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Absolute truth

Endogenous Retroviral Sequences (Ervs), Poof Of Evolution?

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Introduction

One of the most popular alleged 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?
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.

 

ERVS are simply more or less similar to retrovirus genome:

The first problem with this argument is that it’s hard to tell what an ERV is when you meet one. It doesn’t come with a tag attached saying: ” This is an ERV “. It could be that these genes something completely different. That is because if a virus is embedded in it’s complete form, its almost impossible to pass it down to further generations.

 

ERVS are Functional

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

"We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1,743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5' untranslated regions (UTRs)."(Conley, A.B., Piriyapongsa, J. and Jordan, I.K., "Retroviral promoters in the human genome," Bioinformatics 24(14):1563, 2008)

 

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."("Ancient Retroviruses Spurred Evolution Of Gene Regulatory Networks In Humans And Other Primates," ScienceDaily, University of California - Santa Cruz, Nov. 15, 2007.)


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

 

"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."("Retroviral promoters in the human genome,2008"

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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.

 

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?

 

It's slippery slope fallacy again. What if both chimps and humans were infected by the virus, and both got ERV’s in a similar fashion? After all, given their similar physiology, that seems reasonable enough right?


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. to chimps, most ERVs should be in similar spots.

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

"... and two closely related ERV genomes are found in a carnivore (fox) and a ruminant (sheep)."

 

"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."

 

"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
."

How do the authors "explain" this?

"Since cats would be quite likely to scavenge and feed on baboon placentae, a possible exposure to the virus can be envisioned." !!

 

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

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

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


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

 

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
."

 

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 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?

http://evolutiondismantled.com/ervs

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