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Were Retroviruses Created Good? A Critique.

(Return to the ERV FAQ)

The evidence from retroviruses provides powerful evidence for different kinds of creatures having had common ancestors.The following is a critique of an article by a Dr. Yingguang LiuWere Retroviruses Created Good? at a site called Answers in Genesis (AiG), plagiarized here and brought up in various_blogs and discussion fora. The article does not so much argue against common ancestry, as ignore it, and instead attempts to argue for a role for a designer-creator.
The article uses technical terms that mean little to the reader who has not already studied the subject. However, the facts behind these technical terms are very easy to understand. Dr. Liu provides a brief glossary, but in my opinion, it is inadequate for the general reader. To familiarize yourself with the subject of retroviruses, please click on this introductory course which will open in a new window or tab. For further assistance, I have attempted to explain and clarify Liu's writing (which is indented here) at the same time as critiquing it. I will also be adding links throughout this page, both in my quotes of the AiG article, and in my own notes. All such links will be my own.
We begin by examining Dr. Liu's abstract.


  • Abstract: Retroviruses that are not normally present in healthy hosts are called exogenous viruses, ...

More precisely, they are called 'exogenous retroviruses', but usually, they are simply called 'retroviruses', the exogenous bit being implicitly understood. 'Exogenous' means 'originating from outside the body'. Retroviruses, (the human immunodeficiency virus HIV is an example of a retrovirus) reproduce by invading the cells of their hosts and inserting their genetic material into the host cells' DNA. This causes the host cells to create new virus particles.


  • ... while DNA sequences in cellular genomes that are homologous to retroviruses are called endogenous retroviruses (ERVs).

Here, 'homologous to' means 'having the same structure as'. The structure of a retroviral insertion is detailed and distinctive. It is specific to the task of causing the cell to produce new virus particles that can go on to infect new cells. Sequences of DNA with the same detailed structure as retroviral insertions are to be found in the DNA of the cells of all creatures. Each sequence appears in exactly the same position in the DNA of every cell of the body. There are typically hundreds of thousands of these sequences in each and every cell. These are known as 'Endogenous RetroViruses' or ERVs, 'endogenous' meaning 'arising from within the body'.

An essential point to grasp, and which Liu fails to stress sufficiently, is that ERVs are inherited. You and I each began with a single cell, which divided and divided as we developed. Our cells also continue to divide in order to maintain our bodies. At each and every division, our DNA is duplicated, including our host of ERVs. We originally inherited our ERVs from our parents, and they from theirs. This is the distinction between endogenous retroviruses (inherited retroviruses) and exogenous retroviruses (retroviruses acquired by infection).


  • While the belief that all ERVs are remnants of germline infection seems logical,...

It is a conclusion based on evidence, not a 'belief', that ERVs are originally created by exogenous retroviruses infecting germline cells, (egg or sperm cells). We will be looking at the evidence and the reasoning behind this conclusion as we proceed.

  • ... there are also facts against the endogenization theory, such as xenotropic ERVs ...

HorseInAStable.jpgA xenotropic ERV is an ERV that is unable to infect the cells of the species it is inhabiting. We will go into this 'problem' for the endogenization theory (the theory that ERVs are remnants of infections of germ cells) in more detail later. The problem amounts to the same sort of problem one might have if one fails to understand how a horse can come to be in a stable, because the stable door is shut. (The solution involves recognizing that the stable door was not necessarily always shut.)

  • ... and essentiality of some ERVs in host physiology. Syncytins, products of the env gene of HERV-W and HERV-FRD, contribute to human placenta development. Similar genes are also found in mouse and sheep. Indeed, the sheep ERV genes have been shown essential for sheep reproduction. Furthermore, regulation of the human syncytin-1 gene involves a complex regulation network including both viral and host factors.

external image 83471930_7b37b13a1d_o.gifAgain, we will go into this in more detail later, but it is worth noting here that 1) the env (envelope) proteins of retroviruses have the job of binding the retrovirus to the target cell, and they can cause the fusion of more cells to create a syncytium, which is a "supercell" containing multiple nucleii. HIV, for example, combat's T-cells by "swallowing" them into syncytia. This such envproteins are thus ideal candidates for being co-opted by the host as syncytin proteins for their own purposes, binding certain cells of the placenta to create the syncytial cell layers of the placenta. 2) No rational designer would embed this gene, unnecessarily, in an ERV structure. 3) It is often claimed that a common design speaks of a common designer. Here we have uncommon 'designs' in humans, mice and sheep, all involving different env genes, unnecessarily embedded in different ERV structures. If someone wanted to claim that some feature was the product of design, they would not point to syncytia.


  • Conclusion: While intact ERVs with positional polymorphism are likely germline copies of exogenous viruses, ERVs with fixed locations and conserved beneficial genes may have been incorporated into the host genome at the time of creation. Exogenous retroviruses may have been created to help the ERVs and to transfer useful genes between hosts.

'Positional polymorphism' just means 'found in different locations'. The koala retrovirus, KoRV, for example, has been inserted into germ cells in different DNA locations in different groups of koalas. Each example, however, is heritable, and appears in the same location in every cell of the offspring that inherit it. Liu tries to contrast these with "ERVs with fixed locations and conserved beneficial genes", neglecting to mention their non-conserved nonfunctional genes and neglecting to mention ERVs and ERV remnants with fixed locations and no conserved beneficial genes at all - only around 200,000 of them in our genomes. As has already been noted, ERVs with beneficial genes are hardly star witnesses for design anyway.

And it appears that Liu is not, after all, arguing for a designer as much as trying to argue against the natural explanation, that all ERVs are remnants of germline infection. Even if the viral explanation could be shown to be inadequate, it would not mean that the 'design explanation' 'wins'. Neither would it mean that common ERVs do not mean common inheritance for different kinds of creatures - common inheritance is the obvious explanation even if there was a designer. Any proffered explanation requires positive evidence in its favor. We will see, as we go on, whether Liu provides it or not. So far, we have two supposed arguments against the viral explanation, xenotropic ERVs, and a subset of ERVs with components that perform useful or even essential functions. In favor of the design explanation, we have three 'maybes'. Maybe some ERVs just got created, somehow or other (other than via infection) in our genomes. Maybe they got created somehow in order that a few of them could have a component that could do a useful job. Maybe retroviruses were created to transfer useful genes, even though now they transfer any old stuff (in addition to retroviral genomes).

external image Elephantinroom300wide.jpgThe elephant in the room that Liu is desperate to ignore and have us ignore, is that if you and I share hundreds of thousands of ERVs and ERV remnants, each one in a particular location in all of our cells. Whether the parts of some of them that have any function have been scavenged and recycled by evolution, or are there by design, the simple explanation for the fact that we share them is that we inherited them from ancestors we share in common. Similarly, if you and I and Charlie the chimp share hundreds of thousands of ERVs, each one in a corresponding particular location in all of our cells, then the simple explanation is that we have inherited them from ancestors we all share in common. Either that, or the designer had been desperately trying to fool us into falsely concluding common ancestry by designing in a huge mass of unnecessary and misleading features and details pointing to common inheritance.

Let us go on to the next section in Liu's piece,

  • Retroviruses: exogenous and endogenous

  • The main beneficial role of viruses known to date is the ecological role of horizontal gene transfer (DNA transduction) by bacteriophages.12 These viruses enable bacteria to share advantageous traits such as antibiotic resistance.

It is easy to gain an inaccurate impression from this, that transduction is a purely beneficial process. Bacteriophages can transfer any bacterial DNA. It may be advantageous to the bacterium, neutral or detrimental. And antibiotic resistance? What benefits from the transference of resistance? Certainly not humans infected by bacteria with resistance to multiple antibiotics! Beneficial DNA (beneficial to the bacteria) becomes more common in a population of bacteria by simple evolutionary principles – heritable traits, however acquired, will increase in frequency in a population if they confer a survival-to-reproduction advantage.

  • The only family of viruses that are known to transduce genes among eukaryotic organisms (such as vertebrates) is that of the retroviruses. Retroviruses are viruses that have RNA as their genome but make DNA copies of it in the infected cell. They are similar to some bacteriophages (temperate phages) in that both insert their genetic material (DNA provirus) into host cell chromosome(s). This integration of viral and cellular DNA increases the chances of transduction of cellular genes adjacent to a provirus. Some retroviruses are known to transduce tumor genes (oncogenes) into the new host, which, while promoting the proliferation of the infected cell, often bring disaster to the organism.

This underlines the point I made above. DNA transduction by retroviruses does not 'care' what cellular DNA it transfers, nor where it is re-inserted. Such DNA may be beneficial, neutral or detrimental to the infected cell and organism. They can, indeed transduce oncogenes. SeeMechanism of transduction by retroviruses - A Swain and JM Coffin. It hardly argues for a 'creator' of retroviruses when the results of his design are indistinguishable from pure happenstance.

  • While temperate phages only insert a single copy of the provirus into the host chromosome, retroviruses are allowed to insert multiple copies of proviruses into different sites of the same host genome. Integration of proviruses into the host’s germline cells (cells that give rise to eggs or sperm) will result in inherited retroviruses. 3

Temperate phages do not insert proviruses into host chromosomes. They insert prophages. But what does this have to do with retroviruses? Retroviruses do indeed integrate into germline cells, where they become heritable. This is what an endogenous retrovirus is – the remnants of a provirus in a specific location in the genetic inheritance of a creature. Any two creatures sharing multiple ERVs in corresponding locations in their genomes are therefore necessarily related by common ancestry – the ancestors being those who acquired the germline integrations in the first place.

  • On the other hand, the genomes of all vertebrates and humans harbor multiple copies of endogenous retroviruses (ERVs), DNA sequences that have genes and gene organizations homologous to those of retroviruses. Indeed, ERVs constitute about 8% of the human genome, a proportion much larger than the sum of all single-copy genes. fown ge While some ERVs are expressed and some even assembled into intracellular viral particles, most of them are deficient and are rarely transmitted horizontally. In view of this, retroviruses that are normally absent in healthy hosts are called exogenous retroviruses. Are ERVs degenerated germline copies of exogenous viruses which infected the host’s ancestors in history?

After stating that integration of proviruses into germline cells results in inherited retroviruses, Liu now wonders if inherited retroviruses are the result of the integration of proviruses into germline cells! As if to ponder this question, Liu goes on to describe the evidence for the endogenization theory, that the source of heritable endogenous retroviruses is indeed the integration of exogenous retroviruses.

  • Evidences supporting the endogenization theory for the origin of ERVs include the following.

  • (1) Modern exogenous viruses can infect the germline and be inherited like the host’s own genes. 3

  • (2) Some endogenous viruses are replication-competent and infectious. When isolated murine leukemia viruses (MuLV, an endogenous mouse retrovirus) were inoculated into a new host, their proviruses were able to colonize the recipient genome. 5

  • (3) Polymorphism (variation) of the chromosomal positions of an ERV among individuals of the same species suggests independent endogenization events. For instance, proviruses of the Koala retrovirus (KoRV) are found in different loci in different animals. 6

  • (4) Allelic frequency polymorphism (variation in the frequency of finding a DNA sequence among populations) indicates recent endogenization. KoRV is present in koala in northern Australia, but absent in some animals in southern Australia. 6 Similarly, HERV-K113, a provirus located on human chromosome 19p13.11, is rare among Caucasians and more prevalent among Africans, Asians, and Polynesians. 7

  • (5) Negative correlation between degrees of positional polymorphism and sequence polymorphism conforms to the endogenization-degeneration hypothesis. ERVs with fixed chromosomal positions (less positional polymorphism) often demonstrate more sequence polymorphism with deleterious mutations and differences between the 5’ and 3’ long terminal repeats (LTRs), consistently pointing to the hypothesis that the virus infected an early ancestor and degenerated during its long history, 8 while proviruses with varied locations such as KoRV are often intact and infectious, indicating recent or ongoing endogenization.

All Liu is trying to say here in (5) is that ERVs in varied locations such as KoRV are relatively recent, with few mutations, while ERVs in less varied or in singular locations exhibit a greater number of mutations. (Positional polymorphism is when an ERV appears in more than one position in the chromosomes. This may be in more than one position in an individual's DNA, or in the genome of a species, or in the genome of a group of species. Each instance of an ERV in a particular position, however, will be fixed in the sense that it will always be inherited in that position. When we say an ERV is fixed in a population, that means something different. When a genetic feature is fixed in a population, it means that every individual possesses it. Sequence polymorphism means variation in form in a population for a given feature.)

Liu has not listed certain other evidences for the theory that ERVs are the result of germline infections. I'll add to his list here:-

  • (6) The curious case of the phoenix virus. This is a working virus resurrected from inactive ERVs. Why should this experiment have worked if the ERVs were not degenerate proviruses?

  • (7) Viral codon bias. A codon is a triplet of DNA or RNA bases. In translating RNA into a protein, each triplet is translated into a specific amino acid. But the interesting thing is that nearly every such amino acid can be translated from more than one triplet. Now certain types of life forms 'prefer' certain codons over others, and virus' 'preferences' are different. ERVs exhibit the same codon preference, or bias, as exogenous viruses.

  • (8) The phylogenetic evidence from the types of ERVs. Humans, for example, share most of their ERVs with chimpanzees, then, in order of the number of shared ERVs, they share the next highest number with other great apes, then with gibbons, then with old world monkeys and then with new world monkeys. ERVS unique to each species tend to bear the evidence that they are the most recently acquired. The ERVs that are shared among primates are shared in a pattern called a nested hierarchy or tree. A nested hierarchy is a necessary consequence of descent with modification, which is consistent with the 'endogenization theory'. An intelligent designer is not constrained to produce a nested hierarchy of this sort, and where such a hierarchy is maintained in unnecessary detail, as it is, this would make such a hypothetical intelligent designer a bit of a prankster.

  • (9) The phylogenetic evidence from differences in long terminal repeats and from other mutations to ERV genes. Long terminal repeats (LTRs) are sections of DNA at either end of a retroviral insertion. They must be identical at the time of insertion. However, LTRs and ERV contents gradually acquire mutations and begin to differ from one another. Drawing up tables of differences and similarities between orthogolous ERVs in different species produces a nested hierarchy once again.

  • (10) The agreement between (8) and (9), despite the nested hierarchies being derived from different effects - integration in the case of (8) and mutation in the case of (9).

Liu then goes on to discuss what he regards as facts against the endogenization theory.

  • However, there are also interesting facts against the endogenization theory.

  • (1) Endogenization of modern exogenous retroviruses is rarely observed in nature.

The endogenization of modern exogenous retroviruses has been observed in nature. Liu has already mentioned it above - the koala endogenous retrovirus, and he has also described other evidence in support of recent endogenization events. Even if endogenization was judged to be rare, it's rarity would not be evidence against it happening! But we have to be careful about words like 'rare' in evolutionary scenarios. The evidence is that eukaryotic life is some 2 billion years old. As we have some 200,000 ERVs in our genomes, that means one endogenization event that goes on to become fixed in the population, on average, once every 10,000 years. IOW, endogenization can be rare, and still be frequent enough to account for all our ERVs.

  • (2) Most modern ERVs are not actively transposing (moving around or duplicating) in the host cell genome. At least all human ERVs appear fixed in numbers and positions; although some mouse ERVs are capable of expanding in the host genome. Are the human ERVs older, therefore more degenerated and less active? If the human race is younger than the murine race, as evolutionist biologists believe, there is no reason to suppose that the human ERVs are older than those of the mouse.

Liu seems to have a bit of a misunderstanding here about what 'evolutionist biologists believe'. Human beings are not a species that poofed into existence from nowhere, and neither are mice. For both men and mice, they and their ancestors have been around for exactly the same length of time (although there will have been more mouse ancestors, mice happening to breed like - well, like mice). If mice have acquired more ERVs more recently than humans, it is not because they are a more recent species.

  • (3) Xenotropic ERVs reside in cells that have no receptor for them. Instead, envelope (env) proteins of these ERVs bind receptors on cells of other animals. 8 How did these ERVs get into the cell, if they were not built inside? It is no surprise to read speculations like this inRetroviruses, the “Bible” of retrovirology: “It is likely that xenotropic viruses originally inserted into the germ line in a host background that encoded their cognate receptor but that the functional xenotropic viral receptor allele was subsequently lost, probably under selective pressure from exogenous xenotropic viruses.” 9 The term “exogenous xenotropic virus” is difficult to conceive, if not self-contradictory.

ERVs, as has been already explained, get into cells by inheritance, ultimately from the infection of a germline cell by an exogenous retrovirus. Cells that inherit an ERV do not, therefore, need to have the retroviral receptor. Language nitpicking aside, it is not difficult to understand that a species or its ancestors can acquire an ERV and subsequently lose the receptor that made the original acquisition possible. Easier, in fact, than the idea that a designer snuck them into a cell, for no good reason other than to pose us a puzzle.

From Coffin, 1997

  • Genetics of MLV Receptors


  • The ecotropic viruses were the first class of MLVs to be identified. They comprise some of the most intensely studied retroviruses, including exogenous viruses such as Moloney MLV (Mo-MLV) and Friend MLV (Fr-MLV), as well as the endogenous virus of the AKR mouse strain, AKR MLV (AKV). A functional receptor for the ecotropic MLVs is encoded by all strains of laboratory and wild mice of the genus Mus musculus that have been examined to date. The assignment of a single genetic locus for susceptibility to ecotropic MLV infection was consistent with a single gene encoding the receptor protein. The evidence for this came from studies of somatic cell hybrids that were created by fusion of susceptible mouse cells to nonpermissive hamster cells. When cells that retained susceptibility to ecotropic MLV infection were characterized for their mouse chromosomal content, it was possible to assign the receptor gene(s) to the Rec1 locus on chromosome 5 (Gazdar et al. 1977Oie et al. 1978Ruddle et al. 1978).

  • Xenotropic and polytropic MLVs are present as endogenous proviruses in all inbred mice (see Chapter 8). Like ASLV receptors in chickens, the receptor for xenotropic MLV is polymorphic in mice but not in other species. Although xenotropic viruses will not infect cells from inbred strains of mice, they will infect cells derived from some wild mice and species of mice other than M. musculus (Hartley and Rowe 1975;Lander and Chattopadhyay 1984). The genetic locus for susceptibility maps to chromosome 1, and it is inseparable from the gene for the polytropic viral receptor, suggesting that alleles of this gene can serve as the receptor for both polytropic and xenotropic viruses (Kozak 1985Hunter et al. 1991)

  • Xenotropism—the inability of an endogenous retrovirus to infect cells of the species whose germ line it inhabits—is not limited to the endogenous viruses of mice but is also seen with the subgroup E viruses of chickens and with endogenous viruses of cats and primates. It is likely that xenotropic viruses originally inserted into the germ line in a host background that encoded their cognate receptor but that the functional xenotropic viral receptor allele was subsequently lost, probably under selective pressure from exogenous xenotropic viruses.

  • Amphotropic viruses are exogenous MLVs originally isolated from some wild mouse strains. Because of their efficient infection of human cells, the amphotropic env gene is widely used in retroviral vectors (Chapter 9). The distribution of receptor activity for amphotropic viruses among species differs from that of xenotropic and polytropic viruses, as does the map location of the receptor (Garcia et al. 1991). To date, genes encoding receptors for ecotropic and amphotropic MLVs have been cloned and characterized; those for xenotropic and polytropic viruses remain to be discovered.

In other words, certain inbred strains of mice have ERVs derived from viruses that cannot infect them, but which can infect certain wild strains of mice. Liu thinks that a designer with nothing better to do than to mislead us is a better explanation than the explanation that an ancestors of both the wild and the inbred mice acquired the ERVs because the viruses could infect them.

  • (4) Essential beneficial functions of some ERVs and irreducibly complex coordination between ERVs and host DNA sequences argue against the possibility of historical acquisition of ERVs followed by positive selection (see below).

Certain parts of certain ERVs perform essential functions, but the puzzle remains - why do these parts appear embedded in a proviral structure, the rest of which does not perform any beneficial function? Evolutionary theory would lead us to expect that features that can be easily adapted to perform a beneficial function by relatively minor modification will be likely to arise and be positively selected and improved.

The cooption of env genes to act as syncytins is a classic example of this phenomenon. The fact that there are numerous different examples of syncyins based on env genes from different ERVs strengthens the argument for cooption as opposed to that of design.

The 'beneficial function' design argument conveniently ignores the non-functional and the detrimental 'designs'. Why should beneficial features be significant, while neutral and detrimental ones not be?

And this assertion that these systems are irreducibly complex (which is unsupported by any evidence) is a particularly poor one. Irreducible complexity is the notion that a system cannot evolve because it is too improbable that each of its components can arise by variation and selection in the absence of the others. Apart from irreducible complexity being flawed as a basic concept, in this case, it is applied inappropriately even under its own terms. The ERV component does not appear in the host DNA by means of mutation, but by infection. Thus, a major component of this 'irreducibly complex' system appears, almost ready made, in one fell swoop. In fact, this example does illustrate the flaw in the irreducible complexity notion. A component of an 'irreducibly complex' system is not initially required to be a part of the system the observer is scratching his head over. It is sufficient that it performs a function. In this case, that function was that of the env environment protein, i.e. to attach, not placental cells to those of the uterus, but the viruses to the target cells' protein coats.

Consider that, for an ENV that is no longer replication-competent via the viral re-infection route, it is still replication-competent via host organism reproduction. The ERV is 'in the same boat' as the rest of the host's DNA, and the selection pressure on the ERV will be pressure to cooperate with the host DNA.

  • (5) The existence of numerous solo LTRs in genomes suggests retroviral deletions, which may account for frequency polymorphism of some ERVs among populations. In other words, frequency polymorphism is a sign that the sequences are being lost, instead of being added on through endogenization.

Deletions are evidence of the negative selection and loss by genetic drift of non-beneficial ERV DNA. However, as we have seen, novel ERVs are acquired as well as lost. It is hard to see what Liu finds so mysterious about this.

  • Contributions of endogenous retroviruses to the host: syncytins

  • Retroelements including ERVs are normally suppressed from expression or transposition by extensive DNA methylation, RNA interference, heterochromatin formation, etc., to maintain genomic stability of the cell. Failure of the cell to control ERVs can lead to mutations or diseases.8,10,11 As a matter of fact, improper activation of endogenous retroviruses has been associated with many human cancers and autoimmune disorders.11 Complex interplay between retroelements and gene silencing mechanisms suggests ERVs are integral parts of the genome.

So because so many ERVs are still able to create havoc in our cells unless they are 'controlled', that makes them integral parts of the genome! 

  • However, some of these genetic elements are expressed at certain stages of the host’s lifetime to the benefit of the host. Several instances of beneficial ERVs have been noticed. (1) Regulation, mainly activation, of neighboring (downstream) genes during embryonic development of the mouse.12 (2) Regulation of human genes expressed in the placenta (e.g. pleiotropin) and somatic tissues (e.g. apolipoprotein C1 in the liver and β-amylase in the salivary gland).8,13 (3) Immunomodulation, including induction of immunotolerance to self antigens and immunization against exogenous retroviruses.8,13 (4) The env protein of HERV-W and HERV-FRD serving as fusogenic factors (syncytins) during human trophoblast development.14,15 (5) Other roles such as mammalian tissue organization.16 Many of these genes are expressed during genome-wide DNA demethylation in gametogenesis (formation of eggs or sperm) and embryonic development, therefore are important for reproduction.


Basically, Liu is trying to imply that because certain parts of certain ERVs perform an essential function, then at least some ERVs are there by design. 1) Whether they are there by design or not, the best explanation of common ERVs among creatures is common ancestry. This applies to creatures with corresponding ERVs whether or not they are the same kinds of creature. 2) Very few ERVs have parts that perform any beneficial function. What about the other parts that do not? What about all the other ERVs? Why are they there? 3) What is the problem with the notion that components of ERVs can be co-opted by evolutionary processes? It is far more likely that a ready-made approximation to a useful gene gets co-opted than a useful gene arising from complete junk. And a failure to comprehend how ancestors could get by without what is now an essential gene is just that - a failure of comprehension. This study investigates the evolution of syncytin 1 in apes and monkeys. The following diagram taken from the paper maps out just how the HERVW env gene evolved into syncytin 1. Old world monkeys reproduce just fine - indeed with enthusiasm - without a functional syncytin derived from the HERVW env gene.

  • external image F2.medium.gif
  • Evolutionary analysis of Syncytin 1 in hominoids and Old World monkeys. Neighbor-joining tree based on 2,331 bp of Syncytin 1 sequence in 14 primate species, with the bootstrap values of 1,000 replicates indicated in boldface for all the nodes. Gene-inactivating mutations and their corresponding position with respect to the human coding sequence are shown below the branches: asterisks, stop codons; black upward triangles, frameshift insertions; black downward triangles, frameshift deletions. Deletions that do not affect the reading frame are represented as empty downward triangles. Ka/Ksratios according to the PAML free-ratio model are shown in italics above each branch. Dashes indicate branches with Ks = 0. Branch length in the tree corresponds to the number of nucleotide substitutions per codon. In these analyses, the HERV-W family consensus sequence, HERV17 (Jurka 2000), was used as the outgroup, but very similar results were obtained when six sequences representing ancestral HERV-W insertions in the catarrhine lineage derived from the full-length env copies in the human, chimpanzee, and rhesus genome were used. The most parsimonious scenario for the generation of a stop codon in the catarrhine lineage from the original TGC sequence and its reversion in hominoids is represented inside rectangles.

And from Evidence for the Evolutionary Model ,

  • There is no question that some ERVs have functions in organisms, but there are no wholly functional ERVs—only functional components, with the remainder deleted or mutated into non-functionality.

  • For instance, the contribution of enJS56A1 and enJS5F16 (of the mere ~20 enJSRVs) to placental growth/differentiation regulation is achieved solely by their env genes with open reading frames (Dunlap //et al//., 2006Palmarini //et al//., 2000). Although they also have an open gag reading frame (causing gag-gag interaction that restricts pathogenic JSRVs), they are the only ones known to have this (Mura //et al//., 2004). And every studied enJSRV has a closed pol reading frame (Murcia, Arnaud, & Palmarini, 2007).

  • Another example is the transcriptional contribution of LTRs to genes' promoters:

  • 1) Not only are most ERVs not at a loci that even makes it possible for them to contribute to transcriptional activity, but most ERVs have recombined into solo LTRs. Since only the LTRs of active full-length ERVs can contribute (Cohen, Lock, & Mager, 2009, p.107), even most ERVs in the right position have no effect. Just as with enJSRVs, these ERVs represent a very small percentage of the whole.

  • 2) The actual genes of these ERVs contribute nothing—only their promoter sequence-rich LTRs do. Again, just as with enJSRVs, these are examples of functional ERV components, rather than functional ERVs.

  • It is the same with every case observed; again, there are no "functional ERVs;" only a small percentage of ERVs with functional components.

  • But it's a moot point, because we know that ERVs are insertions:

  • The hallmark of an insertion is a displacement of chromosomal DNA, and the hallmark of insertion by integrase is the presents of target site duplication, due to the way it attacks the 5' and 3' phosphodiester bonds with an offset of a few base pairs (Skinner //et al//., 2001). Since ERVs are accompanied by target site duplications and DNA displacement, they are necessarily endogenized/fixed proviral insertions.

  • So 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.

  • For an understanding of scaffolding (p.365-366) and exaptation (p.361-363), including various "paths to exaptation," refer to the first half (p.358-366) of "The Evolution of Complex Organs" by Dr. Gregory (2008).

  • There has been much investigation on the function and regulation of syncytins, especially syncytin-1, which is the envprotein of HERV-W. Syncytin-1 is critical for the formation of syncytiotrophoblast (a layer of fused cells which invades the uterine wall and subsequently develops into parts of the placenta), and its secretion of human chorionic gonadotropin (hCG).15 Efficient tissue-specific expression of syncytin-1 requires cis-acting elements in both the 5’ LTR of HERV-W and host sequences (including an enhancer) upstream of the ERV.17The host enhancer confers placental specificity to the expression of the syncytin gene, with binding sites responsive to cAMP/PKA and putative binding sites for AP-2, Sp-1, and GCMa, all of which are protein factors involved in embryonic development.18,19 GCMa is tissue-specific and has been shown to activate transcription of the syncytin-1 gene.20 Meanwhile, these transcription factors are under the control of host sex hormones such as progesterone. If the syncytins are indeed essential for human reproduction, they appear to be components of an irreducibly complex system that have to be created together to perform the intended function (figure 1).21 Recently, ERV env genes similar to syncytins have been shown to be essential for placenta development of sheep.22 Inhibition of these “viral” genes resulted in abortion in almost all animals. However, the authors of the report still believed in endogenization of these genes, and speculated that “it is likely that some of the host mechanisms governing the reproductive processes [before the endogenization (added for clarification)] may have been lost later during evolution.” The argument is similar to the explanation of xenotropic ERVs quoted above, both depending on “lost” elements which more likely never existed.
  • DNA sequences of Syncytin-1 are conserved in hominidae but appear degenerated in Old World Monkeys.23 While little is known about monkey genomes, complete sequences of the mouse genome are available. Muridae do not have genes orthologous to the HERV syncytins but have unrelated ERVs whose env genes code for similar proteins during placenta development.24 The case is similar in sheep.22Evolutionary biologists call this phenomenon convergent evolution, speculating that hominidae, muridae, and bovidaewere independently infected by different ERVs, which ended up to be harnessed in a similar way for a similar purpose in similar tissues, after the families separated from a common mammalian ancestor. To a creationist, it seems that the human, mouse, and sheep were created with a similar scheme regarding the formation of syncytiotrophoblast, but different viral materials were used.
  • Potential beneficial transduction by retroviruses: retrofection

  • In addition to the beneficial role of ERVs, exogenous retroviruses do transduce cellular nucleic acids other than oncogenes. While bacteriophages enter the host cell by nucleic acid translocation (only the viral DNA or RNA enters the cell), retroviruses penetrate by membrane fusion, allowing viral proteins and anything packaged in the virion to invade the cell. Cellular RNA molecules are frequently packaged in a retrovirus and transferred into other cells. Reverse transcription within the viral particle during the early stages of the viral life cycle is accompanied by high incidences of recombination, resulting in chimerical DNA, partly viral and partly cellular, which is subsequently integrated into chromosomes of the new host. This process is called retrofection. Retrofected cellular genes (retrogenes) have a common 16 nucleotide signature sequence.25 Viral LTR can serve as internal promoters for the expression of retrogenes. An example of a retrogene is the gene for the 7S L RNA, a component of the cytoplasmic signal recognition particle. > 26Because laboratory models of retrofection involved human design, the natural role of retroviruses in horizontal gene transfer still awaits more solid evidence. Unfortunately, there has been no more report in this area since the early 1990s.
  • Conclusion

  • Rather than being added on during evolution by accidental endogenization of exogenous infectious agents, at least some ERVs must have been incorporated into the initial design of eukaryotic life. ERVs with fixed chromosomal positions are more likely integral parts of the host genome created in the host, while the more intact ERVs with positional polymorphism may be germline copies of exogenous viruses. The degenerative nature of mutation forbids the evolution of infectious viruses from ERVs. Exogenous viruses might have been created simultaneously with their endogenous counterparts during the Creation Week. Transmission and propagation of infectious retroviruses among the host population could have helped in maintenance of the endogenous viral sequences via recombination, in a way similar to recombinational DNA repair and modern gene therapy. (Indeed, retroviruses have been used as the classic vectors in gene therapy because of their ability to integrate into host chromosomes.) Interactions between endogenous and exogenous retroviruses may have been perfectly regulated at the time of creation. Additionally, infectious retroviruses may also have played a role in horizontal gene transfer which was ecologically beneficial. Insertional mutagenesis, formation of v-oncgenes, as well as oncogene transduction, are rather dysregulated biological events performed by retroviruses after the Fall, or even after the Flood, when God decided to shorten the human life span. For similar reasons, we do not expect germline infection of modern exogenous viruses to bring benefits to the host, whether on the level of an individual or on the level of a species.



To be continued. Note to self, list points against designer theory.

Note: Liu's citation 12 is available as full text here,
http://www.sciencedirect.com/science/article/pii/S1534580704003259

LTR tutorial http://www.stanford.edu/group/nolan/tutorials/retcl_3_ltrs.html

Reference: Coffin, J.M., Hughes, S.H., and Varmus, H.E., Retroviruses, Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press; 1997. ISBN-10: 0-87969-571-4


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