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Creationist Response To Endogenous Retroviruses


Light_of_Reason
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I found this at the True.Origins archive and have some notions as to how it is wrong, but a more technical explanation from those with a better understanding would prove helpful.

 

PREDICTION 21: NONFUNCTIONAL MOLECULAR

EVIDENCE—ENDOGENOUS RETROVIRUSES

Endogenous retroviruses are molecular remnants of a past parasitic viral infection. Occasionally, copies of a retrovirus genome are found in its host’s genome, and these retroviral gene copies are called endogenous retroviral sequences. Retroviruses (like the AIDS virus or HTLV1, which causes a form of leukemia) make a DNA copy of their own viral genome and insert it into their host’s genome. If this happens to a germ line cell (i.e. the sperm or egg cells) the retroviral DNA will be inherited by descendants of the host. Again, this process is rare and fairly random, so finding retrogenes[51] in identical chromosomal positions of two different species indicates common ancestry.

 

Presumably, the alleged prediction and fulfillment are:

 

If universal common ancestry is true, then the same endogenous retrovirus (ERV) will exist in the same chromosomal location in two or more species.

 

The same ERV exists in the same chromosomal location in two or more species.

 

Since this is the concept of “shared errors” applied to endogenous retroviruses (and since retroviruses are a type of transposon), much of the two preceding responses is applicable. It is not a prediction of the hypothesis of universal common ancestry or the more specific hypothesis of Neo-Darwinism that the same ERVs will exist in the same chromosomal location in two or more species. Evolution does not even predict the existence of ERVs, much less that they will be found at the same location in two or more species. After all, evolutionary theory was considered robust prior to the discovery of ERVs. This is but another example of taking an observation, claiming it as a prediction of evolution, and then using the fact the observation fits the prediction as evidence for the truth of evolution.

 

Moreover, ERVs are inadequate in principle to support Dr. Theobald’s claim of universal common ancestry, because they are not shared by all groups of organisms. To quote Dr. Max once again, “Another limitation [of this argument] is that there are no examples of ‘shared errors’ that link mammals to other branches of the genealogic tree of life on earth. . . . Therefore, the evolutionary relationships between distant branches on the evolutionary genealogic tree must rest on other evidence besides ‘shared errors.’”

 

The claim here is that common ancestry is the only viable explanation for “finding [ERVs] in identical chromosomal positions of two different species.” It is based on the premise that ERVs are (and always have been) nonfunctional products of retroviral infection that have, for the most part, inserted randomly into the genome of the host organism. The presumed nonfunctionality of ERVs is thought to eliminate the explanation of design (because a Designer could have no purpose in placing nonfunctional sequences at the same locus in separate species). The presumed randomness of ERV insertion is thought to eliminate the explanation of chance (because the DNA “chain” is too long for coincidental insertion at the same locus to be a realistic possibility). That leaves common ancestry as the remaining explanation.

 

Again, it is an unprovable theological assertion that God would not place the same nonfunctional sequences at the same locus in separate species. He may have a purpose for doing so that is beyond our present understanding. The objection that placing nonfunctional sequences at the same locus in separate species would make God guilty of deception is ill founded. God cannot be charged fairly with deception when we choose to draw conclusions from data that contradict what he has revealed in Scripture (see Gibson’s comments in the discussion of Prediction 19).

 

In any event, not all ERVs are nonfunctional. Some are transcriptionally active, and studies have revealed ERV protein expression in humans. (Sverdlov, 1.) We simply do not know all that ERVs (or other transposons) may be doing in an organism or what roles they may have played in the past. Sverdlov writes:

 

ometimes the hosts exploit the capacity of TEs [transposable elements] to generate variations for their own benefit. The retroelements can come out as traveling donors of sequence motifs for nucleosome positioning, DNA methylation, transcriptional enhancers, poly(A) addition sequences, splice sites, and even amino acid codons for incorporation into open reading frames of encoded proteins.

 

The number of described cases in which retroelement sequences confer useful traits to the host is growing. Retropositions can therefore be considered as a major pacemaker of the evolution that continues to change our genomes. In particular HERV [human endogenous retrovirus] elements could interact with human genome through (i) expression of retroviral genes, (ii) human genome loci rearrangement following the retroposition of the HERVs or (iii) the capacity of LTRs [long terminal repeats that are common to ERVs] to regulate nearby genes. A plethora of solitary LTRs comprises a variety of transcriptional regulatory elements, such as promoters, enhancers, hormone-responsive elements, and polyadenylation signals. Therefore the LTRs are potentially able to cause significant changes in expression patterns of neighboring genes. (Sverdlov, 1-2.)

 

The functionality of ERV LTRs is suggested by the fact some elements within them are highly conserved. This means that “[t]here probably exists a kind of selection protecting the elements from mutational erosion. . . . It supports the idea that the LTRs (and perhaps other TEs) are of importance for some genomic purposes.” (Sverdlov, 5.) The bottom line is that “[w]e do not know how important the involvement of LTRs is in genome functioning.” (Sverdlov, 5.)

 

Of course, if ERV sequences have a function, then God may have had a functional reason for initially placing them at the same chromosomal location in separately created species. He also may have had a functional reason for designing a system to favor the insertion of certain ERV sequences at certain loci. In other words, maybe retroviruses are a corruption of an original complex system that was designed to facilitate diversification within kinds (per Wood). What was designed as an “altruistic genetic element,” now shows only vestiges of that original benevolent purpose. In that case, the fact ERVs (and other transposons) now have mostly deleterious effects is because the original system has degenerated as a result of the Fall, not because they arose by random processes.

 

In that regard, it is interesting that, in addition to evincing certain functions, some ERVs (and other transposons) also exhibit an insertion bias. Perhaps this is another remnant of a more finely tuned system. Sverdlov writes:

 

But although this concept of retrovirus selectivity is currently prevailing, practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. 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. The S/MARs are thought to be important functional sequences of the genome that anchor chromatin loops to the nuclear matrix subdividing the genome into functional domains. They often neighbor regulatory elements involved in gene expression and DNA replication.

 

A cautious generalization from these findings could be that although TEs can integrate into many sites and may prefer non-coding regions, the de novo integration is frequently targeted at the sites in the vicinity of functionally important elements like transcriptions start points or origins of replication. (Sverdlov, 3.)

 

In addition, LTRs associated with HERVs frequently coincide with genes. This raises the possibility that they are somehow related functionally to those genes.

 

We found frequent coincidences in positions of HERV-K LTRs and mapped genes on human chromosome 19 where the situation with mapped genes is slightly better. Although it would be premature to interpret this result as the indication of the regulatory interplay between closely located LTRs and genes, still some the the coincidences seem interesting. Most striking is the frequent coincidence of the LTRs with Zn-finger or Zn-finger-like genes scattered all over the chromosome. . . . Among other interesting coincidences, the LTRs were often detected in the vicinity of a number of genes (RRAS, EPOR, JAK3 etc.) implicated at different stages of Jak-Strat signal transduction pathway. The frequent coincidences of the LTRs with the genes of similar or concerted functions might suggest either functional involvement of the LTRs in the expression of the genes or their evolutionary relations. (Sverdlov, 4.)

 

The suggestion that the hypothesis of common ancestry would be falsified by the discovery of the same ERV at the same locus in two species that are not believed to have shared a recent common ancestor is incorrect. ERVs simply would join the list of alleged markers for evolution that exhibit homoplasy. And given what is known of retrovirus selectivity, I doubt anyone would be surprised.

 

They also try to critique the 29 Evidences provided by Talk.Origins on this page. Here's the link for those interested.

 

http://www.trueorigin.org/theobald1e.asp

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Of course, if ERV sequences have a function, then God may have had a functional reason for initially placing them at the same chromosomal location in separately created species. He also may have had a functional reason for designing a system to favor the insertion of certain ERV sequences at certain loci.

Jesus wept.

 

You don't need a sophisticated counterargument. They could not be any clearer that God is utterly devoid of scientific utility.

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It is not a prediction of the hypothesis of universal common ancestry or the more specific hypothesis of Neo-Darwinism that the same ERVs will exist in the same chromosomal location in two or more species. Evolution does not even predict the existence of ERVs, much less that they will be found at the same location in two or more species. After all, evolutionary theory was considered robust prior to the discovery of ERVs. This is but another example of taking an observation, claiming it as a prediction of evolution, and then using the fact the observation fits the prediction as evidence for the truth of evolution.

That little bit is the first mistake I came across...

 

Evolution might not predict the existence of ERV's, but the fact that they do exist, and the extreme rarity of their occurance, when coupled with ToE, leads to the prediction that those that are classed as closely related will have more in common than those that are not.

 

When ERV's were discovered, ToE was used to predict the commonality of ERV's in species and that prediction has been confirmed.

It is nothing more than the observation of a fact, making a prediction based on that fact and the theory, and having further facts fit the prediction.

 

 

 

What they've done is try to claim that the ERV argument is that ToE predicts the existence of ERV's... that is a blatent falsehood, and very easily countered.

 

 

Everything else in there is based on the common misrepresentation of the facts and ToE that Creationists love to throw at us...

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I've run into this criticism before, and it's relatively easy to unpack.

 

Notice the following quote: "Again, it is an unprovable theological assertion that God would not place the same nonfunctional sequences at the same locus in separate species. He may have a purpose for doing so that is beyond our present understanding."

 

To summarize, God may have a purpose for common ERV insertions. But the opposite is true also- God may not have a purpose for common ERV insertions. So, God may or may not have a purpose... how do we know if he does?

 

And the creationist is forced to answer: We don't know.

 

And now we see the two words most damning to creationist arguments, "don't know." Whenever you see these words or recognize them hidden in an argument, rest assured that the creationist is making an argument from ignorance.

 

Thus, we can see that what the creationist is really trying to say is the following: "We don't know that God didn't design organisms with homologous ERV insertions, therefore he did."

 

And the rest of the argument lies in tatters.

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And the creationist is forced to answer: We don't know.

 

And now we see the two words most damning to creationist arguments, "don't know." Whenever you see these words or recognize them hidden in an argument, rest assured that the creationist is making an argument from ignorance.

 

Thus, we can see that what the creationist is really trying to say is the following: "We don't know that God didn't design organisms with homologous ERV insertions, therefore he did."

 

And the rest of the argument lies in tatters.

Pretty much what I would have expected creationists to come up with. An utterly weak argument in which they basically try to say, "God only makes it look like evolution happened", because apparently God is either an asshole or has to do it that way for some strange, essoteric reason.

 

Creationists miss the point of coming up with the best interpretation of the evidence. The point remains that if viral remnants are clear indications of common descent, then why is the creationist suddenly abandoning this interpretation when the same evidence indicates relation between the species? It's as though the creationist would have us throw away everything science knows about viruses just so they could maintain the arrogant presumption that we are not connected to the animal kingdom.

 

They can humble themselves before their imaginary Jesus, but they can't humble themselves to the world they actually live in.

 

A thought, though, since creationists are predominantly morons and will try to attack anything they can, it occurs to me that creationists may misunderstand/abuse Zach's point by saying, "Wait a minute! I thought you said it was good to say 'I don't know'." Indeed it is, but it's when the creationist says, "I don't know, therefore {conclusion}" that the appeal is made.

 

The only correct conclusion you can make from ignorance is, "I don't know, therefore I don't know." To a creationist, this is evil, and thus they do everything in their power to avoid this conclusion, not realizing that they disqualify themselves from science in the process.

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I think the strongest point that the True.Origin author makes is that some retroviruses exhibit insertion bias. The strength of the evidence from endogenous retroviruses lies in the supposed randomness of insertion into the host genome and the fact that, in regard to human evolution, humans and chimps share at least 7 common retroviral insertions. The possibility of insertion bias leaves room for the Creationist to say, "Look! Retroviruses are biased, so the ERVs shared by humans and chimps could have been the result of independent insertion!"

 

I personally would like to deny them this, so is there anyone on this board that is more knowledgeable about integration specificity in ERVs? If so, what do you make of this article?

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I think the strongest point that the True.Origin author makes is that some retroviruses exhibit insertion bias. The strength of the evidence from endogenous retroviruses lies in the supposed randomness of insertion into the host genome and the fact that, in regard to human evolution, humans and chimps share at least 7 common retroviral insertions. The possibility of insertion bias leaves room for the Creationist to say, "Look! Retroviruses are biased, so the ERVs shared by humans and chimps could have been the result of independent insertion!"
Yeah, Jason Gastrich tried making an argument like that once, and it didn't work. I immediately shot him down.

 

I can't really say anything about this supposed "insertion bias" (you'll want to ask Zach), but I will say that ERVs mutate way too fast for humans and chimps to have gotten them independently. I mean, that's just an absurd, desperate argument made by people clinging tenaciously to their buttocks archaic fundamentalist belief system. To put it into perspective, the probability of two human individuals aquiring the 7 identical retroviral insertions is astronomical and out-of-the-question.

 

Basically, the creationists can't make this argument, because it doesn't work that way.

 

Conveniently, I happened to have asked Zach about how retroviruses are identified in the genome on the first episode of Evolution 101. I don't know if there's any information you can pull from that audio, but if there is, here's the URL: http://www.infidelguy.com/FLAM_PLAYER_REP/...1130346818.html

 

Besides, that rebuttal on the part of creationists shows that they still fail to understand the point of the argument. They continue to hope and pray that they can find loopholes to get out of damning evidence without actually providing evidence of their own case. This is never going to work.

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All right, here's the deal with that article.

 

Retroviruses don't strictly insert randomly- them seem to prefer areas of the genome that are actively transcribed. This makes sense, of course, because these areas are more available to the protein machinery necessary to insert new sequences. But this doesn't mean that they ONLY insert into genes- the data from the article shows that they're slightly more than twice as likely to insert into a gene than would be predicted by absolute random distribution, but this is still MUCH less than 100%. So there's still a lot of room for insertion in noncoding regions, which would presumably be random.

 

But let's just say, for the sake of argument, that all retroviruses insert nonrandomly, into a finite number of regions. What would we predict to find in the genomes of every animal we sequence? We'd predict that the same retroviruses would be found in the exact same locations in a large number of organisms unrelated by evolutionary theory. For example, we would expect to see a large number of retrovirus insertions in the same chromosomal location of humans, mice, and chickens. And further, we would predict that none of those organisms would have the same hierarchical complement of insertions, since each of them should represent an individual infection. For example, humans would have A, B, and C; mice would have B, D, and E; and chickens would have A, C, and G. However, what we find is that organisms which evolutionary theory predicts share common descent have common insertions, and organisms which are predicted to have a more recent concestor have more common insertions than organisms which are predicted to have a more ancient concestor.

 

So, to summarize: retroviruses aren't completely random, but they're random enough to still give significant evidence to support evolutionary theory. And even if they were completely nonrandom, the data still don't support creationism.

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Thanks Mr. Neil and Zach for your responses. I'm glad to find someone more knowledeable than myself on these issue. I just have an additional question or two.

 

I can't really say anything about this supposed "insertion bias" (you'll want to ask Zach), but I will say that ERVs mutate way too fast for humans and chimps to have gotten them independently. I mean, that's just an absurd, desperate argument made by people clinging tenaciously to their buttocks archaic fundamentalist belief system. To put it into perspective, the probability of two human individuals aquiring the 7 identical retroviral insertions is astronomical and out-of-the-question.

 

Can you recommend any articles or books or anything of the like that will go into more detail regarding the mutation rate of ERVs and the astronomical improbability of two humans acquiring 7 identical retroviral insertions? I would just like to have them on hand for the purpose of debate. While your explanation makes some intuitive sense to me, Creationists, as you know, show a remarkable aptitude for being dense.

 

But let's just say, for the sake of argument, that all retroviruses insert nonrandomly, into a finite number of regions. What would we predict to find in the genomes of every animal we sequence? We'd predict that the same retroviruses would be found in the exact same locations in a large number of organisms unrelated by evolutionary theory. For example, we would expect to see a large number of retrovirus insertions in the same chromosomal location of humans, mice, and chickens. And further, we would predict that none of those organisms would have the same hierarchical complement of insertions, since each of them should represent an individual infection. For example, humans would have A, B, and C; mice would have B, D, and E; and chickens would have A, C, and G. However, what we find is that organisms which evolutionary theory predicts share common descent have common insertions, and organisms which are predicted to have a more recent concestor have more common insertions than organisms which are predicted to have a more ancient concestor.

 

Zach, I think I basically follow your argument here, though I'm unsure what you mean by "hierarchical complement of insertions." I guess I didn't realize insertions were hierarchical.

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Zach, I think I basically follow your argument here, though I'm unsure what you mean by "hierarchical complement of insertions." I guess I didn't realize insertions were hierarchical.
He basically means that species that are more closely related on the evolutionary branching system have more insertions in common than species that are farther apart. For example, you're going to find more common insertions between humans and chimps than you would between humans and any other primate, and you'll find more ERV insertions in common between humans and primates than you would between humans and rodents, etc. The farther apart any two species are on an evolutionary branch, the fewer ERVs they'll have in common.

 

There's a graph somewhere on the Talk Origins site that demonstrates this. I think it's buried somewhere in the "29+ Evidences" article. I don't have time to go looking for it, so I'm trusting that you'll be able to find it on your own.

 

Also, if I can find a link about ERVs, I'll gladly post it later, along with a link to that graph, in case you haven't found it.

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Thanks for the explanation Mr. Neil. I'll continue to dig on my own until I get a better understanding of the big picture. Interestingly, I came across a couple of posts by the dearly departed WinAce over on Christian Forums that shed more light on the topic.

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retrovirus.gif

 

Here's the graph that Neil was talking about. I have a PDF of that article that I can send you if you like.

 

Retrovirus mutation rates were first characterized in this paper: J Virol. 1988 Aug;62(8):2817-22. Point mutations occur at a rate of 2 X 10^-5 per base pair, and insertions occur at a rate of 10^-7 per base pair. This is higher than mutation rates in other organisms by at least an order of magnitude. For example, the basal mutation rate in humans (measured by comparing pseudogenes of humans and chimps) has been estimated to be about 2.5 X 10^-8.

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