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Are ERV's evidence for common ancestry ?

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1 Are ERV's evidence for common ancestry ? on Tue Mar 25, 2014 5:19 pm

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Why would functionality negate endogenization? Why do retroviruses form syncytia? What are reverse transcriptase and integrase doing in ERVs? What are they for?


Well, here are some notes: The definitive response on ERV’s and Creation, with Dr. Jean Lightner



Refutation Of Endogenous Retrovirus - ERVs - Richard Sternberg, PhD Evolutionary Biology

http://www.metacafe.com/watch/4094119

Sternberg, R. v. & J. A. Shapiro (2005) How repeated retroelements format genome function. Cytogenet. Genome Res. 110: 108-116

Endogenous retroviruses regulate per iimplantation placental growth and differentiation - 2006 http://www.pnas.org/content/103/39/14390.abstract.

Retrovirus in the Human Genome Is Active in Pluripotent Stem Cells - Jan. 23, 2013

Excerpt:

"What we've observed is that a group of endogenous retroviruses called HERV-H is extremely busy in human embryonic stem cells," said Jeremy Luban, MD, the David L. Freelander Memorial Professor in HIV/AIDS Research, professor of molecular medicine and lead author of the study. "In fact, HERV-H is one of the most abundantly expressed genes in pluripotent stem cells and it isn't found in any other cell types.

http://www.sciencedaily.com/releases/2013/01/130123133930.htm

Transposable Elements Reveal a Stem Cell Specific Class of Long Noncoding RNAs - (Nov. 26, 2012)

Excerpt:

The study published by Rinn and Kelley finds a striking affinity for a class of hopping genes known as endogenous retroviruses, or ERVs, to land in lincRNAs. The study finds that ERVs are not only enriched in lincRNAs, but also often sit at the start of the gene in an orientation to promote transcription. Perhaps more intriguingly, lincRNAs containing an ERV family known as HERVH correlated with expression in stem cells relative to dozens of other tested tissues and cells. According to Rinn, "This strongly suggests that ERV transposition in the genome may have given rise to stem cell-specific lincRNAs. The observation that HERVHs landed at the start of dozens of lincRNAs was almost chilling; that this appears to impart a stem cell-specific expression pattern was simply stunning!"

http://www.sciencedaily.com/releases/2012/11/121125192838.htm

Retroviruses and Common Descent: And Why I Don’t Buy It - September 2011

Excerpt: If it is the case, as has been suggested by some, that these HERVs are an integral part of the functional genome, then one might expect to discover species-specific commonality and discontinuity. And this is indeed the case.

http://www.uncommondescent.com/evolution/retroviruses-and-common-descent-and-why-i-dont-buy-it/

Some (inconsistencies) ERVs that don't fit into the naturalistic evolutionary assumption of common descent: PTERV1 in chimpanzee, African great apes and old World monkeys but not in humans and asian apes (orangutan, siamang, and gibbon).

http://www.sciencedaily.com/releases/2005/03/050328174826.htm

Conservation and loss of the ERV3 open reading frame in primates.

http://www.ncbi.nlm.nih.gov/pubmed/15081124

ERV3 sequences were amplified by PCR from genomic DNA of great ape and Old World primates but not from New World primates or gorilla, suggesting an integration event more than 30 million years ago with a subsequent loss in one species. From ancestral infectious retroviruses to bona fide cellular genes: role of the captured syncytins in placentation.

http://www.ncbi.nlm.nih.gov/pubmed/22695103

We focus on the recent discovery of genes derived from the envelope glycoprotein-encoding (env) genes of endogenous retroviruses that have been domesticated by mammals to carry out an essential function in placental development… Remarkably, the capture of syncytin or syncytin-like genes, sometimes as pairs, was found to have occurred independently from different endogenous retroviruses in diverse mammalian lineages such as primates–including humans–, muroids, leporids, carnivores, caviids, and ovis, between around 10 and 85 million years ago. Retroviruses push the envelope for mammalian placentation

http://www.pnas.org/content/109/7/2184.

short Domestication of the syncytin genes represents a dramatic example of convergent evolution via the cooption of a retroviral gene for a key biological function in reproductive biology. In fact, syncytin domestication from a retroviral envelope gene has been previously shown to have independently occurred at least seven times during mammalian evolution… Based on this data, certain cases of widespread and similar retroviral genes are attributed to convergent evolution. Many more cases of anomalous ERVs

http://www.uncommondescent.com/intelligent-design/life-project-architecture/#comment-449621

Interestingly, it seems these ERVs are ordered by usefulness in placental function, and not by common descent. This is a phenomenon predicted by common design. The Human Lineage Was Somehow “Purged”

- Cornelius Hunter - April 2012

Excerpt: Another such feature is the lack of endemic infectious retroviruses in humans. The problem is that these viruses are present in the other primates, and so according to evolutionists these viruses must be present in their common ancestor which, again according to evolution, would be an ancestor of humans as well.,, In other words, when evolution spontaneously created humans our DNA must have been “purged.” We got a do-over! Hilarious.

http://darwins-god.blogspot.com/2012/04/unbelievableevolution-in-complete-free.html


More Counterpoints on ERVs - JonathanM -

May 2011 Excerpt:

'In the absence of a feasible naturalistic mechanism to account for how evolution from a common ancestor could have occurred, how can we be so sure that it did occur? In such a case, one ought to reasonably expect there to be some quite spectacular evidence for common ancestry. Unfortunately for Darwinists, however, the evidence for common ancestry is paper thin on the ground.'

http://www.evolutionnews.org/2011/05/more_points_on_ervs046761.html


there are many studies suggesting non-random and preferential positioning of retrovirus sequences. This kind of data refutes the claims of re-used ERV sites having to be an ‘amazing coincidence’ if not by common descent. Perpetually mobile footprints of ancient infections in human genome

http://www.sciencedirect.com/science/article/pii/S0014579398004785


Although not available for HERVs at this point, the results for other retroelements demonstrate that transcriptionally active genome regions might be preferred targets for retrovirus integration and that the site selection during retroposition can be influenced by many factors A good example of retroelement–host interaction gives the study of de novo insertions of Ty1 and Ty3 yeast retrotransposons that are analogues of endogenous retroviruses. Most of the integration sites were found clustered upstream of the genes transcribed by RNA polymerase III. There were identified `hot spots’ containing integration sites used up to 280 times more frequently than predicted mathematically. A recent study of the de novo retroviral integration demonstrated also preference for scaffold- or matrix-attachment regions (S/MARs) flanked by DNA with high bending potential. Integration specificity of the hobo element of Drosophila melanogaster is dependent on sequences flanking the integration site

http://link.springer.com/article/10.1023%2FA%3A1003712619487


We analyzed the integration specificity of the hobo transposable element of Drosophila melanogaster. Our results indicate that hobo is similar to other transposable elements in that it can integrate into a large number of sites, but that some sites are preferred over others, with a few sites acting as integration hot spots. Large-scale discovery of insertion hotspots and preferential integration sites of human transposed elements

http://nar.oxfordjournals.org/content/38/5/1515.full

We first discovered that most TEs insert within specific ‘hotspots’ along the targeted TE… Finally, we performed a global assessment to determine the extent to which young TEs tend to nest within older transposed elements and identified a 4-fold higher tendency of TEs to insert into existing TEs than to insert within non-TE intergenic regions. Our analysis demonstrates that TEs are highly biased to insert within certain TEs, in specific orientations and within specific targeted TE positions. TE nesting events also reveal new characteristics of the molecular mechanisms underlying transposition. Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0020234

Chromosomal regions rich in expressed genes were favored for HIV integration, but these regions were found to be interleaved with unfavorable regions at CpG islands. MLV vectors showed a strong bias in favor of integration near transcription start sites, as reported previously. ASLV vectors showed only a weak preference for active genes and no preference for transcription start regions. Thus, each of the three retroviruses studied showed unique integration site preferences, suggesting that virus-specific binding of integration complexes to chromatin features likely guides site selection. ERVs are known to have highly targeted insertion points, even in different species, in separate infections. -



Integration of retroviral vectors - 2012

http://www.sciencedirect.com/science/article/pii/S095279151200129X

Several members of the retrovirus family show distinct pattern for preferential integration into the host genome. Despite many years of investigation, precise mechanisms of target site selection and the fundamental interplay of viral integrase and host cell proteins are still unknown. Excellent article for addressing the ERV argument for human evolution. http://evolutiondismantled.com/ervs Endogenous Retroviruses (ERVs)

http://www.detectingdesign.com/pseudogenes.html#Endogenous Endogenous Retroviruses (ERVS)

A Case for Common Descent or A Case for Incorrect Presupposition?

http://www.whoisyourcreator.com/endogenous_retroviruses.html

Evolution or Creation - WHAT'S ERVs GOT TO DO WITH IT? -



The definitive response on ERV's and Creation, with Dr. Jean Lightner and Wazooloo



Last edited by Admin on Sun Jul 13, 2014 10:32 am; edited 1 time in total

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http://www.uncommondescent.com/evolution/retroviruses-and-common-descent-and-why-i-dont-buy-it/

The second point worthy of note is that it shouldn’t surprise us that ERV elements can be found occupying the same genetic loci across multiple taxa. This is indicative of the specificity of the target site preference. Such target sites might exist by virtue of the fact that they are most conducive to their successful reproduction (e.g. the necessitude for expression of the ERV’s regulatory elements; the activity of the host’s DNA correction system, etc). Mitchell et al. (2004) suggest “that virus-specific binding of integration complexes to chromatin features likely guides site selection.”

I asked evolutionary biologist Richard Sternberg about his take on the ERV question. He wrote back to me,

Now, the story that these seemingly defunct retroviruses provide compelling evidence for common descent on the one hand, and support for the notion of non-designed junk on the other, is based on an interpretation that is almost thirty years old and contradicted by recent data. For one thing, ERVs are markedly taxon-specific and they all have non-random chromosomal distributions. The mouse and rat have different ERV families and yet many of them occupy similar genomic sites. This is explained by the insertion machineries having preferences for specific DNA targets or chromatin profiles. So while one can find some retroviral sequences occupying a position shared between by two species, it cannot be ruled out that such similarity is due to constraints on integration. In yeast, for example, the ERV Ty repeatedly inserts into the promoters of transfer RNA genes. And human and mouse “jumping genes” such as Alu and B1/B2, respectively, are not homologous and yet thay have the same linear pattern of placement. Such genomic profiles look like inherited accidents from afar but close inspection reveals that they are independent events. Appearances can be deceiving.

In 2001, Barbulescu et al. identified ten different HERV-Ks in the human genome. Eight of them were unique to the human genome. Intriguingly, a ninth HERV-K was detected in the human, chimpanzee, bonobo and gorilla genomes, but not in the orang-utan genome. The tenth was found in humans, chimpanzees and bonobos. They also reported,

We identified a human endogenous retrovirus K (HERV-K) provirus that is present at the orthologous position in the gorilla and chimpanzee genomes, but not in the human genome. Humans contain an intact preintegration site at this locus. These observations provide very strong evidence that, for some fraction of the genome, chimpanzees, bonobos, and gorillas are more closely related to each other than they are to humans. [emphasis added]

Could this be evidence for a site-specific target bias rather than common ancestry?

A recent study by Spradling et al. (2011) documented Drosophila P elements preferentially transpose to replication origins. They report,

P element insertions preferentially target the promoters of a subset of genes, but why these sites are hotspots remains unknown. We show that P elements selectively target sites that in tissue-culture cells bind origin recognition complex proteins and function as replication origins.

Summary & Conclusion


In summary, the stupendous claim that there is overwhelming evidence that humans and chimpanzees have common ancestry is an overstatement. The arguments for common ancestry based upon shared ERV elements needs to be considered in the context of other evidence as well (such as that from embryology), which clearly militates against the paradigm of common descent. And then there is still the lack of any feasible naturalistic evolutionary mechanism which can account for the complexity of life. When all the facts are in, I am inclined to be very skeptical of not just the claims of neo-Darwinism to be able to explain all of life, but also that the observed molecular patterns are robust evidence for the common ancestry model. If it is the case, as has been suggested by some, that these HERVs are an integral part of the functional genome, then one might expect to discover species-specific commonality and discontinuity. And this is indeed the case.





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3 Re: Are ERV's evidence for common ancestry ? on Sat Jul 12, 2014 12:18 pm

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http://whoisyourcreator.com/topics/endogenous-retroviruses-ervs/

Endogenous Retroviruses (ERVS)
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:

Virus attaches its surface proteins to host cell receptor proteins.
RNA virus particle (virion) enters a host cell’s cytoplasm, where the protective coat of the virus is removed.
Specialized enzymes called transcriptase transcribe viral RNA into a DNA viral molecule.
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.
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:

“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.”
http://www.physorg.com/news114266805.html
“Initially, HERVs and other retroelements were studied almost exclusively as a potential cause of disease.”
http://www.pnas.org/cgi/content/full/101/suppl_2/14572#REF65
“Because they no longer seem to serve a purpose or cause harm, these remnants have often been referred to as ‘junk DNA.’”
http://www.newyorker.com/reporting/2007/12/03/071203fa_fact_specter
“The human endogenous retroviruses (HERVs) are remnants of ancient infections of retroviruses and they were previously thought to be inactive junk DNA.”
http://64.233.167.104/search?q=cache:R1s9I7PxC3kJ:cmb.molgen.mpg.de/
brew/papers/HELS_oja_final.ps+expression+of+human+endogenous+retroviruses+
oja&hl=en&ct=clnk&cd=2&gl=us&ie=UTF-8
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?

“‘But these sorts of ancient interactions may have influenced how humans are able to combat these retroviruses today. These proteins help protect us against current retroviruses.’ Indeed, HERV-K may well have helped to shape the modern APOBEC3G defense.”
Rockefeller University, “New Evidence Of Battle Between Humans And Ancient Virus,” July 23, 2008, ScienceDaily.
http://www.sciencedaily.com/releases/2008/07/080721112616.htm
“We propose a model in which Iris has “switched sides,” having been recruited by host genomes to combate baculoviruses and retroviruses, which employ homologous envelope genes to mediate infection.”
http://genetics.plosjournals.org/perlserv/?request=get-document&doi=
10.1371%2Fjournal.pgen.0010044
“These results suggest that the loss of ERV3 mRNA expression is associated with susceptibility to choriocarcinoma.”
http://www3.interscience.wiley.com/cgi-bin/abstract/112716625/ABSTRACT
“They also block exogenous retrovirus replication by receptor interference or antisense mRNA.”
http://lib.bioinfo.pl/pmid%3A17199106
“The HERV-W env gene product has also been shown to block infection by an exogenous retrovirus, suggesting that the expressed HERV-W env gene could have a beneficial function to the host (Ponferrada et al., 2003Down).”
http://vir.sgmjournals.org/cgi/content/full/85/5/1203
“Thus, HERV-W Env confers host cell resistance to infection by SNV. This is the first report of a human endogenous retrovirus gene product blocking infection by any exogenous retrovirus.”
http://www.ncbi.nlm.nih.gov/pubmed/12664292
“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.”
http://www.pnas.org/cgi/content/full/101/30/11117
“Of note in this respect is the observation that endogenous Jaagsiekte sheep retrovirus (JSRV) blocks the entry of the corresponding exogenous virus.”
http://www.pnas.org/cgi/content/full/101/suppl_2/14572#REF65
“However, in the case of both Fv4 and Rmcf, the mode of defense is by the domesticated env gene blocking the receptor required for retrovirus entry.”
http://genetics.plosjournals.org/perlserv/?request=get-document&doi=
10.1371%2Fjournal.pgen.0010044
By Chance, What Made ERV Elements Change From Viral Activities to Cellular Activities and Create New Essential Genes?



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“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?

“We also present evidence that the functional TF binding sites of the human b3GAL-T5 LTR promoter were present in the original consensus sequence for this class of LTRs. Upon similar analysis of other ERV sequences, we have concluded that this evolutionary history is shared by certain other LTR gene promoters, and may be a general phenomenon.”
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T39-
4GXVG6Y-1&_user=10&_rdoc=1&fmt=&_orig=search&_sort=d&view=
c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=
19c2ea074bec5e7313b36ce1630e38a8
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?

“During primate evolution, the LTRs were self-replicated and stably integrated into various host chromosomal site.”
http://www.jbc.org/cgi/content/full/280/42/35184
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?

“The question arises as to whether HERV elements can continue to change our genomic landscape through active retrotransposition or recombination events. While no direct evidence indicates that such events are ongoing in the human genome, members of the HERV-K family appear to be the most likely candidates for playing such a role.”
http://www.genetics.org/cgi/content/full/171/3/1183
“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.”
http://www.ncbi.nlm.nih.gov/pubmed/11704760?ordinalpos=1&itool=EntrezSystem2.
PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus
“As for the elimination of the numerous copies produced by such rapid and extensive bursts, it is not yet clear whether recombination occurs continuously through time, thus slowly and regularly decreasing large amounts of DNA, or if there is any mechanism that would activate large recombination events following bursts of amplification, as proposed by some authors (Rabinowicz 2000).”
http://mbe.oxfordjournals.org/cgi/content/full/20/4/528
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.)

“No current transposition activity of HERVs or endogenization of human exogenous retroviruses has been documented so far.”
http://www.pnas.org/cgi/content/full/101/suppl_2/14572
“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.”
http://www.pnas.org/cgi/content/abstract/101/6/1668
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?

“Integration into the host-cell genome is a critical step in the retrovirus life cycle. In particular, the choice of the integration site is crucial for retroviral replication, since integration at a site incompatible for high-level transcription may impair production of the progeny virus … Target site selection might be influenced by several factors, including the function of cellular proteins that interact with integrase, the viral protein that catalyzes the integration reaction. Interestingly, a common functional feature that unifies these cellular co-factors is that, to a different extent, they are all involved in the regulation of chromatin structure or transcription. Inappropriate retroviral integration might lead to insertional mutagenesis and cellular transformation, as recently observed in a gene therapy clinical trial exploiting retroviral vectors for gene transfer into hematopoietic progenitors. Thus, the deeper understanding of the molecular mechanisms regulating integration site selection is also essential for the design of safer and more effective gene transfer vectors.”
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed&Cmd=ShowDetailView&
TermToSearch=15168737&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.
Pubmed_ResultsPanel.Pubmed_RVAbstractPlus
“Thus, each of the three retroviruses studied showed unique integration site preferences, suggesting that virus-specific binding of integration complexes to chromatin features likely guides site selection.”
http://www.iscid.org/boards/ubb-get_topic-f-1-t-000167.html
“While the PIC is capable of directing integration of the viral DNA into any chromosomal location, different retroviruses have clear preferences for integration in or near particular chromosomal features. The determinants of integration site selection are under investigation but may include retrovirus-specific interactions between integrase and tethering factors bound to the host cell chromosomes.”
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B7CT7-4HJ20NX-5&_user=
10&_origUdi=B6WSN-49TP1CG-5&_fmt=high&_coverDate=12%2F31%2F2005&
_rdoc=1&_orig=article&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5
=373115706749716ff8fdc6aa26485094
“Replication of retroviruses and retrotransposons depends on selecting a favorable chromosomal site for integration of their genomic DNA. Different retroelements meet this challenge by targeting distinctive chromosomal regions. Despite these differences, recent data hints at a common targeting mechanism —tethering of integration complexes to proteins bound at favorable sites.”
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WSN-49TP1CG-5&_user=10&_rdoc=1&_fmt=&
_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=
0&_userid=10&md5=5f51596c964fb5c3abe56a9e60d7ae24
“Each retrovirus, they discovered, showed distinct preferences for genome integration.”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=509317
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
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

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Moreover, researchers have recently identified an important function for a large proportion of the human genome that has been labelled as ERVs. They act as promoters, starting transcription at alternative starting points, which enables different RNA transcripts to be formed from the same DNA sequence.

‘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).’4

And,

‘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.’5

Moreover, researchers have recently identified an important function for a large proportion of the human genome that has been labelled as ERVs.

So we’re not just talking about a small scale phenomenon. These ERVs aid transcription in over one fifth of the human genome! ‘

http://creation.com/large-scale-function-for-endogenous...


Conley, A.B., Piriyapongsa, J. and Jordan, I.K., Retroviral promoters in the human genome, Bioinformatics 24(14):1563–1567, 2008.


"The human genome is composed of more than just DNA sequences that produce proteins. In fact, only about 2% to 3% of the genome directly encodes information specifying the sequence of proteins. Despite this small percentage, about 80 to 90% of the entire genome is copied into RNA—a phenomenon that has been termed pervasive transcription.2,3 A large proportion of this activity produces long non-coding RNAs (lncRNAs). These lncRNA encoding regions are actually very similar to protein-coding genes in their regulation and genomic structure.4,5 And they are located all over the genome, between protein-coding genes as well as inside them. Some even partially overlap protein-coding sequences."

http://www.icr.org/article/8170/

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