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Endogenous Retroviruses: evidence of Evolution? Think again!

Endogenous Retroviruses (ERVS)

virus

virus (Photo credit: twenty_questions)

(Visit Who’s your Creator and Evolution Dismantled)

A Case for Common Descent or Another Evolutionary Blunder?

(Because research in regard to endogenous retroviruses has been heavily focused on human endogenous retroviruses (HERVs), many of the cited references include research pertaining exclusively to them.)

Research on ERVs has mostly produced inaccurate, inconsistent, and biased conclusions due to the presupposition that ERVs were originally dangerous viruses that somehow got embedded in germ cell (ones that can be inherited). In addition, most of the research has been spent on attempting to link them directly to disease as well attempting to prove that ERVs miraculously ‘evolved’ into essential genetic material.

Overview of the ERV Controversy

Evolutionists claim that a virulent strain of ancient viruses called retroviruses plagued vertebrates (and most non-vertebrates) as they evolved throughout time. After their initial outward communicable infection (exogenous), evolutionists also claim that these viruses were able to insert their DNA into their host’s germ cells, which are all sperm and egg related cells. Any viral DNA that integrates into the DNA of a host’s germ cell would be automatically passed down (inherited) to all offspring and that type of transmission and is called endogenous.
ERVs are considered ‘proviral,’ which means they a latent form of an original virus that can no longer replicate and infect. Because all ERVs lack and have different genetic material than that of exogenous retroviruses, evolutionists commonly refer to ERVs as “retrovirus-like elements” or “remnant sequences.”
ERV integration points within chromosomes are typically located at the identical position (loci) of related species. Evolutionists believe that integration sites are random upon insertion into the germline from exogenous retroviral infections and claim that those shared loci could only have occurred by common descent. This case of presupposition is why ERVs have been the poster child for biological evolution.

ERV 101

First, all viruses are complex parasites that cannot survive independently from a host cell. They act as delivery mechanisms that insert their viral genetic information into host cells, which is where they reside and reproduce:

  • “Viruses are nanomachines built within the cell factory and designed to invade neighboring cells. Their building relies on timely and dynamically regulated assembly of individual components, including nucleic acids, proteins, and lipids, in specific cell locations. Their invading strategies rely on complex interactions with the cell plasma membrane, involving several viruses and cellular proteins organized in dynamic complexes that are able to mediate viral penetration into the cell interior without rupturing the outside-inside plasma membrane frontier required for cell survival.”
    American Society for Microbiology, “Virus Entry, Assembly, Budding, and Membrane Rafts (CONCLUDING REMARKS AND PROSPECTS),” June 2003.
    http://mmbr.asm.org/cgi/content/full/67/2/226

What makes retroviruses particularly interesting is that they are the only viruses that have the ability to splice foreign genetic elements into the host cell as well as they are the only viruses whose genome consists of RNA that reverse transcribes to DNA. The steps of retroviral infection are:

  1. Virus attaches its surface proteins to host cell receptor proteins.
  2. RNA virus particle (virion) enters a host cell’s cytoplasm, where the protective coat of the virus is removed.
  3. Specialized enzymes called transcriptase transcribe viral RNA into a DNA viral molecule.
  4. Viral DNA molecule uses another specialized enzyme called integrase to enter the cell’s nucleus and fully integrates its viral DNA into the host cell DNA.
  5. Host cell machinery transcribes viral DNA molecule into RNA proteins or viral particles (virions).

For more information on retroviruses and reverse transcription:
http://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=rna%20virus&rid=mcb.section.1408#1436 
http://www.microbiologybytes.com/virology/Retroviruses.html 
http://pathmicro.med.sc.edu/flash/ltr-sl.htm
http://www.web-books.com/MoBio/Free/Ch1E3.htm
http://www.retrovirology.com/content/3/1/67

The number of ERVs in the human genome is over 100,000 and, depending on the research paper, they account for 1-10% of the DNA in most mammals. If you throw in all the fragmented ERV derivatives, about 50% of human DNA is comprised of ERV elements. Up until now, they have been mostly and erroneously thought of as useless ‘junk’ DNA that is disease related:

About 85-90% of ERV elements are promoter and enhancer elements called solitary long terminal repeats (solo LTRs). The remaining 10-15% represent genetic sequences typically known to identify ERVs (gag, pol and env genes flanked by two LTRs). Because ERV sequences differ and have less genetic material than exogenous sequences, evolutionists claim that mutations, deletions, and homologous recombination altered ERV sequences so that they are now considered only remnants of previous exogenous infections: 

  • “Most (85%) of the LTR retroposon-derived ‘fossils’ consist only of an isolated LTR, with the internal sequence having been lost by homologous recombination between the flanking LTRs …Finally, LTR retroposons appear to be teetering on the brink of extinction, if they have not already succumbed.”
    http://www.nature.com/nature/journal/v409/n6822/full/409860a0.html
  • “ERVs become defective over time due to frameshift or nonsense mutations introduced during host DNA replication or via recombinational deletion of the internal region to leave a solo LTR structure. Solo LTRs are approximately tenfold more abundant than their undeleted, full-length counterparts.”
    http://jvi.asm.org/cgi/content/full/79/19/12507
  • “Over time, replication-competent ERVs accumulate in-frame stop codons and frame-shift mutations as a result of host DNA replication and, within the human genome sequence, these processes have led to the inactivation of almost every element. Another mechanism by which ERVs are inactivated is via recombinational deletion between the two viral LTRs, which removes the internal region leaving a solo LTR structure. Solo LTRs are typically 10–100 times more numerous than their more intact, undeleted counterparts.”
    http://www.pnas.org/cgi/content/full/101/14/4894
  • “They are thought to be remnants of ancient germ line infections by exogenous retroviruses …The majority of these LTR elements, however, lack sequence similarity to retroviral genes within their internal region or constitute solitary LTRs. About 40 families identified so far have at least some members that show discernible homology to coding regions of retroviruses, but most of them have not yet been analyzed in depth.”
    http://jvi.asm.org/cgi/content/full/79/1/341
  • “Within the published human genome sequence, there are over 98,000 human endogenous retroviruses (HERVs), but all are defective, containing nonsense mutations or major deletions.”
    http://jvi.asm.org/cgi/content/full/79/19/12507
  • “Although HERVs have retained some similarity to their exogenous counterparts, they have acquired many mutations over the course of evolutionary time so that, with a few exceptions, they are now defective and incapable of producing protein.”
    http://genomebiology.com/2001/2/6/reviews/1017.1
  • “Moreover, none are intact; all have lethal mutations.”
    http://www.current-biology.com/content/article/abstract?uid=PIIS0960982201004559

Because ERVs were originally cast off as ‘junk’ DNA, evolutionary-based research was primary geared towards looking for how they might relate to disease. While no direct correlation was ever found, other research discovered that essential genetic material is directly attributed to ERVs. That’s when the confusion began:

  • “The evolutionary origin of viruses has long fascinated evolutionary biologists. Are they remnants of an ancestral lifestyle, or more recent escapees from traditional genomes?”
    http://genetics.plosjournals.org/perlserv/?request=get-document&doi=
    10.1371%2Fjournal.pgen.0010044
  • “Exogenous retroviruses may have originated from ERVs and ERV-Ls in particular may represent an intermediate between retrotransposons and exogenous viruses.” 
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=524511
  • “Where do virus-specific genes come from is a much harder question … This model implies that, at the early stages of evolution, including the LUCA stage, the entire genetic system was, in a sense, “virus-like” … Thus, viral comparative genomics seems to provide substantial support for the non-cellular model of early evolution.”
    http://www.biology-direct.com/content/1/1/29
  • “Technologies to interrogate the relationship between transcription factors and repetitive sequences are currently much limited. Most genomewide analyses of gene regulation, transcription factor binding sites, and other functional genomics, including the ENCODE project designed to catalog all sequence elements in 1% of the human genome, tend to ignore the functional aspect of repetitive elements. The results reported here suggest that it may be valuable to take a deeper look at the role of these elements in the evolution of gene regulatory networks.” 
    http://www.pnas.org/cgi/content/full/104/47/18613
  • “However, the activities (expression levels) of individual HERV sequences are mostly unknown …The data suggests that in many cases the retroviral sequence has been used as a building block for something else than retroviral proteins, for example human gene exons. However, for some HERVs there may be an alternative explanation: the retroviral transcripts may have RNA-mediated activities. We need to study the active elements more closely to discover the possible functions of retroviral transcripts.”
    http://www.biomedcentral.com/1471-2105/8/s2/s11
  • “These are endogenous viruses and some animal species have thousands of copies of these A-type viruses in their chromosomal DNA. Their function remains unknown.”
    http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.3287
  • “Their functions, if any, in the host remain an enigma, except for env genes driving differentiation of the syncytiotrophoblast in the placenta.” 
    http://www.retrovirology.com/content/3/1/67
  • “The expression of endogenous retroviruses and their control is not well understood.” 
    http://www3.niaid.nih.gov/labs/aboutlabs/lpvd/retroviralMolecularBiologySection/

FUNDAMENTAL PROBLEMS FOR ERVS BEING CONSIDERED GERMLINE INFECTIONS OF EXOGENOUS RETROVIRUSES INSTEAD OF INTRINSIC ESSENTIAL GENETIC MATERIAL

By Chance, How Did ERV Related Elements Insert Themselves into Germ Cells Thousands of Times Without Fatalistic Damage to the Host?

  • Genetic alterations to germ cells are rare and have been mostly found to harm overall genetic fitness, not improve it. What would make retroviruses an exception?
    “In short, the notion that molecules of germ cells … are in states of perpetual change is not, in our present understanding of cell biology, tenable. This doesn’t mean that “molecular change” does not occur; only that mechanisms provoking such change in germ cells are likely instantaneous and stochastic and probably often lethal (Maresca and Schwartz 2006) – which will preclude their persistence into future generations.”
    http://www.mitpressjournals.org/doi/abs/10.1162/biot.2006.1.4.357
  • Having healthy and strong germ cells is mandatory to produce a viable zygote, so why would harmful viral-infected egg/sperm cells be considered more fit (positive selection) versus ones without retroviral DNA?
  • Apoptosis is an accepted biological phenomenon, so why wouldn’t most germ cells with viral-infected DNA be eliminated?
    “Apoptosis, or programmed cell death, is a normal component of the development and health of multicellular organisms. Cells die in response to a variety of stimuli and during apoptosis they do so in a controlled, regulated fashion … The latter occurs when T-cells recognise damaged or virus infected cells and initiate apoptosis in order to prevent damaged cells from becoming neoplastic (cancerous) or virus-infected cells from spreading the infection.”
    http://www.sgul.ac.uk/depts/immunology/~dash/apoptosis/ 
    “Apoptosis occurs during the normal development of multicellular organisms and continues throughout adult life.”
    http://www.sgul.ac.uk/depts/immunology/%7Edash/apoptosis/disease.htm
  • Evolutionists claim that retroviruses were in a dormant cycle (lysogenic) upon insertion and were intact before mutations, deletions, and recombination deleted and disabled them. What prohibited the thousands of retroviruses from changing into an infectious cycle (lytic), thus weakening or killing the embryo (especially in hosts with long gestation periods) and weakening or killing young and adult hosts?
  • Why would populations with harmful viral-infected germ lines be under positive selection and become prevalent and “fixed” over non-infected populations? (The supposed ‘evolution’ of ERV elements changing into beneficial genetic material must be assumed to have occurred after fixation.)
  • Geneticists have problems with controlling retroviruses (vectors) for gene therapy, so how would ERV elements randomly invade healthy germ and somatic cells without damage, thus be eliminated by ‘purifying selection’?
    “Scientists have tried to take advantage of the virus’s biology and manipulate its genome to remove human disease-causing genes and insert therapeutic genes. However, viruses, while effective, introduce other problems to the body, such as toxicity, immune and inflammatory responses, and gene control and targeting issues.”
    http://www.genome.gov/10004764
  • There are at least 98,000 different ERVs sequences and 158,000 ERV-like elements just in the human genome. Why is it that only ERVs have supposedly invaded germ cells hundreds of thousands of times, but no other virus has been discovered to do the same?

How is it that ERVS are Considered Copies of Disease Producing Exogenous Retroviruses but None Have Been Proven to Directly Cause Disease?

  • “Whether other examples of pathogenic endogenous retroviruses will be found, particularly in the human, is unknown. Numerous reports of retroviral particles in human tumor specimens have not been verified. For now, it appears that few, if any, replication-competent human endogenous retroviruses capable of causing disease exist.”
    http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=cmed.section.4250
  • “HERVs have frequently been proposed as etiological cofactors in chronic diseases such as cancer, autoimmunity and neurological disease. Unfortunately, despite intense effort from many groups, there remains little direct evidence to support these claims, and moreover some studies have served only to muddy the waters for others.”
    http://genomebiology.com/2001/2/6/reviews/1017
  • “Retroviral activity might cause disease … although a causal role of HERVs in these conditions is highly uncertain.”
    http://www.biomedcentral.com/1471-2105/8/s2/s11 
  • “The causative or disease-promoting association of HERV protein expression with germ cell tumors, mammary carcinomas, various autoimmune diseases, and neurological disorders, such as schizophrenia, has yet to be conclusively demonstrated.”
    http://www.pnas.org/cgi/content/full/101/suppl_2/14572#REF65
  • “Although it is generally accepted that the integration of retroelements can cause significant harm by disrupting or disregulating essential genes, the role of HERV expression in the etiology of malignancies and autoimmune and neurologic diseases remains controversial.” 
    http://www.pnas.org/cgi/content/full/101/suppl_2/14572 
  • “Overall, while a number of articles highlight some steps in determining the role of HERVs, it will be crucial in the next few years to establish firmly clear associations of HERVs that may contribute to the pathology of disease states and/or aetiology “
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1809191 
  • “Tumor development is a multistep process in which both genetic and epigenetic events cooperate for the emergence of a malignant clone. The possibility that endogenous retroviruses promote the expansion of a neoplastic clone by subverting immune surveillance has been proposed, but remained elusive … Future work should now be aimed at the identification of a possible role of such genes in human tumorigenesis.”
    http://cancerres.aacrjournals.org/cgi/content/full/65/7/2588
  • “Many still manage to generate proteins, but scientists have never found one that functions properly in humans or that could make us sick.”
    http://www.newyorker.com/reporting/2007/12/03/071203fa_fact_specter 
  • “This illustrates that HERV expression is not automatically higher in malignant tissues.” 
    http://www.liebertonline.com/doi/abs/10.1089/aid.2006.22.551?
    cookieSet=1&journalCode=aid

By Chance, What Made ERVS Evolve from Being the Cause of Exogenous Infection into Elements that Resist Exogenous Infection?

By Chance, What Made ERV Elements Change From Viral Activities to Cellular Activities and Create New Essential Genes?

  • “Apart from detecting ERVs, the thesis demonstrates their expression in bovine tissue for the first time. It involves, moreover, a controlled expression and, therefore, valuable for the protection of the host. As shown in the thesis, this expression occurs mainly in the endocrine glands and in embryos, and so could be linked to the protection of the embryo.”
    Basque Research, “PhD Thesis Describes 35 Hitherto Unknown Families Of Endogenous Retroviruses, After Analysing Cattle And Horses,” December 1, 2010, Medical News Today.
    http://www.medicalnewstoday.com/articles/209622.php
  • “Conventional wisdom says that evolution is driven by small changes–point mutations–to the genetic code. If a change is beneficial, the mutation is passed onto future generations.
    Now it appears that another level of evolution occurs that is not driven by point mutations. Instead, retroviruses insert DNA sequences and rearrange the genome, which leads to changes in gene regulation and expression. If such a change in gene regulation is beneficial, it is passed onto future generations.”

    http://www.physorg.com/news114266805.html
  • “In some cases, transcription factor binding sites that interact with cell type-specific nuclear factors could be identified, demonstrating that the expression of HERVs is regulated in a complex and diverse manner comparable to cellular genes … Our data reveal that the activity of endogenous retroviruses is regulated differentially and is cell type specific, similar to normal gene regulation … Taken together, our findings suggest that HERVs behave like normal cellular genes and are a permanent component of the transcriptome of a cell.”
    http://jvi.asm.org/cgi/content/full/79/1/341
  • “It appears that each of the functioning genes was originally formed from mobile elements and that in some process of molecular evolution a coding sequence was derived that could be translated into a protein that is of some importance to human biology. In one case (AD7C), the coding sequence is 99% made up of a cluster of Alu sequences. In another example, the gene BNIP3 coding sequence is 97% made up of sequences from an apparent human endogenous retrovirus. The Syncytin gene coding sequence appears to be made from an endogenous retrovirus envelope gene … These observations contribute an additional bit to the growing mass of evidence that indicates that mobile elements/repeats are not always junk and have made important contributions to the “host.”
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=534736
  • Note that syncytin-1 is regulated differently in different tissues and at different times:
    “Syncytin-1 is a captive envelope glycoprotein encoded by one of human endogenous retroviruses W. It is expressed exclusively in the placental trophoblast where it participates in cell-to-cell fusion during differentiation of syncytiotrophobast. In other tissues, however, syncytin-1 expression must be kept in check because inadvertent cell fusion might be dangerous for tissue organization and integrity.”
    http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=
    PubMed&list_uids=16427621&dopt=Citation

How Could ERVS Create a Specie-Specific Regulatory Network that Controls the Expression of Cells in a Collective Manner?

  • “The ancient retroviruses–distant relatives of the human immunodeficiency virus (HIV)–helped a gene called p53 become an important “master gene regulator” in primates, according to a study published this week in the online early edition of Proceedings of the National Academy of Sciences … Scientists have long wondered how a master regulator such as p53 gained the ability to turn on and off a broad range of other genes related to cell division, DNA repair, and programmed cell death. How did p53 build its complex and powerful empire, so to speak.
    Using the tools of computational genomics, the UCSC team gathered compelling evidence that retroviruses helped out. ERVs jumped into new positions throughout the human genome and spread numerous copies of repetitive DNA sequences that allowed p53 to regulate many other genes, the team contends.
    Thus, p53 was crowned “guardian of the genome,” as biologists now call it. Its job is to coordinate the surveillance system that monitors the well-being of cells. Indeed, p53 is so important that when it fails, cancer often results. About half of all human tumors contain a mutated or defective p53 gene.”

    http://www.physorg.com/news114266805.html
  • “We report that human ERVs actively shape the p53 transcriptional network in a species-specific manner … At least one ERV insertion likely reshaped the transcriptional landscape of its surrounding genomic area and was instrumental in creating a new gene that became part of the human-specific p53 regulatory network … We discovered a unique distribution pattern of p53 sites within repetitive sequences of the human genome, and several ERV families emerged as being substantially enriched for p53 sites in their LTRs.”
    http://www.pnas.org/cgi/content/full/104/47/18613
  • “The reasons why genes are expressed when and where they are in the spatial domains of the developing organism are revealed in network “architecture,” that is, in the total aggregate pattern of regulatory linkages. Definitive regulatory functions emerge only from the architecture of intergenic linkages, and these functions are not visible at the level of any individual genes …
    Gene regulatory networks are inhomogeneous compositions of different kinds of subcircuits, each performing a specific kind of function. This concept is important, because it holds the key to network design principles.” 

    http://www.pnas.org/cgi/content/full/102/14/4935

By Chance, What Made Unrelated ERVS in Unrelated Species Create Almost the Same Gene (Convergent Evolution)?

  • “ERVWE1/Synctin-1 and ERVFRDE1/Syncytin-2 are specific to primates and thus do not exist in other placentae. However, this apparent endogenous retrovirus hihacking for placentation use is not restricted tot he primates. Indeed two unique endogenous envelope genes of retroviral origin have been found in the mouse, i.e. Syncytin-A and –B … Altogether the date strongly argue for convergent evolution of endogenous retroviral envelopes to serve for placentation in mammals.”
    http://atlasgeneticsoncology.org/Genes/ERVWE1ID40497ch7q21.html

By Chance, What Made Two Unrelated ERV LTRS Evolve Independently in Creating the Same Regulatory Roles for the Same Gene (Convergent Evolution)?

  • “We demonstrate that both the human and rodent neuronal apoptosis inhibitory protein (NAIP) genes, involved in preventing cell death, use different ERV sequences to drive gene expression. Moreover, in each of the primate and rodent lineages, two separate ERVs contribute to NAIP gene expression. This repeated ERV recruitment by NAIP genes throughout evolution is very unlikely to have occurred by chance. We offer a number of potential explanations, including the intriguing possibility that it may be advantageous for anti-cell death genes like NAIP to use ERVs to control their expression. These results support the view that not all retroviral remnants in our genome are simply junk DNA.”
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1781489#id2960616

By Chance, What Made ERV LTRS Immediately Turn into Essential Gene Regulators Upon Insertion?

By Chance, What Made LTRS Acquire Transcription Abilities for Essential Genes?

  • “Endogenous retrovirus (ERV) elements have been shown to contribute promoter sequences that can initiate transcription of adjacent human genes …
    These data illustrate the potential of retroviral sequences to regulate human transcription on a large scale consistent with a substantial effect of ERVs on the function and evolution of the human genome.”

    http://www.ncbi.nlm.nih.gov/pubmed/18535086
  • “Despite the general selection against ERVs near genes, the number of examples of promoters and enhancers derived from ERVs is steadily increasing. The evolutionary process of “exaptation” of noncoding functional elements from viruses and transposons to benefit the host is not well understood beyond a few examples.
    http://www.pnas.org/cgi/content/full/104/47/18613
  • “HERVs have been found to contribute physiologically in other human tissues. In particular the vast numbers of residual LTRs contain regulatory elements known as promoters, enhancers, silencers and polyadenylation signals that can specifically interact with the cellular expression of proteins. HERV-derived promoters have been found in roughly a quarter of all the human promoter regions so far examined. In many such instances, the viral promoter has only a minor function. However, in 2003, Dunn and colleagues demonstrated that an LTR of the ERV-L family is the dominant promoter of the gene responsible for the enzyme galactosyltransferase in the human colon and small intestine.31 Andersson and her colleagues have produced clear evidence for developmental and physiological roles for HERV-R (also known as ERV-3), showing that it is highly expressed in many human fetal tissues including adrenal cortex, kidney tubules, tongue, heart, liver and central nervous system as well as in the sebaceous glands of normal skin.”
    http://www.jrsm.org/cgi/content/full/97/12/560 
  • “Here, we describe mapping of transcriptional start sites within solitary and proviral LTRs of the HERV-K (HML-2) human-specific subfamily of endogenous retroviruses. Surprisingly, the transcription was initiated predominantly from the very 3¢ termini of the LTR R regions. The data presented here may shed light on adaptive coevolution of human endogenous retroviruses with their host cells.”
    http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WXR-
    4HRMTVY-1&_user=10&_rdoc= 1&_fmt=&_orig=search&_sort=d&view=c&_acct=
    C000050221&_version=1&_urlVersion=0&_userid=10&md5=
    9a8359dcf66d451223e17972617f87c3
  • “While both LTRs were shown to promote transcription in vivo and in vitro, their respective activity and tissue specificity appeared to differ even though they shared a high degree of sequence identity … The results from this study illustrate how slight variations in transcriptional regulatory sequences can have a profound effect on promoter activity and demonstrate the complex regulatory effects of human endogenous retrovirus elements on human gene expression.” 
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=164795
  • “By germline insertion, a long terminal repeat (LTR) of an intracisternal A-particle type IAP retrovirus has overtaken the transcriptional control of the rat oncomodulin (OM) gene, which codes for a high affinity Ca2+-binding protein with modulatory capacity.”
    http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WB5-4J3P0MR-5&_
    user=10&_origUdi=B6T39-4GXVG6Y-1&_fmt=high&_coverDate= 03%2F01%2F2006&_
    rdoc=1&_orig=article&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=
    db4a9ec49fd48c70f7bdbf5d97495bb0 

Where is the Proof that ERV LTRS can “Self-Replicate” and Why Don’t We See them Doing it Now?

By Chance, What Made the Same ERV Transcribe Differently Between Supposedly ‘Closely Related’ Species? 

  • “Based on analysis of finished BAC chimpanzee genome sequence, we characterize a retroviral element (Pan troglodytes endogenous retrovirus 1 [PTERV1]) that has become integrated in the germline of African great ape and Old World monkey species but is absent from humans and Asian ape genomes … Six out of ten of these genes, for which there are expression data, show significant differences in transcript expression between human and chimpanzee.”
    http://biology.plosjournals.org/perlserv/?request=get-document&doi=
    10.1371/journal.pbio.0030110&ct=1
  • “We report that human ERVs actively shape the p53 transcriptional network in a species-specific manner.”
    http://www.pnas.org/cgi/content/full/104/47/18613
  • “Most HERVs are active in at least some tissues, though tissue specificity is common for most elements. We analyzed multiple tissues from several Old World monkeys using retroviral pol-based DNA microarrays and quantitative PCR methods to determine their ERV expression profiles. The results demonstrate that while many ERVs are active in nonhuman primates, overall the tissue expression specificity is unique to each species. Most striking is that while the majority of HERVs analyzed in this study are expressed in human brain, almost none are expressed in Old World monkey brains or are only weakly expressed.”
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472034

By Chance, What Made the Same ERV Transcribe Differently Among Different Cell Types Within the Same Organism?

  • “Furthermore, there is evidence that transcription of at least some HERV families may be differentially regulated depending on the cell type. Characterization of promoter activities of HERV-K, HERV-H, HERV-E, ERV9, and HERV-W families, the most intensively studied HERVs, revealed specific cell type preferences for each HERV family, and even individual elements of one family showed significant variation in transcription pattern. In some cases, transcription factor binding sites that interact with cell type-specific nuclear factors could be identified, demonstrating that the expression of HERVs is regulated in a complex and diverse manner comparable to cellular genes.”
    http://jvi.asm.org/cgi/content/full/79/1/341

Where is the Evidence that Genetic Recombination Creates New Exogenous and Endogenous Retroviruses as well as Novel Beneficial Genetic Elements?

Why are there NO Examples of an ERV that Has Been Recently “Endogenized” or Examples of ERVS that Have A Direct Exogenous Counterpart? 

(Note: Go to “Examples of biased research/articles” regarding KORV Koala virus.)

If ERV Elements Deteriorate Rapidly, Why Did Only One ERV Remain Active and Continue to Infect All Placental Mammals Over a 70 Million Year Period? 

Evolutionists point to “lack of selection pressure” to explain why ERVs deteriorate rapidly, but then point to “bursts” of copy numbers when they need ERVs to be conserved:

  • “Southern blot analysis of a large series of mammalian genomic DNAs shows that HERV-L-related elements—so-called ERV-L—are present among all placental mammals, suggesting that ERV-L elements were already present at least 70 million years ago. … Phylogenetic analyses allowed the establishment of a plausible evolutionary scheme for ERV-L elements, which accounts for the high level of sequence conservation and the widespread dispersion among mammals … One rather striking feature of our results is the observation of a high level of sequence conservation among ERV-L elements. It is generally admitted that such sequence conservation is a common feature of functional genes, whereas noncoding sequences as well as pseudogenes diverge more rapidly, due to the lack of any selection pressure …
    Rather, a scheme in which sequence conservation is the unnecessary consequence of the transpositional activity of the transposable element itself (which requires both transcription activity and coding capacity), independent of any possible selective pressure imposed by the host, appears more plausible and would account for the data. According to this scheme, a functional sequence present in an ancestor of mammalian species would survive only if active, simply by generating a sufficiently high number of copies, so that despite the fact that such elements are submitted to genetic drift, as any pseudogene-like sequence, and also to elimination through transposon excision, there still remain functional copies of the founder element. Evidence for the transpositional activity of ERV-L elements is provided by the occurrence of bursts in both the primate and mouse branches, which resulted in large increases in ERV-L copy numbers.”

    http://jvi.asm.org/cgi/content/full/73/4/3301

Why Are Closely Related ERV Elements Found in Supposedly Non-Related Species?

  • “… and two closely related ERV genomes are found in a carnivore (fox) and a ruminant (sheep).”
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120 
  • “We have sequenced and characterized an endogenous type D retrovirus, which we have named TvERV(D), from the genome of an Australian marsupial, the common brushtail possum (Trichosurus vulpecula). Intact TvERV(D) gag, pro, pol, and env open reading frames were detected in the possum genome. TvERV(D) was classified as a type D retrovirus, most closely related to those of Old World monkeys, New World monkeys, and mice, based on phylogenetic analyses and genetic organization.” 
    http://jvi.asm.org/cgi/content/full/75/5/2499
  • “For instance gamma-retrovirus was isolated from trophoblastic cells of the baboon placenta. This virus was found 7o be very closely related antigenically and by sequence homology to the endogenous RD114 virus in cats (which is itself unrelated to endogenous FeLV). Benveniste and Todaro observed, like we did for jungle fowl, that only certain species of the cat genus, Felis, possessed this endogenous genome related to the baboon ERV. In contrast, all species of baboons carry this virus so it would appear to have been present in the germ line of primates much longer than in cats. Thus it seems evident that a horizontal, infectious event occurred to transfer the virus from baboons to cats, whereupon it became endogenous in the new species.”
    Note: Evolutionists make up ridiculous scenarios without any supporting evidence or proven genetic capabilities:
  • “Since cats would be quite likely to scavenge and feed on baboon placentae, a possible exposure to the virus can be envisioned.”
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120

If ERVS Are Intrinsic, Essential and Functional Genetic Elements, Why Wouldn’t Integration Sites Be identical?

Do ERV Elements Have Random Integration Sites? 

The premise that ERV integration would prove evolution to be true is purely based on presupposition, instead of objective research and empirical evidence. Random or non-random insertion (if it was the case) is impossible to conclude due to an utter lack of realistic testing. To replicate the supposed original insertion, the EXACT genetic sequence of the original integrated ERV must be inserted in closely several related species. This has never been done, nor is it plausible:

  • There are no exogenous retroviral counterparts of any ERV. Therefore, it is impossible to reconstruct a sequence from one that supposedly was degraded by deleterious mutations, deletions, recombination, and insertions of other repetitive elements.
  • Even if a precise ERV sequence was known, cloning techniques using vectors do not precisely replicate anything without problems:
    “Scientists have tried to take advantage of the virus’s biology and manipulate its genome to remove human disease-causing genes and insert therapeutic genes. However, viruses, while effective, introduce other problems to the body, such as toxicity, immune and inflammatory responses, and gene control and targeting issues.”
    http://www.genome.gov/10004764

What has the Presupposition of Evolutionary Science Done for Research on ERVS?

Evolutionists claim that creationists lack the ability to properly assess biological sciences due to their presupposition that God created life and that common descent is nonsense.
We submit that the opposite is true and that evolutionary-based presuppositions have resulted in a general lack of knowledge and a grievous hindrance in scientific research, discovery, and progress.
In this following quote, note that Francis Collins states, “It’s a radical concept, one that a lot of scientists aren’t very happy with …” Why in the world would any scientist NOT be excited by a new discovery? It’s because many evolutionists are so zealous in their belief of evolution, that they are angered and threatened by any contradictory evidence that might challenge any of its doctrine. How very pathetic …:

  • “‘It’s a radical concept, one that a lot of scientists aren’t very happy with,’ said Francis S. Collins, director of the National Human Genome Research Institute. ‘But the scientific community is going to have to rethink what genes are, what they do and don’t do, and how the genome’s functional elements have evolved.’
    ‘I think we’re all pretty awed by what we’re seeing,’ Collins said. ‘It amounts to a scientific revolution.’
    For half a century, the core concept in biology has been that every cell carries within its nucleus a full set of DNA, including genes. Each gene, in turn, holds coded instructions for assembling a particular protein, the stuff that keeps organisms chugging along.
    As a result, genes were assigned an almost divine role in biological ‘dogma,’ thought to govern not only such physical characteristics as eye color or hair texture, but even much more complicated characteristics, such as behavior or psychology. Genes were assigned blame for illness. Genes were credited for robust health. Genes were said to be the source of the mutations that underlay evolution.
    But the picture now emerging is more complicated, one in which illness, health, and evolutionary change appear to be the work of almost fantastical coordination between genes and swaths of DNA previously written off as junk.
    ‘If the surprising amount of RNA transcribed from genomic ‘junk’ proves to be a powerful regulator of genes, understanding it will be critical in the fight against genetic disease, medical researchers predict. A big push is underway, for example, to develop so-called ‘RNA interference’ drugs, designed to turn off gene activity by mimicking the effects of RNA.’
    ‘For medicine, it could be good news if disease is mainly caused by ‘regulators’ ” in the genome, not mutations in genes themselves,’ said Lander. ‘It suggests that [cures] might be a matter of tweaking the controls – turning them up here, dialing them down there. Nothing about the gene is broken, but the dial may be powered up too high or turned low.’”

    http://www.boston.com/news/globe/health_science/articles/2007/09/
    24/dna_unraveled/?page=4

The Difference Between Creation and Evolution Presupposition in ERV Research

We all have presuppositions that lead to biased thinking. In the area of ERV genetic research, almost all grants start with the presupposition that ERVs began as dangerous viruses, so the natural focus would be on the connection to disease.

Because creationists believe that all initial genetic elements were created good, their natural focus would be on the beneficial effects of ERVs.

It’s now obvious that the money would have been better spent using a creation presupposition. The 20-30 years of evolutionary biased research on ERVs (commonly referred to as ‘junk DNA’ by evolutionists) has proven to be one of evolution’s biggest blunders. Evolutionists have already begun to spin it and we can’t wait to hear their defense!

Misc. Examples of biased and inaccurate research and publications:

  • FeLVs were previously thought to activate certain harmful genes, but were later found non-related:
    “We have previously reported that the long terminal repeat (LTR) region of feline leukemia viruses (FeLVs) can enhance expression of certain cellular genes such as the collagenase IV gene and MCP-1 in trans (S. K. Ghosh and D. V. Faller, J. Virol. 73:4931–4940, 1999)…
    Unlike their exogenous FeLV counterparts, neither nearly full-length endogenous FeLV molecular clones (CFE-6 and CFE-16) nor their isolated LTRs were able to activate collagenase IV gene or MCP-1 expression in transient transfection assays … Endogenous, nonleukemogenic FeLV LTRs, therefore, do not transactivate cellular gene expression, and this property appears to be specific to exogenous, leukemogenic FeLVs.”

    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=112408
  • Outdated and unproven theories continue to be cited by current research papers:
    (Note that the papers are from 1967, 1969, and 1973 respectively.)
    “Many endogenous retroviruses do not readily re-infect their own host cells but can infect other species in vitro or in vivo. Thus the endogenous ALV of chickens infects cells of quail, pheasants and turkey more readily than the chicken [22,23]. Jay Levy studied New Zealand black mice with auto-immune disease and discovered an endogenous MLV strain that could infected human and rat cells but not murine cells. He coined the term ‘xenotropic’ for viruses that only infect foreign species [68] in contrast to ‘ecotropic’ and ‘amphotropic’ strains. Thus the reservoir of infection may be a DNA provirus in the chromosomes of one species while the virus produced from it may infect other species.”
    http://www.retrovirology.com/content/3/1/67
  • Classifications of ERV elements included mixing up rabbit ERVs with human ERVs:
    “RERV-H is a recently identified retro-element of rabbits that was originally thought to be an exogenous human retrovirus, denoted HRV-5 (Griffiths et al., 2002Down). Currently, it is unknown how RERV-H sequences came to be present in human DNA preparations. Laboratory contamination would be one obvious mechanism but cannot explain several observations, notably its disproportionate detection in autoimmune diseases and cancer (Rigby et al., 1998Down; Brand et al., 1999Down; Griffiths et al., 1999Down; Murovska et al., 2000Down; Kozireva et al., 2001Down), and its detection by RT-PCR in tissue homogenates separated by sucrose gradient centrifugation (Griffiths et al., 1997Down).”
    http://vir.sgmjournals.org/cgi/content/full/84/1/215
  • Research papers consistently exaggerate their findings:
    Title of research article: “Evidence for genomic rearrangements mediated by human endogenous retroviruses during primate evolution.”
    Text: “Although repeated sequence elements such as HERVs have the potential to lead to chromosomal rearrangement through homologous recombination between distant loci, evidence for the generality of this process is lacking … Here we show, by phylogenetic and sequence analysis, that at least 16% of these elements have undergone apparent rearrangements that may have resulted in large-scale deletions, duplications and chromosome reshuffling during the evolution of the human genome.” 
    http://www.ncbi.nlm.nih.gov/pubmed/11704760?ordinalpos=1&itool=EntrezSystem2.PEntrez.
    Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus
  • Endless claims with no absolutely no evidence to substantiate them:
    “As active agents, repeats have reshaped the genome by causing ectopic rearrangements, creating entirely new genes, modifying and reshuffling existing genes, and modulating overall GC content.” 
    http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0030110&ct=1
  • Researchers attempt to clone ERV sequences, which ‘reactivate’ them by using foreign vectors. However, vectors only produce active viral particles of an imprecise ERV sequence, so it’s back to square one. Here is a little insight on the utter confusion of interpreting cloned ERVsequences:
    “The EAV-HP clones have an env region related to EAV-E51, while part of the LTR and the gag region are identical to those of ART-CH and EAV-E13. EAV-E51 and related clones were previously designated as a subfamily of the EAV-0 family. The relationship among the EAV-0 elements and the related E51, E13, and E33 clones, as well as EAV-HP clones reported here, suggests that these elements would best be regarded as members of one family of ERVs, designated EAV. There were two recent reports suggesting the existence of new endogenous elements in the chicken genome with close sequence identity to the ALV-J env. Although the env sequences of these elements initially published are identical to that of EAV-HP, the authors have designated these elements as a new family of endogenous viruses called ev/J. To avoid the confusion of assigning different names for the same elements, there is a need to systematically look at the characteristics of the different endogenous elements to devise a universal system of nomenclature for these elements.”
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?&pubmedid=10627540
  • The persistent use of erroneous dating techniques is based on unproven data:
    Example: “Mutation rates for each element were estimated independently for each HERV-K locus. First, pairwise distances were calculated using the Kimura two-parameter correction in the PAUP*4.0b program for all homologous sequence pairs among the species for which sequence information was available. Each distance was then divided by the years since the two species in each pair shared a last common ancestor on the basis of accepted primate divergence dates (GOODMAN et al. 1998). These were then averaged to obtain a mutation rate for each HERV-K locus (substitutions per site per year). Next, the divergences between the two LTRs of each element were calculated. The corrected distances between the 5′ and 3′ LTR sequences of each element within species were averaged to obtain LTR divergence values (substitutions per site) for each element. The LTR divergence value was then divided by the mutation rate to give the integration time estimate for each HERV-K element.”
    http://www.genetics.org/cgi/content/full/171/3/1183
    The truth about ‘molecular clock’ adjustments:
    “The high frequency of these events casts doubt on the accuracy of integration time estimates based only on divergence between retroelement LTRs.” 
    http://www.genetics.org/cgi/content/full/171/3/1183 
    “Review of the history of molecular systematics and its claims in the context of molecular biology reveals that there is no basis for the “molecular assumption.””
    http://www.mitpressjournals.org/doi/abs/10.1162/biot.2006.1.4.357 
    “For more than two decades, biologists have used mitochondrial DNA to peer into the past, to time the divergences of organisms from each other, and to map human migrations. Now a wash of sequence data reveals that in many cases, the main assumption underlying this “molecular clock” doesn’t hold up: The clock ticks at different rates in different lineages and at different times.” 
    http://www.sciencemag.org/cgi/content/summary/283/5407/1435
    “For more than two decades, biologists have used mitochondrial DNA to peer into the past, to time the divergences of organisms from each other, and to map human migrations. Now a wash of sequence data reveals that in many cases, the main assumption underlying this “molecular clock” doesn’t hold up: The clock ticks at different rates in different lineages and at different times.”
    http://www.sciencemag.org/cgi/content/summary/283/5407/1435
  • This entire paper is an example of research based upon admitted rough estimations, admitted bias, admitted difficult evaluations, admitted unrealistic comparisons, and admitted lack of data. Yet, it presents conclusions as if they are factual:
    http://mbe.oxfordjournals.org/cgi/content/full/20/4/528

ERVs are Functional

If ERVs are found to have function, it would be highly likely that they didn’t originate from retroviruses. It would be inconceivable that viral non-functional ERVs somehow became functional. Evidence has surfaced that they do have function.

“We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1,743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5′ untranslated regions (UTRs).”[1]

“Now it appears that another level of evolution occurs that is not driven by point mutations. Instead, retroviruses insert DNA sequences and rearrange the genome, which leads to changes in gene regulation and expression. If such a change in gene regulation is beneficial, it is passed onto future generations.”[2]

The previous quote is very telling. There are many thousands of ERV sequences in our genome and in that of chimps. Does this mean that all are beneficial?

“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.”[3]

As we can see, it has been discovered that ERVs aid transcription in one fifth of the human genome!

“The ancient retroviruses … helped a gene called p53 become an important “master gene regulator” in primates. …the UCSC team gathered compelling evidence that retroviruses helped out. ERVs jumped into new positions throughout the human genome and spread numerous copies of repetitive DNA sequences that allowed p53 to regulate many other genes, the team contends. … Thus, p53 was crowned “guardian of the genome,” as biologists now call it. Its job is to coordinate the surveillance system that monitors the well-being of cells. Indeed, p53 is so important that when it fails, cancer often results. About half of all human tumors contain a mutated or defective p53 gene.”[4]

“We report that human ERVs actively shape the p53 transcriptional network in a species-specific manner … At least one ERV insertion likely reshaped the transcriptional landscape of its surrounding genomic area and was instrumental in creating a new gene that became part of the human-specific p53 regulatory network … We discovered a unique distribution pattern of p53 sites within repetitive sequences of the human genome, and several ERV families emerged as being substantially enriched for p53 sites in their LTRs.” [5]

“Taken together, our findings suggest that HERVs behave like normal cellular genes and are a permanent component of the transcriptome of a cell.”[6]

One scientist said about junk DNA, of which ERVs are all part:

“The failure to recognize the full implications of this – particularly the possibility that the intervening noncoding sequences may be transmitting parallel information … may well go down as one of the biggest mistakes in the history of molecular biology.”[7]

Apoptosis
Because ERVs have function, it is implausible that they are the product of retroviruses. And there is more evidence to back up this idea. Apoptosis is a process of the body that kills infected cells – ERV-infected cells included. If ERVs really were introduced by retroviruses, we should expect apoptosis to have ridden them long ago. The fact that we have so many ERVs indicates that they could not possibly have come about as a result of retroviruses – apoptosis should have ridden most, if not all, of the cells.

“Apoptosis, or programmed cell death, is a normal component of the development and health of multicellular organisms. Cells die in response to a variety of stimuli and during apoptosis they do so in a controlled, regulated fashion. The latter occurs when T-cells recognize damaged or virus infected cells and initiate apoptosis in order to prevent damaged cells from becoming neoplastic (cancerous) or virus-infected cells from spreading the infection.”[8]

Because apoptosis would kill ERV-containing cells, why is it that we still have ERVs hundreds of thousands of years after supposedly being inserted by retroviruses?

The evidence points to the idea that ERVs didn’t come from retroviruses. But if they are not the product of retroviruses, why is the positioning of many human ERVs so similar to the positioning of chimp ERVs? The answer seems to be in the overall similarity of the human and chimp genomes: since our DNA is 93.7 — 95% similar[9, 10, 11] to chimps, most ERVs should be in similar spots.

Similar ERVs in Unrelated Organisms
Another problem for the typical evolutionary explanation is that very similar ERVs exist in unrelated animals.

“… and two closely related ERV genomes are found in a carnivore (fox) and a ruminant (sheep).”[12]

“We have sequenced and characterized an endogenous type D retrovirus, which we have named TvERV(D), from the genome of an Australian marsupial, the common brushtail possum (Trichosurus vulpecula). Intact TvERV(D) gag, pro, pol, and env open reading frames were detected in the possum genome. TvERV(D) was classified as a type D retrovirus, most closely related to those of Old World monkeys, New World monkeys, and mice, based on phylogenetic analyses and genetic organization.”[13]

“For instance gamma-retrovirus was isolated from trophoblastic cells of the baboon placenta. This virus was found to be very closely related antigenically and by sequence homology to the endogenous RD114 virus in cats (which is itself unrelated to endogenous FeLV). Benveniste and Todaro observed, like we did for jungle fowl, that only certain species of the cat genus, Felis, possessed this endogenous genome related to the baboon ERV. In contrast, all species of baboons carry this virus so it would appear to have been present in the germ line of primates much longer than in cats. Thus it seems evident that a horizontal, infectious event occurred to transfer the virus from baboons to cats, whereupon it became endogenous in the new species.”[14]

How do the authors “explain” this?

“Since cats would be quite likely to scavenge and feed on baboon placentae, a possible exposure to the virus can be envisioned.”[14]

This is hopeful imagination at best!

More Problems
It is interesting to note that ERVs are different than the retroviral genomes from which they are supposed to have originated. Evolutionists usually explain this away by claiming that the ERV sequences have evolved to the point where they are quite different from their ancestral genomes. If this is so, then there is consequently very little to lead us to the conclusion that ERVs are derived from retroviruses!

If ERVs really are a product of retroviruses, how could they have been inserted into reproductive cells thousands of times without fatal damage to the host? Having healthy and strong reproductive cells is mandatory to produce a viable zygote, so why would viral-infected reproductive cells be considered more fit than ones without ERVs? Furthermore, how could they survive for hundreds of thousands of years in two different species? It is quite incredible.

Changes to the reproductive cells are rare and often harm the animal. So why should we believe that ERVs were inserted many thousands of times?

“In short, the notion that molecules of germ cells … are in states of perpetual change is not, in our present understanding of cell biology, tenable. This doesn’t mean that “molecular change” does not occur; only that mechanisms provoking such change in germ cells are likely instantaneous and stochastic and probably often lethal (Maresca and Schwartz 2006) — which will preclude their persistence into future generations.”[15]

How could it be that unrelated ERVs in different species created essentially the same gene?

“ERVWE1/Syncytin-1 and ERVFRDE1/Syncytin-2 are specific to primates and thus do not exist in other placentae. However, this apparent endogenous retrovirus hijacking for placentation use is not restricted to the primates. Indeed two unique endogenous envelope genes of retroviral origin have been found in the mouse, i.e. Syncytin-A and –B … Altogether the data strongly argue for convergent evolution of endogenous retroviral envelopes to serve for placentation in mammals.”[16]

One may argue that convergent evolution is the answer, as the author did, but this explanation has no real scientific basis. Convergent evolution is only ever used to explain similarities between organisms that are otherwise unrelated. But then why shouldn’t we consign other ‘proof-of-evolution’ similarities to convergent evolution?

Conclusion:

The word ‘virus’ means toxic or poison, and that is how most evolutionists perceive them. However, if 50% of our DNA is made up viral elements, wouldn’t that indicate that they might be essential genetic elements and that these viral elements just might be another regulatory network in organisms? This is just another case why evolutionary-based science is a menace to scientific research, discovery, and progress http://whoisyourcreator.com/evolution_menace.html

In summary, a very strong case can be made pointing to the view that ERVs were not inserted by retroviruses. They have function, should have been ridden by apoptosis, are different than their ancestral genomes, and it is incredible that the organisms did not die after being infected with so many viral genes. With so many problems, how can evolutionists continue to use ERVs as evidence for evolution?

God Bless! Deus te abençoe!

References

 

1.Conley, A.B., Piriyapongsa, J. and Jordan, I.K., “Retroviral promoters in the human genome,” Bioinformatics 24(14):1563, 2008.
2.”Ancient Retroviruses Spurred Evolution Of Gene Regulatory Networks In Humans And Other Primates,” ScienceDaily, University of California – Santa Cruz, Nov. 15, 2007. http://www.physorg.com/news114266805.html

3.Conley, A.B., Piriyapongsa, J. and Jordan, I.K., Reference 1.

4.”Ancient Retroviruses Spurred Evolution Of Gene Regulatory Networks In Humans And Other Primates,” ScienceDaily, University of California – Santa Cruz, Nov. 15, 2007. http://www.physorg.com/news114266805.html

5. Ting Wang, Jue Zeng, Craig B. Lowe, Robert G. Sellers, Sofie R. Salama, Min Yang, Shawn M. Burgess, Rainer K. Brachmann, and David Haussler, edited by Eric H. Davidson, “Species-specific endogenous retroviruses shape the transcriptional network of the human tumor suppressor protein p53,” PNAS, November 20, 2007 vol. 104 no. 47 18613-18618. http://www.pnas.org/cgi/content/full/104/47/18613

6. Wolfgang Seifarth, Oliver Frank, Udo Zeilfelder, Birgit Spiess, Alex D. Greenwood, Rüdiger Hehlmann, and Christine Leib-Mösch (author contributions), “Comprehensive Analysis of Human Endogenous Retrovirus Transcriptional Activity in Human Tissues with a Retrovirus-Specific Microarray,” Journal of Virology, January 2005 vol. 79 no. 1 341-352. http://jvi.asm.org/cgi/content/full/79/1/341

7. Mattick, J., cited in: Gibbs, W.W., “The Unseen Genome: Gems Among the Junk,” Scientific American, 289(5):26–33, November 2003; pp. 29–30.
8. Reproductive and Cardiovascular Disease Research Group. http://www.sgul.ac.uk/depts/immunology/~dash/apoptosis/

9. Nature, May 27, 2004, pp. 382-388.

10.New Scientist News Service 23 September 2002.

11. The Washington Post, Monday, September 30, 2002, A7.

12. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120

13.Gregory J. Baillie and Richard J. Wilkins, “Endogenous Type D Retrovirus in a Marsupial, the Common Brushtail Possum (Trichosurus vulpecula),” Journal of Virology, March 2001 vol. 75 no. 5 2499-2507. http://jvi.asm.org/cgi/content/full/75/5/2499

14. Robin A Weiss, “The discovery of endogenous retroviruses,” Retrovirology, 2006; 3: 67. Published online 2006 October 3. doi: 10.1186/1742-4690-3-67. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120

15. http://www.mitpressjournals.org/doi/abs/10.1162/biot.2006.1.4.357 (The quote seems to have disappeared since we first took it from this address.)

16. Gimenez J, Mallet F., “ERVWE1 (Endogenous Retroviral family W, Env(C7), member 1),”Atlas Genet Cytogenet Oncol Haematol, September 2007. http://AtlasGeneticsOncology.org/Genes/ERVWE1ID40497ch7q21.html

17. Jennifer F. Hughes and John M. Coffin, “Human Endogenous Retroviral Elements as Indicators of Ectopic Recombination Events in the Primate Genome,” Genetics, November 2005 vol. 171 no. 3 1183-1194. http://www.genetics.org/cgi/content/full/171/3/1183

18. Hughes JF, Coffin JM, “Evidence for genomic rearrangements mediated by human endogenous retroviruses during primate evolution,” Nature Genetics, 2001 Dec;29(4):487-9. http://www.ncbi.nlm.nih.gov/pubmed/11704760?ordinalpos=1&itool=EntrezSystem2PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus

19. C. Vitte and O. Panaud, “Formation of Solo-LTRs Through Unequal Homologous Recombination Counterbalances Amplifications of LTR Retrotransposons in Rice Oryza sativa L.,” Molecular Biology and Evolution (2003) 20 (4): 528-540. First published online: March 5, 2003. http://mbe.oxfordjournals.org/cgi/content/full/20/4/528

One response to “Endogenous Retroviruses: evidence of Evolution? Think again!

  1. sdf May 3, 2016 at 03:18

    You could definitely see your enthusiasm in the work you write.
    The arena hopes for more passionate writers such
    as you who aren’t afraid to say how they believe.
    Always go after your heart.

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