[QUOTE=User55;4309303]Mark found some straws to clutch at after being presented with some facts about endogenous retroviruses. In this thread, I will be presenting a critique of the article he links to.[/QUOTE]
[quote]Do Endogenous Retroviral Sequences (ERVs) Prove Evolution?
One of the most popular evidences for evolution on the internet is Endogenous RetroViral sequences (ERVs). Evolutionists think that a type of virus called a 'retrovirus', once inserted genetic information into one of our ape ancestors' genome. So how is this evidence for evolution?

[/quote]

It is virologists and geneticists who study retroviruses (such as HIV). Retroviruses reproduce by invading a cell, reverse-transcribing their RNA genomes into DNA, snipping the host cell's DNA and inserting their own DNA (the provirus). This DNA is then "read" by the host cell's machinery, and new virus particles are produced. A provirus is a complex structure - string of DNA containing a characteristic set of genes whose function is to get viruses reproduced. A provirus also exhibits a telltale repetition of original host DNA either side of the insertion point. When a retrovirus infects us, it does not infect every cell of the body, and it inserts (integrates, in the jargon) in different locations in each cell it does infect.
But our cells are full of retroviral integrations, in every cell, each one in the exact same location going from cell to cell. They bear all the characteristics of proviruses, the same set of genes, the same telltale record of integration, but they mostly do not function as proviruses any more. They are broken. Some parts of some of them now serve the host organism (more on this later), but the bulk of the DNA involved does nothing. The only way these structures can be in the same places in every cell is by inheritance, not by direct infection, and certainly not by design by any sane designer. The explanation is that each one is duplicated from an ancestral sperm or egg cell. Many thousands of them, from many thousands of ancestors.
[quote]Scientists have noticed that chimps and humans have ERV genetic sequences at very similar points in our DNA. And so the story goes: our common ancestor acquired these ERVs and since humans and chimps are closely related, we should have them in similar spots in our genomes. We do. If we and chimps didn't evolve from a common ancestor (which first acquired the ERVs), how is it possible that we and chimps have ERVs in almost precisely the same locations? The only plausible explanation, evolutionists say, is evolution. But this is far from the truth. If we can show that ERVs are not the product of retroviruses, this evidence for evolution would fall flat.[/quote]
This should be good. To show that ERVs are not of retroviral origin, the author will need to explain the presence of uniquely retroviral genes for such things as reverse transcriptase, which transcribes the RNA genome of a retrovirus into the DNA of a provirus, and integrase, which snips the host DNA and integrates the provirus, leaving the characteristic duplication of the original host DNA on either side of the integration site. The author will also need to explain why live, functioning retroviruses can be easily resurrected form ERV DNA sequences. Let's see if such explanations are forthcoming.
[quote]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.[/quote]
Some sub-components of some ERVs are functional. Others do nothing, and yet others are implicated in diseases, particularly late-onset cancers. There is no attempt by the author to explain why he thinks it would be highly likely that they didn't originate from retroviruses. What he can and cannot conceive is of little interest. What we are looking for is evidence and reasoning. The evidence, BTW, of function (some bits of some ERVs do have function) has been produced by virologists and geneticists, not by creationists vainly trying to conduct damage limitation, not by those who battle them, but by people who hope to make a contribution to human wellbeing, aided and informed by evolutionary theory, which is already accepted as settled science.
[quote][quote][COLOR="#B22222"]"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][/COLOR][/quote][/quote]
All proviruses contain promoters. That is how they get the host cell to reproduce retroviruses. Any promoter left lying around will promote some DNA downstream of it, regardless of what it is. Some transcriptions will be harmful, so the promoter will be negatively selected. Most will be neutral, and will therefore hang around in the genome. Some, a few, will be advantageous, and will tend to spread through the population. It is curious that an article that tries to discredit the evidence from ERVs for evolution - starts by admitting that retroviral integrations (insertions) are a source of variation that is subject to natural selection! This can only happen if the retroviruses are heritable - have been endogenized, in the jargon - and have thus entered the gene-pool. Thus, in a few short paragraphs, the author has already contradicted himself. He says, "It would be inconceivable that viral non-functional ERVs somehow became functional", and then quotes, "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."
I do wonder whether Mark has actually read and thought about this article.
To be continued.



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]

[QUOTE=User55;4309357]To be continued.[/QUOTE]
[QUOTE]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.
[COLOR="#B22222"][QUOTE]"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][/QUOTE][/COLOR]
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?

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This, to put it charitably, is nuts. There is only one type of cell that does not undergo apoptosis - cancer. Like those of poor Henrietta Lacks. Cells live, they die, but they also reproduce. In fact viruses induce apoptosis, but they also reproduce. And the immune system is not perfect - otherwise all diseases would have become extinct a very long time ao.
[quote]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.[/quote]
Well, a brief look at the literature would have prevented this boob. Retroviruses do not target specific locations - even going from cell to cell in the same organism with absolutely identical DNA in each cell! This is a crucial part of the evidence for common descent, and the author has completely failed to face up it. For multiple ERVs to be found in corresponding locations in every cell of two individuals by coincidence would be a coincidence so remote that it staggers belief.
[QUOTE]Similar ERVs in Unrelated Organisms
Another problem for the typical evolutionary explanation is that very similar ERVs exist in unrelated animals.
[QUOTE][COLOR="#B22222"]"... 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][/COLOR][/QUOTE]
How do the authors "explain" this?
[QUOTE][COLOR="#B22222"]"Since cats would be quite likely to scavenge and feed on baboon placentae, a possible exposure to the virus can be envisioned."[14][/COLOR][/QUOTE]
This is hopeful imagination at best![/QUOTE]
It certainly is hopeful imagination to think that this weighs against the evidence for common descent from corresponding ERVs. Remember, the argument rests on the discovery of ERVs in corresponding locations in the DNA of two different species. Once again, the author fails utterly to address the case. It is either stupid, lazy or dishonest of the author to present this as having any relevance whatsoever.
More later. Teh stoopid is getting me down.
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

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?
Possible Responses

"The article said: 'It would be inconceivable that non-functional ERVs somehow became functional.' No, they evolved."

If this explanation were true, there would be almost nothing to lead us to the conclusion that ERVs arose from retroviruses! And this is the very point in question. Indeed, sequences inserted by harmful viruses virtually never become beneficial functioning pieces of DNA!
Of great interest is the fact that genetic recombination (or the like) has not been observed to change ERVs.
"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." [17]

"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."[18]

"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)."[19]

"The article asked us how harmful ERVs could survive for hundreds of thousands of years in two different species when reproductive cells won't tolerate this. Answer: they evolved so that they were not harmful."

This answer does not explain the problem. It would take many, many years for ERVs to evolve, whereas the animal/zygote would be killed immediately when these ERVs hadn't yet evolved.