From a piece by one Dr. Sean DeVere Pitman, M.D.

From a piece by one Dr. Sean DeVere Pitman, M.D. Source, http://www.detectingdesign.com/pseudogenes.html#Endogenous

I Googled him. He only seems to come up on creationist websites.

Here we go. As usual, my fisking is in red. 

Endogenous Retroviruses (ERVs)

Updated: April, 2012

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The case for common descent:

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        Endogenous retroviruses or "ERVs" are viral elements that are thought (concluded) to have inserted themselves into the genomes of various creatures - to include humans and apes.  ERVs are thought by many to be among the strongest evidences supporting the theory of common descent.  For example, it is argued that the same ERVs in the same locations in the genomes of both humans and apes are best explained by a shared common ancestry between humans and apes.  In other words, the common ancestor(s) of humans and apes must have been the one(s) to initially experience the ERV insertion into its genome (their genomes).  Then, later, when human and ape ancestors split off from this common ancestral lineage, the same ERV sequences were maintained in the same places in the genomes of both lineages (all related lineages).  

        This argument seems rather straightforward and even downright obvious at first approximation.  However, there are several potential problems with this theory.

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Signs of function:

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        One problem is that a number of ERVs, or at least portions of ERVs, are being discovered to be functionally beneficial. (Why is this a problem?) 

       The ERV known as enJSRV has been shown to "regulate trophectoderm growth and differentiation in the peri-implantation ovine conceptus. This work supports the hypothesis that ERVs play fundamental roles in placental morphogenesis and mammalian reproduction." ³⁵  

         In fact, ERVs elements are thought to control or aid in the transcription of over 20% of human genome⁴⁶ and can trigger premature transcriptional termination at a distance. (Link)

         It is also interesting to consider that ERVs and other supposedly "parasitic" DNA elements are found far more often in the genomes of more "complex" organisms - suggesting again that non-coding portions of DNA once thought to be nothing but "junk DNA" and evolutionary remnants are actually playing important functional roles in the genomes of more functionally complex organisms.  

     "With the accumulation of genomic sequence data, certain unexplained patterns of genome evolution have begun to emerge. One striking observation is the general tendency of genomes of higher organisms to evolve an ever decreasing gene density with higher order. For example, E. Coli has a gene density of about 2 Kb per gene, Drosophila 4 Kb per gene and mammalian about 30 Kb per gene. Much of the decreased density is due to the increase in the accumulation of non-coding or 'parasitic DNA' elements, such as type one and two transposons. Current evolutionary theory does not adequately account for this observation (81). In addition mammals appear to have retained the presence of at least some copies of non-defective 'genomic retroviruses', such as intercysternal A-type particles (IAP's) or endogenous retroviruses (ERVs). It is currently difficult to account for the selective pressure that retains these genomic viruses . . ." ³⁸

        In this same line, a subsequent paper presented evidence that proposes potential reasons for the previously observed "selective pressure" and the actual need for ERVs within the genomes of complex organisms like humans.  In the journal Bioinformatics, Conley et. al. write:  

       "We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5' untranslated regions (UTRs)...

        Our analysis revealed that retroviral sequences in the human genome encode tens-of-thousands of active promoters; transcribed ERV sequences correspond to 1.16% of the human genome sequence and PET tags that capture transcripts initiated from ERVs cover 22.4% of the genome. These data suggest that ERVs may regulate human transcription on a large scale." ⁴⁶

        ERVs are also being shown to be protective against infection by harmful exogenous retroviruses:

        "A possible biological role hypothesized for ERVs is to help the host resist infections of pathogenic exogenous retroviruses, affording a selective advantage to the host bearing them. For instance, some avian and murine ERVs can block infection of related exogenous retroviruses at entry by receptor interference; mouse Fv-1 blocks infection at a preintegration step, also can be viewed as an ERV." ⁵⁰

ERVs may also aid in modulating the activity of the immune system:

     "For example, the HERV-K sequence of the human teratocarcinoma derived virus type (HTDV), is reported to be able to make retrovirus like particle and can express gag, pol and env genes via vectors. Also, ERV 3 can express env gene in embryonic placental tissues. Such reports may now explain the numerous early observations of being able to find viral particles in human tissues. Although some HERV's are expressed in mammary tumors, the feline RD114, ERV-3, and HERV K10+ are all expressed in placental tissues. What then is the significance of nondefective ERVs and why is expression so common in embryos? . . . I and Venables et al. in the Boyd group have proposed that some of these HERV's may function during embryo implantation to help prevent immune recognition by the mother's immune system. . . 

       In addition, the ERV gag gene product may also be immuno-modulatory. The p70 (gag) of mouse IAP has been cloned and expressed and shown to be identical to IgE binding factor (IgE-BF) which is a regulator of B-cell ability to produce IgH. More recently, it has been reported that endogenous gag is Fv-1, an-Herv.L like endogenous virus which confers resistance to MLV tumors. Although some researchers disagree with the immunomodulatory role of p15E, an immune suppressing activity in culture assays has been clearly established. These supporting results seem sufficiently clear to warrant a serious investigation that both the env and gag gene products of ERV's may modulate immunity." ³⁸

        So, it isn't a necessary default that all ERV-like sequences are functionless evolutionary remnants of random viral infections as originally proposed by prominent evolutionists such as Richard Dawkins or Douglass Theobald.  This fact was highlighted by Richard Sternberg in a 2002 issue of Annals of the New York Academy of Sciences in the following statement: 

         "The selfish DNA narrative and allied frameworks must join the other ‘icons’ of neo-Darwinian evolutionary theory that, despite their variance with empirical evidence, nevertheless persist in the literature." ⁴⁷

Similar support for this concept is noted by Dr. Wang from the Haussler lab:       

        "These results raise new questions about the role of so-called 'junk DNA,' the vast regions of the genome that don't code for proteins. ERVs fall into that category. Many scientists once believed that such DNA served no purpose, but new data from the Haussler lab and other labs are challenging that view." ⁴⁸

It is a very common bleat from creationists that some components of some ERVs perform useful, and even essential functions for their host organisms. We know. It is real scientists doing real science that discovered this. So much for the conspiracy theory that "evolutionist" scientists try to suppress the truth. It is also a dishonest strawman argument to say that the proof of common descent rests on the assertion that ERVs are "junk" DNA. Nobody claims this. Follow these links to see what I say about function in ERV DNA.

ERVs do stuff. Doesn't that prove that they didn't originate from retroviruses, but were designed?

ERVs promote the transcription of host DNA. Doesn't this prove they are designed?

ERVs are essential in reproduction (syncytin and the formation of the placenta). How can this be?

Aren't the same ERV genetics in the same places in different species because they have to do the same job?

But how can you rule out design as an explanation?

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Origin of ERVs from exogenous retroviruses - or visa versa?: 

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       There is also some evidence that exogenous retroviruses are occasionally derived from ERVs - instead of the other way around. 

    "Exogenous retroviruses may have originated from ERVs and ERV-Ls in particular may represent an intermediate between retrotransposons and exogenous viruses." ⁴⁹

        This concept is supported by the observation that there are no known examples of current exogenous retroviral insertions into the modern human genome.  Also, there are no known infectious exogenous counterparts of any human endogenous retroviruses known to exist today.  This is a very curious finding considering the striking commonality of ERVs within the human and ape genomes if the prevailing hypothesis that these ERV sequences were in fact derived from exogenous infective retroviruses.  

    “No current transposition activity of HERVs or endogenization of human exogenous retroviruses has been documented so far.” ⁵¹

    “Most of these elements represent ancient retroviral infections, as evidenced by their wide distribution in primate species, and no infectious counterparts of human endogenous retroviruses (HERVs) are known to exist today.” ⁵²

  

         This opens up the possibility that at sometime in the past all exogenous retroviruses were originally derived from ERVs - - not necessarily the other way around with ERVs originally being derived from exogenous retroviral infections.  In other words, it is possible that all sequences that are now thought to be viruses or viral elements were originally derived from functional genetic sequences that have since suffered degenerative changes and loss of genetic controls, resulting in various parasitic features that we see in many viruses today - as well as the resulting harmful effects of this loss of regulation such as tumor development and the association of numerous types of cancers and neoplastic processes.

This is just, simply, incorrect. Comparison of the whole genome sequences of common chimps, bonobos and humans indicate that, although the vast majority of retrovirally derived endogenization are shared between these species, there are some that are unique to each of them. Hardly a surprise, considering that retroviruses persist in the environment.

See How many ERVs are shared, in common locations, in the genomes of humans and chimps?

And yes, it is known to be the case that ERVs can produce viable virions, (it's part of the retroviral replication cycle after all - and again, a discovery by real scientists) but this does not support the case that all ERVs were designed into genomes. All the evidence points in the other direction. And how do you explain common disabling mutations in ERVs in what evolutionary science says are closely related species? The coincidences are much too numerous to be credible.

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Non-random viral insertions:

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        Beyond this, it has also been shown that the insertions of ERVs are not entirely random despite this common belief - even among mainstream scientists.  ERVs actually show a preference for certain fairly specific locations in various genomes.  

     "Although retrovirus integration can occur throughout the genome, local "hot spots" for integration exist where a strong preference for particular sites over others can be demonstrated statistically. Recent work with HIV and murine leukemia virus has implied that there is also a preference for integration into transcribed regions of the host genome, in the case of murine leukemia virus, near transcriptional start sites. The basis for these preferences is unknown, but they may reflect interaction of the pre-integration complex with specific proteins or with specific DNA sequences or structures that are associated with transcription." ³⁶ 

     "But although this concept of retrovirus selectivity is currently prevailing, practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified 'hot spots' containing integration sites used up to 280 times more frequently than predicted mathematically." ⁴³

Not nearly specific enough to account for the vast majority of ERVs that are in precisely corresponding locations in chimp and human DNA. See Don't retroviruses target particular locations in the DNA? Doesn't this explain corresponding ERVs? And take a course in probability theory.

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The odds against similar ERV germline insertions:     

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        In order for an ERV to be in the same location in differing populations via common descent one of two things had to have happened.  Either many individuals in the same population were infected by the save virus which inserted itself into the same position in all the different individuals (highly unlikely scenario), or there was a very significant population bottleneck where only a very few individuals (like just one individual) were infected and then the offspring of that individual subsequently overtook the entire population to achieve fixation of the viral sequence within all individuals of the population.

        In short, a viral event would have had to overtake all of the individuals in population for each different ERV sequence in the genome (hundreds of thousands of them), and each ERV would have had to inject itself into gametic cells while not harming the reproductive fitness of the host - - and all of this would have had to happen many times in different species. The odds do not seem all that likely - especially when one considers the very high detrimental mutation rate for humans and apes and the very real odds that detrimental mutations would lead toward rapid genetic meltdown and extinction during extended population bottlenecks.

The writer does not seem to understand sexual reproduction. Just as with mitochondrial Eve and Y-chromosome Adam, genetic sequences can be traced back to single individuals. We have all inherited our common ERVs from a large number of ancestors. Some ERVs disappear from the population, some are to be found in subsets of the population, and some become fixed. It's not a matter of "overtaking" (a curiously creationist conception of evolution), but of intermixing.

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Inconsistent phylogenies:

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        Another interesting aspect of ERVs is that they do not always show the expected evolutionary pattern of "inheritance".  According to the proposed phylogenetic tree (shown to the right) chimps are closer to humans than to gorillas.  Given this scenario, gorillas and chimps would only be expected to share an ERV if this same ERV were also present in humans. However there are some ERVs that don't seem to fit this pattern. For example, the K family of ERVs (HERV-K provirus) is present in chimps and gorillas, but not in humans.⁴⁰  Also, portions of ERVs known as CERV 2 and CERV 1 elements are present in chimpanzee, bonobo and gorilla (non-orthologous) but are absent in human, orangutan, old world monkeys, new world monkeys.³⁹  

        The usual explanation for such findings, of course, is that humans lost this or that particular ERV along the way. Of course, this post-hoc argument could be used to explain any aberrancy.  It seems somewhat difficult to imagine, however, how an entire human population could loose ERVs that are preserved in both chimps and gorillas? - outside of yet another significant population bottle neck that is. 

        There are also other even more problematic phylogenetic inconsistencies with ERVs:

       "We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates. This is particularly relevant for the human/great ape lineage. For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee. Our Southern analysis shows that human and orangutan completely lack PTERV1 sequence (see Figure 2A). If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely (Figure S3). . .

        Several lines of evidence indicate that chimpanzee and gorilla PTERV1 copies arose from an exogenous source. First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon, making it unlikely that endogenous copies existed in a common ancestor and then became subsequently deleted in the human lineage and orangutan lineage. Second, the PTERV1 phylogenetic tree is inconsistent with the generally accepted species tree for primates, suggesting a horizontal transmission as opposed to a vertical transmission from a common ape ancestor. An alternative explanation may be that the primate phylogeny is grossly incorrect, as has been proposed by a minority of anthropologists." [emphasis added] ⁴²

     "Inconsistencies do exist with phylogenetic analyses and are often explained by ad hoc arguments without positive evidence." ( Link - last accessed 3/10/09)

        In fact, it seems like just about any finding or data set can be explained within the evolutionary paradigm using this or that "ad hoc" explanation to make the data fit the theory.  This produces a problem of bias when it comes to interpreting data sets. Such biases in the interpretation of ERV phylogenies have been recognized for some time now.  For example, according to Posada and Crandal, in a 2001 paper published in Molecular Biology and Evolution:

        "Wrong models of [retroviral] evolution lead to the estimation of trees that are in agreement with biochemical and immunological evidence and with previous phylogenetic studies. . .

        When examining the results of the present study, only those trees estimated according to simple, likely wrong, models of evolution agree with current evidence. In most of the reconstructed trees, different genera appear as monophyletic groups. These groups have normally high bootstrap values indicating that, given the data sets at hand, we can be confident in the nodes defining these clusters. When more complex, more realistic, models of evolution are employed, fewer genera are recovered as monophyletic, the level of support is lower, and the topologies are very different from the assumed "known" trees.

        Phylogenetic bias, by which "incorrect" models can give "correct" answers, has been identified in simulation studies. Why this bias occurs is a question that remains unsolved. . . 

        One possible factor contributing to the bias is most likely a problematic alignment, in which sequences belonging to the same group (genus) are easily aligned, whereas the opposite is true for sequences belonging to different groups. Complex models might be confounded when trying to extract information from the bad intragroup sequence alignment, while simpler models use basically the observed patterns. This would warrant a word of caution for the estimation of phylogenies from highly divergent data sets."  ⁴⁵

The writer seems to be unaware of incomplete lineage sorting.  Explained at the link.

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The sheer number of ERVs:  

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        Not too long ago it was thought that around 30,000 ERVs existed within the human/ape genomes, comprising between 1-8% of each. ^37,41,43  As of the 2005 Chimpanzee Sequencing and Analysis Consortium, where the entire chimpanzee genome was compared to the human genome, it is now thought that approximately 200,000 ERVs, or portions of ERVs, exist within the genomes of both humans and apes - totaling around 127 million base pairs (around 4% of the total genomic real estate).⁶³  Some authors suggests a 45% ERV origin for the human genome at large (Mindell and Meyer 2001) and 50% for mammalian species in general ( Link ), if all small fragments of ERV sequences are included in the estimate. In any case, of these hundreds of thousands of recognizable portions of ERVs, the vast majority of them seem to match up, at the very same loci, between humans and chimps.  As suggested in "Table 2" from the paper (to the right), less than 1% of the ERVs are lineage specific for either humans or apes.  In other words, the vast majority of ERVs are shared or "orthologous" between humans and chimps (a significant increase from the seven or so that were once thought to infect both humans and chimps at identical locations ( Link ).

That's right. Endogenization in common ancestors explains them. "Design", as an explanation, doesn't work. 

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ERV Summary

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       For many this finding alone (of near universal homology among ERVs between species) might suggest overwhelming evidence in favor of common ancestry - not to mention the nested hierarchical patterns that most of these ERVs display between species.  Certainly, it does not seem rational to deny a common origin of some kind.  However, given the ever increasing discoveries of functionality for various elements of ERVs, in all their various forms and fragments, combined with the difficulty to explain truly exogenous sources for their existence, the theory of a common evolutionary ancestry becomes less tenable.  The existence of ERVs or parts of ERVs at the same or similar places mostly doing the same or similar jobs over so much of the genome (often at a very high level of integrated complexity) in similar creatures strongly favors the theory of a common designer.

        The Darwinian mechanism of random mutations and function-based natural selection is simply inadequate to explain the high-level functional complexity of ERV elements within very complex and heavily integrated genomes.  Also, the fact is that there simply are no known examples of exogenous retroviruses inserting themselves into the germ lines of humans or chimps, or any other animal for that matter.  If the common descent hypothesis were in fact true, that such events have occurred in the past at very rapid rates, one should expect to see at least a few real time examples of such.  Why are there no such examples in action?  The requirement for so many tens and hundreds of thousands of neutral retroviral infections to have achieve fixation in the original germ-line ancestry of humans and chimps, requiring very small population bottlenecks over long periods of time, is also strongly inconsistent with the hypothesis of common descent on many levels, while being right in line with the hypothesis of original intelligent design with degenerative changes acting over subsequent periods of time.  

       But why would any intelligent designer deliberately design retroviral elements as part of the genomes of highly complex living things?  Aren't retroviral insertions almost always functionally detrimental?  Given that so many beneficial features are now known to be tied to these endogenous retroviral elements, that much of our genome is actually controlled by these elements, that we wouldn't be able to live without them, it seems much more likely that the original genome was in fact designed with these elements in place at the very beginning - that they have always been vital to the existence of humans, apes, and all other complex organisms.  However, as is always the case when complex reproductive machines or lines of code are subject to random mutations and natural selection, degenerative changes take place whereby parasitic elements are quickly realized through the loss of pre-existing complexities that used to control or modify their activities.   It is far more likely, therefore, that exogenous retroviruses that currently plague humanity (like HIV, HTLV-1, Hep-B, etc) where originally derived from endogenous retroviral sequences that suffered degenerative changes.  Like a cancer less that has escaped the normal systems of control and regulation, these exogenous viruses became "selfish" and parasitic, attacking and feeding off the host instead of contributing to the ideal function of the host. 

       There are many real time examples of such degenerative changes that result in parasitic functionality - such as the TTSS toxin injector system in bacteria that evolved through the loss of pre-existing structural elements from the rotary bacterial flagellum.  The TTSS system is now used by toxic bacteria - like the bacteria that cause Bubonic Plague or "Black Death" (Yersinia pestis).   Such are better referred to as devolutionary changes rather than evolutionary changes since they are based on a loss, rather than a true gain, of novel functional complexity.

        See also the following excellent Review Article on ERVs.

Armwaving evidence free opinionating. For an example of ongoing endogenization, BTW, go to  The Koala's Tale. 

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