answer is because it looks better. We can quickly convert this to say there were at least 60nt changes in the exons overall, definitely more though if they were honest. The most honest they could have been was to say, the changes were somewhere between 60-~593nt (593nt: the difference between consensus and source, disregarding possible mutational difference within the two sequences, which could change this number to >593nt potentially ~1000nt) changes depending on which source sequence you compare the consensus to [approximately 0.63-6.3% of the overall sequence changed]). Take a closer look at the source sequences used to find the most frequent nucleotides at each position... K104 5p13.3, 30496205-30487114bp, K108 7p22.1a 4622057-4631528bp, K109 6q14.1 78427019-78436083bp, K113 19p12b 21841536-21841542bp, K115 8p23.1a 7355397-7364859bp, AC025420 12q 58683749-58694798bp, AP000776 11q 191266bp, Y17833 HERK q19 8807bp(10, 11) (assembled from human chromosomes 5, 7, 6 , 19, 8, 11, and 12).(7) WHY DIFFERENT CHROMOSOMES? The evolutionary biologist would tell you it was to repair the damaged sequences which occurred over time. However this is preposterous! Unless that same evolutionary biologist can show that each of these HERV sources was from the original exogenous virus, this makes no sense. This is the biggest flaw in the ERV line of evidence so far. It was not from one part of the DNA they found many open reading frames, it was a Frankenstein attempt to create a virus out of human DNA by picking bits and pieces from various different chromosomes to create a virus that would function. YET! Why do you think they didn’t include other members of the HERV-K family? Was it simply too much work for them... or do you think they only picked the parts of the HERV-K family that would most likely make a virus? They missed out: HERV-K102, K18, K2, K101, K111 etc etc. Now by no means was this experiment useless, in fact I believe this experiment is vital to targeting viral proteins and using drugs to fight off viruses like HIV. I congratulate the researchers on their hard work. 

Even if the evolutionary biologist claims that the HERV sequences from all over the genome, in different chromosomes was once the fabled initial ancient exogenous virus. This is unfortunate since the literature says: “All of ‘these’ proviruses are known to be unique to humans, indicating integration into the germ-line within the last 6 million y, when the human lineage is believed to have diverged from the chimpanzee lineage”(12) and “HERV-K(HML-2), may have replicated in human ancestors less than 1 million years ago”(12) referring to the ancient virus which is trying to be resurrected as the phoenix virus.The preferable and testable theory is that it is homologous recombination causing what is observed. Admittedly I concede there is no mention of protein folding in your paper, I must have used my memory of a paper I previously read:“Reconstitution of an Infectious Human Endogenous Retrovirus” by Lee et. al. 2007. They used the HERV-K(HML-2)genes, and they admitted their first attempt failed because after they fixed up what they thought were the right deletions, mutations etc, the proteins didn’t fold properly and were functionless.(13 )Moreover, I might actually be right that there would have been protein folding problems with the phoenix virus, if they left in the sequences which had “deletions” before the env gene, this would have possibly caused protein folding problems.

The above comments do not address the matter of codon usage bias. Phoenix is discussed below.

Here's a very funny discussion on viral codon usage bias at Science Blogs - ERV.

d) What is the design purpose of re-transcribable promoters? 

I would need more specifics on this question. If he is talking about small promoters.. than obviously probability would tell you these promoters are very possible:TATATAA sequences or ATATTA etc… As for what their design could be? The science says it. “A total of 114 of the ERV-derived transcription start sites can be demonstrated to drive transcription of 97 human genes, producing chimeric transcripts that are initiated within ERV long terminal repeat (LTR) sequences and read-through into known gene sequences.” (5) This basically means it is a form of a catalyst to increase the frequency of those 97 humans genes worth promoting.

This is a non-answer. Retroviruses form LTRs as part of their proviruses, which act as powerful promoters for proviral genes (they also often promote "native" genes too). These cause native RNA polymerase II to transcribe the retroviral genes. The problem, from the point of view of the retrovirus, is that the polymerase does not normally transcribe promoters, but the retrovirus needs a way of preserving the promoter-forming potential through the RNA part of the replication cycle. This is accomplished by the special structure of the LTRs themselves. Endogenous retroviral promoters have no need to be re-transcribed if they are original design features. They make no sense as designed features, only as features resulting from endogenization.

If my probability answer wasn’t sufficient for you, and the fact they can drive transcription of at least 97 human genes(14) isn’t enough, another answer is it gives that part of the genome a way to escape epigenetic changes. When the DNA is transcribed to RNA and then reversed back to DNA to be later transcribed, it may lose its epigenetic changes which can happen over generations. This may preserve the sequence, or at least “Reversing Epigenetic Repression”(15). This may also be a reason for why it is such a well conserved piece of sequence. Barry sounds like he is referring to late phase transcription for late viral proteins. If this is the case, I would need examples of this. I don’t believe this actually happens in ERV’s. –see my image I sent to you for an explanation of late phase transcription of late viral proteins, edited out the figure legend for anonymity purposes. -Figure 1 (a diagram for this particular mechanism which I illustrated for educational presentations [the obvious difference is this virus has DNA not RNA]). LTR’s accumulate due to the results of reverse transcriptase actions (16) I wouldn’t (nor could I) extrapolate that to say this therefore must be a virus.

Drop a promoter anywhere in a genome, there is a good chance it will promote the transcription of something. A design hypothesis is hardly needed to explain this. The same with epigenetic resetting. But maybe my question wasn't well framed. The issue is, how do retroviruses ensure that LTR promoters are produced during retrotranscription in a way that the ability to reproduce them is preserved through transcription and retrotranscription? (Link to page from University of South Carolina School of Medicine). If ERVs are not of retroviral origin, why do endogenous LTR promoters exhibit the same structure as retroviral LTRs, according to the design hypothesis? Why are they different to native promoters?

e) What were the HERVs that generated the consensus sequence that generated Phoenix designed for? 

As we have discussed in my posts today and a few weeks ago, the consensus sequences have many function other than that of viral endogenisation.

There is no HERV-K "consensus sequence" in the genome. The consensus sequence generated by Dewannieux et. al. (8) is a fully functional provirus.

We already established the genes that make up the consensus sequence were derived from the HERV of which, we have identified functions which a designer could use to benefit the organism. –See Question B, etc. I wouldn’t call it a ‘provirus’, it might give people the wrong impression. I would call it a synthetic virus. –See Question C on why the Phoenix virus is highly artificial:differences in sequence size (0.65-17.5%), assembled from human chromosomes 5, 7, 6, 19, 8, 11, and 12. With exclusions of the sequences with deletions of 292ntat the start of the env gene (3% of the total sequence), they aligned and separated the genes by one frameshift, which is not seen in the human chromosome, most likely came with an unknown number of deletions (x% of the total sequence), added the CMV promoter 567nt(6% of the whole sequence)(9), the authors said the exons had at least 20aa changes, also known as, somewhere between 60-~593nt (or more) changes (0.63-6.3%), this adds up to at least 10.28-32.8% change from the original chromosomal sequences, plus an unknown x% for frameshift alignment-see Question C. I have contacted the authors of the paper to find out more details of the experiment and I will share them here if they are willing to present them. Hopefully to fill in the ‘x’% etc.

I would be most interested to see any response from the authors. Flambeau takes all his details from their paper, so the insinuation of dishonesty appears to be grandstanding on his part. The endogenization hypothesis has it that very similar ERVs are either the result or amplification of the same provirus or derive from very closely related retroviruses. The hypothesis also includes the notion that they may be divergent due to insertions, deletions, and associated frameshifts. And to the question, "WHY DIFFERENT CHROMOSOMES?", the answer would be, "If these structures are endogenized, why on earth not?" The endogenization hypothesis says that retroviruses can endogenize virtually anywhere in nuclear DNA. Are these hypotheticals reasonable? Of course. Are they vindicated? Well, It appears so. Flambeau has failed to explain why a set of perfectly reasonable (according to the endogenization hypothesis) procedures actually produced a replication-competent retrovirus. 

f) What is the design purpose of both exogenous and endogenous KoRV? 

My answer would be the same as the evolutionary biologists: to spread variability and diversity, but I would add, for the negative effects it is another example of the consequences for living in a fallen world.

There are much better ways to spread variability and diversity than by using the cumbersome, scattergun approach of retroviruses integrating error-prone reverse transcriptase products all over the genome with the most common result being oncogenesis (9), especially for an omni-everything supernatural designer. Regarding the "fall", an "explanation" absent of evidence is no explanation at all.

KoRV is not part of any original koala genome "design" It is not present in certain populations of koalas, and it closely resembles the gibbon ape leukemia virus. The parsimonious explanation is that KoRV is in the process of endogenization in koalas.

There are much better ways to spread variability and diversity, for example, the best technique thus far is recombination. However, a combination of all events would be the best way to spread diversity, therefore, attacking the KORV’s usefulness out of context, should fall on deaf ears, especially when most evolutionary biologists agree with me that indeed this is one of their purposes: “Retroviruses facilitate the rapid evolution”.(17) Once again, it’s misleading to present information about the “most common result being oncogenesis” when, historically, the majority of the research was focused on how junk DNA can cause disease. The literature: “there is an unfortunate tendency for researchers and science writers to proclaim the demise of junk DNA”(18) and other studies suggest ERV’s should no longer be considered junk DNA.(19) Your answer: “The parsimonious explanation is that KoRV is in the process of endogenization in koalas” and my own answer, are not mutually exclusive. Therefore our answers are both valid a combination of both would be most accurate, not only may they be in the process of endogenization, but their purpose is to spread variability and diversity.(17)

Time for a reminder that functionality is not necessarily indicative of design. An intelligent, omni-everything designer would not need to use such haphazard and often destructive methods. Read my page again. There is no way in which endogenous KoRV could be an original part of the koala genome. Endogenous KoRV is absent in some koala populations, and where it is endogenous, it is endogenous in a wide variety of loci. And it causes cancers. It may increase genetic diversity, or it may drive koalas to extinction. That it is mutagenic does not imply that it was intelligently designed to be so. And if it was the exogenous form that was designed, then we are right back to square one, in which commonly located endogenized reroviruses are a slam-dunk case for relatedness.

And one more word about the supposedly "fallen" world. This is what makes this design position non-science. If it works, it's designed. (There is never any further justification of this). And if it doesn't work, it is because of "Adam" and his "sin". In this way, it doesn't matter what reality looks like. It's heads I win, tails you lose. The trouble is that it goes absolutely nowhere in explaining why things are as they are, and not some other way. It has no explanatory power whatsoever.

g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations? 

Easy, if they didn’t share common disabling mutations, you wouldn’t get the unique mammalian ERV benefits I have mentioned today and a few weeks ago. Additionally, to address the point of why they are in similar locations (but not exactly the same location) the science says that for certain genes to have “x” gene activity/transcription frequency they need to be at certain locations. Promoters and enhances are likely to be just at the right number on those particular chromosome. This also makes me want to go into genetic crossover, recombination and many other things which can happen, because the further genes are from the loci the greater chance that they will be separated by a crossover. 

If the components of ERVs that are adaptive for the host require mutations, then that supports endogenization over design. We are not talking about "similar" locations, but precisely corresponding locations, down to single base-pair resolution. Promoters and enhancers do indeed need to be in certain locations relative to the genes that that they regulate, but the whole package, regulators + regulatees may be placed anywhere. The requirement of functionality is not a reason for these genetic complexes to be in precisely corresponding locations in different species. Syncytins provide the falsification of this particular notion. They are present in completely different locations, even different chromosomes in different lineages. See (10).

If the components of ERV’s that are adaptive for the host require mutations, I would agree that this supports endogenization. However, of course I don’t actually believe ‘common disabling mutations’ exist in the frequency reported by the literature [I should have put inverted comma’s for the phrase to avoid confusion]. I would argue these ‘common disabling mutations’ and other polymorphisms were not mutations and were simply original design features. Not all, but some. To present phylogenetic diagrams, as some evolutionary biologist do, that show the differences between ERVs in species, isn’t evidence that the ERV was inherited by evolution through natural selection from ‘ancestral’ species. Of course the ERV location is down to the base pair, all genetic locations are either chromosome or base pair resolution. However, as seen below, they are not in the exact same place, they are in similar places:the chimpanzee ERV-K (CERV-K):NW_001229127, it is 13136186:13151505it corresponds to NC_018912.2 homo sapiens (Chromosome 1) 13150809-13136882a change in 5’ end of ~600nt and a change in 3’ end of 700nt (and this is our closest ‘cousin’). The list of ERV searches could go on and on. You can find this information yourself by using the U.S Department of Health and Human Services National Institute of Health, Basic Local Alignment Search Tool.(20) Obviously I cannot do a BLAST of phoenix ERV’s because they are not located in chimpanzees (human specific). The requirement of functionality is not a reason for these genes to be in precisely the same locations, I agree 100%. However, there is much more at stake than the function of the gene. “The relationship between the function of a segment of genomic DNA and its chromosomal position is an important focus”.(21) There are plenty of studies that will discuss the importance of “how gene expression is affected by changes in its chromosomal position or sequence context”.(22) It is disingenuous for someone to say that the genes which are at similar locationsis more evidence for ERV’s. It tries to spin a mistruth that genes would share equivalent activity potentially anywhere on the chromosome and on any chromosome and maintain functional and sufficient transcriptional frequency. Obviously the work by Capecchi et. al.1989 tries to demonstrate that genes are usually only conserved or protected closer to the centromere, than at the ends of the chromatid as those locations are subject to change more frequently. (23, 24) All geneticists are aware that chromatin structure can be predicted by correlating gene targeting frequencies, similar to how aspects of chromatin structure are reflective of histone acetylation, DNA methylation, DNase hypersensitivity and they are associated with genetic expression.(21, 25, 26) In this case if you look at any suspected ERV, you can see that not only do they influence the ‘human’ genes beside them. They are also influenced from epigenetics (27) and the above mentioned mechanisms. Another commonly known regulator of transcription is the locus control region, of which ERV-9 has been responsible for: “serve a relevant host function in regulating the transcription of beta-globulin LCR”.(28) Therefore, for most species, you wouldn’t put a gene like ERV-W, the gene responsible for such proteins as syncytins in a place similar to that of ERV-9 since it would ruin the gene transcription near it, and they are not themselves affected by other genes as you pointed out, and would only be required during gestation.

This wanders way off the question, which was, "If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?" Re. the reality of commonly located ERVs, see "Amount of shared ERVs". And given the high degree of genetic similarity between chimps and humans, if one has mutations in its ERVs, the other will have largely the same mutations. So are ERVs, generally, highly mutated?

From Human Evolution: Genes, Genealogies and Phylogenies, Graeme Finlay, 

In the early 1980s, ERVs were discovered in the human genome.Their presence was first inferred from the appearance of viral particles that were seen to be budding from cells comprising reproductive tissues, including testicular tumours. These virus particles did not have te capacity to infect other cells, and thus appeared to be defective. (Later research sowed that human ERVs are riddled with inactivating mutations that preclude the production of infectious viruses.) Genetic analysis showed that cells producing these particles possessed messenger RNA molecules encoding the full suite of retroviral genes: gag, prt, pol and env. 
[Lower R, Lower J and Kurth R (1996). The viruses in all of us: characteristics and biological significance of human endogenous retrovirus sequences. Proceedings of the National academy of Sciences of the USA 93, 5177-84; Bromham L (2002). The Human Zoo: endogenous retroviruses in the human genome. Trends in Ecology and Evolution 17, 91-7; Bannert N and Kurth R (2004). Retroelements and the human genome: new perspectives on an old relation. Proceedings of the National Academy of Sciences of the USA 101 (Suppl. 2), 14572-9; Kurth R and Bannert N (2010). Beneficial and detrimental effects of human endogenous retroviruses. International Journal of Cancer 126, 306-14]



And, again, Phoenix provides a good indication. The consensus sequence is replication-competent. None of the contributing HERV-Ks are. No function for a complete HERV-K has been identified. The same can be said for any complete ERV (an ERV that has the same full structure as a provirus in the nuclear DNA of a somatic cell). All design proponents can point to is a subset of ERVs where a sub-component has been shown to perform some function, and in none of these cases can a reasonable case for deliberate, intelligent design be made.

Two bonus questions have occurred to me since this discussion began.

h) What is the design purpose of giving some people HERVs and not others?
i) What is the design purpose of creating different syncytins in different placental lineages? 

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2. Bhat RK, Rudnick W, Antony JM, Maingat F, Ellestad KK, Wheatley BM, et al. Human endogenous retrovirus-K(II) envelope induction protects neurons during HIV/AIDS. PloS one. 2014;9(7):e97984.
3. Contreras-Galindo R, Kaplan MH, Contreras-Galindo AC, Gonzalez-Hernandez MJ, Ferlenghi I, Giusti F, et al. Characterization of human endogenous retroviral elements in the blood of HIV-1-infected individuals. Journal of virology. 2012;86(1):262-76.
4. Kitamura Y, Ayukawa T, Ishikawa T, Kanda T, Yoshiike K. Human endogenous retrovirus K10 encodes a functional integrase. Journal of virology. 1996;70(5):3302-6.
5. Conley AB, Piriyapongsa J, Jordan IK. Retroviral promoters in the human genome. Bioinformatics (Oxford, England). 2008;24(14):1563-7.
6. Overbaugh J, Miller AD, Eiden MV. Receptors and Entry Cofactors for Retroviruses Include Single and Multiple Transmembrane-Spanning Proteins as well as Newly Described Glycophosphatidylinositol-Anchored  and Secreted Proteins. Microbiology and Molecular Biology Reviews. 2001;65(3):371-389. doi:10.1128/MMBR.65.3.371-389.2001.
7. Marlene Belfort, M. Joan Curcio, Neal F. Lue, Telomerase and retrotransposons: Reverse transcriptases that shaped genomes. PNAS vol. 108 no. 51 20304–20310, doi: 10.1073/pnas.1100269109
8. Identification of an infectious progenitor for the multiple-copy HERV-K human endogenous retroelements, Marie Dewannieux, Francis Harper, Aurélien Richaud, Claire Letzelter, David Ribet, Gérard Pierron, Thierry Heidmann
Genome Res. 2006 December; 16(12): 1548–1556. doi: 10.1101/gr.5565706
PMCID: PMC1665638
9. Shojima T, Hoshino S, Abe M, et al. Construction and Characterization of an Infectious Molecular Clone of Koala Retrovirus. Journal of Virology. 2013;87(9):5081-5088. doi:10.1128/JVI.01584-12.
10.Retroviral envelope syncytin capture in an ancestrally diverged mammalian clade for placentation in the primitive Afrotherian tenrecs. Cornelis et. al. PNAS > vol. 111 no. 41 > Guillaume Cornelis,  E4332–E4341, doi: 10.1073/pnas.1412268111

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