Are Endogenous Retroviral Sequences (ERVs) Evidence for Evolution?

Endogenous retrovirus

Endogenous retrovirus.
Image credit: FreeDigitalPhotos.net by user ‘jscreationzs’

Introduction

Don’t be put off by the big name. Endogenous means something that comes from within the organism or cell. This helps us understand that an EndogenousRetroViral sequence is a piece of DNA which was put in by a virus.

This is one of the few stronger evidences for the theory of evolution. Evolutionists think that a type of virus, called a ‘retrovirus’, once inserted DNA into our supposed ape ancestor. Scientists have noticed that chimps and humans have these bits of viral DNA (“ERVs” for short) at very similar spots in our DNA. So they say: 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.

However, if we can show that ERVs were not put in by retroviruses, this would not be evidence for the theory of evolution.

ERVs are Functional

If ERVs are found to have function, they would be highly unlikely to have come from retroviruses. It’s hard to think that viral DNA could be injected into an ape’s genome and somehow be functional. Evidence has surfaced that they do have function.

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

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

The previous quote is very telling. There are tens of thousands of ERVs in human and chimp genomes. 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]

ERVs are important in much of the genome. Does that means ERVs absolutely didn’t come from retroviruses? No, but there are certainly some questions evolutionists need to answer.

Apoptosis

<pApoptosis is a process of the body that kills dangerous cells. Foreign DNA injected into a cell by a virus would surely trigger the cell to commit suicide (apoptosis). So if tens of thousands of ERVs were really introduced by retroviruses, we should expect apoptosis to have ridden most of them long ago. The fact that we have so many ERVs indicates they could not have been injected by retroviruses – apoptosis should have ridden most of the cells.

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

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

Now, evolutionists might ask why the positioning of human ERVs are so similar to the positioning of chimp ERVs if viruses didn’t put them in the common ancestor? The answer seems to be in the overallsimilarity of the human and chimp genomes: since our DNA is fairly similar[9, 10, 11] to chimps, we’d expect most ERVs should be in similar spots.

Similar ERVs in Unrelated Organisms

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

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

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

How do the authors “explain” this?

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

This is hopeful imagination at best!

More Problems

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

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

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 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, a lot of explaining must be done before using ERVs as evidence for evolution.

Possible Responses

  1. “The article said ERVs couldn’t be injected by viruses and be functional. No, ERVs evolved their functions later.”
    But this is the very point in question. Sequences inserted by harmful viruses virtually never become beneficial functioning pieces of DNA. To say that they “just evolved” is ad hoc.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]

  2. “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.

References

  1. Conley, A.B., Piriyapongsa, J. and Jordan, I.K., “Retroviral promoters in the human genome,” Bioinformatics 24(14):1563, 2008. Back to text
  2. “Ancient Retroviruses Spurred Evolution Of Gene Regulatory Networks In Humans And Other Primates,” ScienceDaily, University of California – Santa Cruz, Nov. 15, 2007. http://www.physorg.com/news114266805.html Back to text
  3. Conley, A.B., Piriyapongsa, J. and Jordan, I.K., Reference 1. Back to text
  4. “Ancient Retroviruses Spurred Evolution Of Gene Regulatory Networks In Humans And Other Primates,” ScienceDaily, University of California – Santa Cruz, Nov. 15, 2007. http://www.physorg.com/news114266805.html Back to text
  5. Ting Wang, Jue Zeng, Craig B. Lowe, Robert G. Sellers, Sofie R. Salama, Min Yang, Shawn M. Burgess, Rainer K. Brachmann, and David Haussler, edited by Eric H. Davidson, “Species-specific endogenous retroviruses shape the transcriptional network of the human tumor suppressor protein p53,” PNAS, November 20, 2007 vol. 104 no. 47 18613-18618. http://www.pnas.org/cgi/content/full/104/47/18613 Back to text
  6. Wolfgang Seifarth, Oliver Frank, Udo Zeilfelder, Birgit Spiess, Alex D. Greenwood, Rüdiger Hehlmann, and Christine Leib-Mösch (author contributions), “Comprehensive Analysis of Human Endogenous Retrovirus Transcriptional Activity in Human Tissues with a Retrovirus-Specific Microarray,” Journal of Virology, January 2005 vol. 79 no. 1 341-352. http://jvi.asm.org/cgi/content/full/79/1/341 Back to text
  7. Mattick, J., cited in: Gibbs, W.W., “The Unseen Genome: Gems Among the Junk,” Scientific American, 289(5):26–33, November 2003; pp. 29–30. Back to text
  8. Reproductive and Cardiovascular Disease Research Group. http://www.sgul.ac.uk/depts/immunology/~dash/apoptosis/ Back to text
  9. Nature, May 27, 2004, pp. 382-388. Back to text
  10. New Scientist News Service 23 September 2002. Back to text
  11. The Washington Post, Monday, September 30, 2002, A7. Back to text
  12. Gregory J. Baillie and Richard J. Wilkins, “Endogenous Type D Retrovirus in a Marsupial, the Common Brushtail Possum (Trichosurus vulpecula),” Journal of Virology, March 2001 vol. 75 no. 5 2499-2507. http://jvi.asm.org/cgi/content/full/75/5/2499 Back to text
  13. Robin A Weiss, “The discovery of endogenous retroviruses,” Retrovirology, 2006; 3: 67. Published online 2006 October 3. doi: 10.1186/1742-4690-3-67. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120 Back to text
  14. http://www.mitpressjournals.org/doi/abs/10.1162/biot.2006.1.4.357 (The quote seems to have dissapeared since we first took it from this address. If anyone knows where it went, don’t hesitate to contact us.) Back to text
  15. Gimenez J, Mallet F., “ERVWE1 (Endogenous Retroviral family W, Env(C7), member 1),”Atlas Genet Cytogenet Oncol Haematol, September 2007. http://AtlasGeneticsOncology.org/Genes/ERVWE1ID40497ch7q21.html Back to text
  16. Jennifer F. Hughes and John M. Coffin, “Human Endogenous Retroviral Elements as Indicators of Ectopic Recombination Events in the Primate Genome,” Genetics, November 2005 vol. 171 no. 3 1183-1194. http://www.genetics.org/cgi/content/full/171/3/1183 Back to text
  17. Hughes JF, Coffin JM, “Evidence for genomic rearrangements mediated by human endogenous retroviruses during primate evolution,” Nature Genetics, 2001 Dec;29(4):487-9. http://www.ncbi.nlm.nih.gov/pubmed/11704760?ordinalpos=1&itool=EntrezSystem2PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlusBack to text
  18. C. Vitte and O. Panaud, “Formation of Solo-LTRs Through Unequal Homologous Recombination Counterbalances Amplifications of LTR Retrotransposons in Rice Oryza sativa L.,” Molecular Biology and Evolution (2003) 20 (4): 528-540. First published online: March 5, 2003. http://mbe.oxfordjournals.org/cgi/content/full/20/4/528 Back to text
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