What do you mean by “air tight”?
Sure.
With so many claiming that it’s only around 7 or 14, an important question is; just how many ERVs do humans share with chimpanzees? The answer is that humans and chimpanzees share virtually all of them. We know this is the case for two reasons; examination of indel variation, and whole-genome analysis.
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The Talk Origins article you quote is out of date. There are at least 100,000 endogenous retroviruses and almost all are shared with chimps.
As to your point about it not being airtight. Science isn’t about of “proving” things. Rather science judges the merits of competing models in terms of their fit to the data. Unsuccessful hypothesis are never “disproven” because can always come up with contrived stories to save our hypothesis. ERVs provide very strong evidence for common ancestry. But one could always claim god is trying to fool us by making it look like we share common ancestry with other primates.
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Nice article, but it’s written so as to be nearly opaque to a non-expert, as it uses a host of unexplained terms, makes many unexplained connections, and alludes to many arguments and facts rather than making them explicitly.
I thought it demonstrated clearly enough that there is sufficient evidence to conclude that nearly all ERV insertions are at identical loci in both lineages. But I guess it’s up to @thoughtful to decide that.
What I find interesting is that she was quoting from an article written by Jonathan McLatchie (presumably not a non-expert) in which he was summarizing and responding to the article I linked. Yet, somehow @thoughtful came away thinking that there were only about seven insertions in common. I don’t really think that is her fault, TBH.
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It does, but I’m not sure it’s comprehensible. Maybe if she read it and asked questions?
Thank you for thinking of me. I got about 2/3 of the way through and my eyes are glazing over, more because I’m tired than because it’s poorly written although that may be true too. I’ll have to come back to it.
I’m pretty new to this subject, would you please be able to explain why the article I’m pretty knew to this subject and not being a scientists, would you be able to explain what is wrong with the explanation given in article from creation.com that you attached that claims that what evolutionists say are matching ERVs aren’t viruses, but something else. The article said:
“ERVs
Earlier, in a series of papers, I argued that the origin of RNA viruses can be understood as genetically modified ERVs which acquired virulence genes and thus became disease-causing agents.2,3,4 The ‘VIGE-first hypothesis’ holds that RNA viruses have their origin in ERVs, and that ERVs were created for/with a purpose. ERVs are made of two genes, gag and pol , which are also found in all modern RNA viruses. This fact is also the most vital argument for why endogenous retroviruses are always interpreted as remnants of ancient genomic invasions of RNA viruses. The pol gene encodes a large protein with four distinct enzymatic activities: a protease, a reverse transcriptase, an RNase, and an integrase. To produce the individual proteins, the protease, which is synthesized first, proteolytically releases the other three enzymes from the precursor sequence. The transcribed, full-length ERV RNA then functions as a template for reverse transcriptase, the enzyme that catalyzes the synthesis of a double-stranded RNA-DNA hybrid.
Next, the RNase enzyme removes the RNA part, and the remaining single-stranded DNA forms a circular molecule. This circular single-stranded DNA serves as a template for the synthesis of a second DNA strand. The double-stranded DNA copy can now be put back in the genome with the help of the integrase enzyme. The position where this happens is determined by repetitive DNA sequences flanking the ERV element and/or by the sequence specificity of the endonuclease (integrase).13,14 Alternatively, the RNA molecule can be packed in a capsule consisting of three proteins, which are specified by the gag gene, and the whole thing looks very much like a virus. Why this packaging is necessary is unclear, but it may prevent the RNA molecule from docking to the wrong places in the cell. On the other hand, the protein-coated viral-like particles may contain biologically active molecules which have to be protected and/or delivered to the right places. In other words, we are dealing with a subcellular transport system.
In 2018, two publications addressing this possibility appeared simultaneously in Cell .15,16Neurons use a virus-like construct to pass on messenger RNAs that code for the building blocks of that virus-like construction. These building blocks are known as activity-regulated cytoskeleton-associated protein (ARC). Although the ARC protein was for a long time suspected to be involved in learning and memory processes, nobody knew how or why. ARC is homologous to the gag proteins, which are found in all RNA viruses and ERVs. Although ARC is required for synaptic plasticity and cognition, and mutations in this gene are linked to autism and schizophrenia, its biological function is largely undefined.
The publications in Cell now shed some light on this matter. Jason Shepherd and colleagues from the University of Utah, USA, transferred the ARC gene into bacteria, and observed that ARC proteins self-assemble into capsids which look very much like virus coats.15 The researchers concluded that that neuronal ARC gene encodes a repurposed retrotransposon gag protein that packages intercellular RNA to mediate intercellular communication in the nervous system. Purified ARC capsids are taken up and transfer ARC mRNA into the cytoplasm of neurons. Apparently, the neurons need ARC in such large amounts that they require a special delivery system. Furthermore, these results show that ARC exhibits molecular properties similar to those of retroviral gag proteins. Of course, the authors spun an evolutionary story around their findings, claiming that ARC is derived from a vertebrate lineage of Ty3/gypsy retrotransposons. In a comment on a Dutch media site, Shepherd admitted: “Other neuroscientists would have laughed at me if I had claimed something like that before.” His response identifies the junk DNA hypothesis of the Darwinian paradigm as a science stopper, and shows that questioning junk DNA still induces scoff and laughter from a scientific community blinded by the erroneous idea that our genome is made of viruses.
In the same issue of Cell , a research group from the University of Massachusetts further disclosed another function of ARC proteins.16 They discovered that the motor neurons of fruit flies control muscles by releasing extracellular vesicles which are packed with ARC capsids. Here too, the ARC protein forms capsid-like structures. They bind dArc1 mRNA in neurons and they are uploaded into extracellular vesicles that are transferred from motor neurons to muscles. The more active the neurons are the more capsids are delivered. These results point to a trans-synaptic mRNA transport mechanism involving retrovirus-like capsids and extracellular vesicles. The paper also reports how cultured genetically modified mouse neurons, which do not express the ARC gene, integrated ARC capsids and started to use the delivered ARC mRNAs. Again, we see a sophisticated delivery system at work, not viruses . The researchers asked whether this form of transport may also play a role in the delivery of additional mRNAs and proteins, and perhaps may promote the spread of Alzheimer’s and other neurological disorders.16
Considering these novel facts, we are compelled to also ask whether the ERV system itself is some sort of common delivery mechanism, since ERV-like vesicles readily leave and enter cells of the placenta. Unfortunately, nobody is really interested in studying this fascinating possibility. Still, it has recently been reported that ERVs can act as DNA regulatory elements17,18 as long non-coding RNAs,19,20 and as triggers for the innate immune system.20 ERVs in the human genome are able to bind ‘signal transducer and activator of transcription’ 1 (STAT1), an effector of the interferon (IFN) pathway involved in immune responses. The enrichment of ERVs in IFN-regulated genes suggest that they play an active role as regulators of essential immune system genes.21 creation.com claim that what evolutionists say are matching ERVs aren’t viruses, but something else. The article said:
“ERVs
Earlier, in a series of papers, I argued that the origin of RNA viruses can be understood as genetically modified ERVs which acquired virulence genes and thus became disease-causing agents.2,3,4 The ‘VIGE-first hypothesis’ holds that RNA viruses have their origin in ERVs, and that ERVs were created for/with a purpose. ERVs are made of two genes, gag and pol , which are also found in all modern RNA viruses. This fact is also the most vital argument for why endogenous retroviruses are always interpreted as remnants of ancient genomic invasions of RNA viruses. The pol gene encodes a large protein with four distinct enzymatic activities: a protease, a reverse transcriptase, an RNase, and an integrase. To produce the individual proteins, the protease, which is synthesized first, proteolytically releases the other three enzymes from the precursor sequence. The transcribed, full-length ERV RNA then functions as a template for reverse transcriptase, the enzyme that catalyzes the synthesis of a double-stranded RNA-DNA hybrid.
Next, the RNase enzyme removes the RNA part, and the remaining single-stranded DNA forms a circular molecule. This circular single-stranded DNA serves as a template for the synthesis of a second DNA strand. The double-stranded DNA copy can now be put back in the genome with the help of the integrase enzyme. The position where this happens is determined by repetitive DNA sequences flanking the ERV element and/or by the sequence specificity of the endonuclease (integrase).13,14 Alternatively, the RNA molecule can be packed in a capsule consisting of three proteins, which are specified by the gag gene, and the whole thing looks very much like a virus. Why this packaging is necessary is unclear, but it may prevent the RNA molecule from docking to the wrong places in the cell. On the other hand, the protein-coated viral-like particles may contain biologically active molecules which have to be protected and/or delivered to the right places. In other words, we are dealing with a subcellular transport system.
In 2018, two publications addressing this possibility appeared simultaneously in Cell .15,16Neurons use a virus-like construct to pass on messenger RNAs that code for the building blocks of that virus-like construction. These building blocks are known as activity-regulated cytoskeleton-associated protein (ARC). Although the ARC protein was for a long time suspected to be involved in learning and memory processes, nobody knew how or why. ARC is homologous to the gag proteins, which are found in all RNA viruses and ERVs. Although ARC is required for synaptic plasticity and cognition, and mutations in this gene are linked to autism and schizophrenia, its biological function is largely undefined.
The publications in Cell now shed some light on this matter. Jason Shepherd and colleagues from the University of Utah, USA, transferred the ARC gene into bacteria, and observed that ARC proteins self-assemble into capsids which look very much like virus coats.15 The researchers concluded that that neuronal ARC gene encodes a repurposed retrotransposon gag protein that packages intercellular RNA to mediate intercellular communication in the nervous system. Purified ARC capsids are taken up and transfer ARC mRNA into the cytoplasm of neurons. Apparently, the neurons need ARC in such large amounts that they require a special delivery system. Furthermore, these results show that ARC exhibits molecular properties similar to those of retroviral gag proteins. Of course, the authors spun an evolutionary story around their findings, claiming that ARC is derived from a vertebrate lineage of Ty3/gypsy retrotransposons. In a comment on a Dutch media site, Shepherd admitted: “Other neuroscientists would have laughed at me if I had claimed something like that before.” His response identifies the junk DNA hypothesis of the Darwinian paradigm as a science stopper, and shows that questioning junk DNA still induces scoff and laughter from a scientific community blinded by the erroneous idea that our genome is made of viruses.
In the same issue of Cell , a research group from the University of Massachusetts further disclosed another function of ARC proteins.16 They discovered that the motor neurons of fruit flies control muscles by releasing extracellular vesicles which are packed with ARC capsids. Here too, the ARC protein forms capsid-like structures. They bind dArc1 mRNA in neurons and they are uploaded into extracellular vesicles that are transferred from motor neurons to muscles. The more active the neurons are the more capsids are delivered. These results point to a trans-synaptic mRNA transport mechanism involving retrovirus-like capsids and extracellular vesicles. The paper also reports how cultured genetically modified mouse neurons, which do not express the ARC gene, integrated ARC capsids and started to use the delivered ARC mRNAs. Again, we see a sophisticated delivery system at work, not viruses . The researchers asked whether this form of transport may also play a role in the delivery of additional mRNAs and proteins, and perhaps may promote the spread of Alzheimer’s and other neurological disorders.16
Considering these novel facts, we are compelled to also ask whether the ERV system itself is some sort of common delivery mechanism, since ERV-like vesicles readily leave and enter cells of the placenta. Unfortunately, nobody is really interested in studying this fascinating possibility. Still, it has recently been reported that ERVs can act as DNA regulatory elements17,18 as long non-coding RNAs,19,20 and as triggers for the innate immune system.20 ERVs in the human genome are able to bind ‘signal transducer and activator of transcription’ 1 (STAT1), an effector of the interferon (IFN) pathway involved in immune responses. The enrichment of ERVs in IFN-regulated genes suggest that they play an active role as regulators of essential immune system genes.21
I actually agree it’s rather dry reading. Not because it’s badly written, but it is rather technical and has a lot of molecular biology vernacular. It’s all tables full of numbers, abbreviations, and DNA sequences in multi-step figures with arrows all over the place.
Sadly some of the evidence for evolution, which really is very good evidence for evolution, takes personal effort on the part of the reader to understand. Science can be very complicated, and some of the strongest evidence is laborious to wrap one’s head around. It’s probably why so many creationist responses to it also totally miss the mark because it appears to be based on misunderstandings and only cursory reading with little comprehension. I suppose this is the problem with a lot of science when it comes down to it, be it vaccines and so on.
I think it is sadly also human nature to read things we already know we don’t agree with way too little interest or patience.
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Hi Elliot,
Let me answer as a former retrovirologist.
False. Their GENOMES have THREE genes, gag, pol, and ENV.
The rest of that paragraph and the following paragraph are less wrong, but irrelevant to their point (you’ll find this a lot in ID/creationist propaganda).
No, viruses transport between cells. That’s probably why they strategically omitted the entire existence of the env gene and the protein it encodes.
Of course, the connection to junk DNA as a category (which is not a hypothesis and is produced by non-Darwinian mechanisms) was not made by Shepherd.
No, there was no generalization about junk DNA in anything Shepherd wrote or said. This is common in ID/creationist propaganda too–if even a few hundred base pairs of junk DNA is found to have a function, this somehow means that all of it does.
Elliot, there’s an obvious question that arises. Creation.com has plenty of money. Why isn’t anyone there studying this?
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It’s probably sufficient to simply appreciate that the scientific evidence conclusively shows that the number of ERV’s sharing common loci between the chimp and human genomes is in the hundreds of thousands, not just 7 as Jonathan McLatchie claimed. You can then delve into the specifics of how we know that at your leisure, if you are sufficiently interested.
Have you any thoughts on why McLatchie failed to mention that part of the article in any of the three posts he wrote discussing it?
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There are members of the group here who are probably far more qualified than I to get into the specifics.
For my part: If I see someone using an old, burnt out CRT monitor from an ancient computer as a door stop, I am smart enough to realize that old, burnt out CRT monitors were not deliberately created to serve as door stops.
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There abides Omphalism. Nobody who understands the implications thinks that is a good argument.
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Thanks for that information.
The article said:
“On the other hand, the protein-coated viral-like particles may contain biologically active molecules which have to be protected and/or delivered to the right places. In other words, we are dealing with a subcellular transport system.”
You replied:
“No, viruses transport between cells. That’s probably why they strategically omitted the entire existence of the env gene and the protein it encodes.”
The article also said:
“In the same issue of Cell, a research group from the University of Massachusetts further disclosed another function of ARC proteins. They discovered that the motor neurons of fruit flies control muscles by releasing extracellular vesicles which are packed with ARC capsids. Here too, the ARC protein forms capsid-like structures. They bind dArc1 mRNA in neurons and they are uploaded into extracellular vesicles that are transferred from motor neurons to muscles. The more active the neurons are the more capsids are delivered. These results point to a trans-synaptic mRNA transport mechanism involving retrovirus-like capsids and extracellular vesicles. The paper also reports how cultured genetically modified mouse neurons, which do not express the ARC gene, integrated ARC capsids and started to use the delivered ARC mRNAs. Again, we see a sophisticated delivery system at work, not viruses. The researchers asked whether this form of transport may also play a role in the delivery of additional mRNAs and proteins, and perhaps may promote the spread of Alzheimer’s and other neurological disorders.”
So the author think ERVS look like ERVS but aren’t ERVS but something else. Sorry if you’ve already addressed this, but I’m pretty new to this subject. How would you respond?
Thanks
Elliot
Evolution has co-opted ERV genes. It’s very cool but doesn’t change any paradigms. Viruses are extremely sophisticated delivery systems. Capsid proteins self-assemble in vitro, no design there.
More specifically,
This is just deceptive gobbledygook. Retroviruses are enveloped, so packaging a retrovirus-like capsid into an extracellular vesicle (i.e., the envelope) produces something that is very virus-like. It explains why they strategically omitted the envelope gene from their description of the genome.
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Well, what made me curious is why the article you linked also said that a bunch of other people were claiming it. 
I didn’t get a chance yet to find the section of the talkorigins article that McLatchie cited that claimed there were only 7. Also the last time I was reading about ERVs was when @ColtCorrea posted about the video he was working on I think? I was doing a search and he had posted on the Biologos forum a few years ago (if I’m remembering where I read it correctly) that there were “at least 16” that shared common loci.
So what is the truth here?
And I know I will never be able to gain sufficient knowledge to figure that out on my own. But I’m still curious about this. 
The truth is that McLatchie was quote-mining his source. If you actually read it, you will find that over 95% of the insertions in question were found to be non-homologous by the assay used. The other 5% were unable to be determined by that method, which doesn’t mean they were homologous. The authors then tried another, more sensitive method on that 5% remainder. A couple of those couldn’t be determined by that method either, but the remainder were found to be non-homologous. So claims to have found a great many insertions that were inconsistent with the standard phylogeny were refuted by the very paper used to support the claim.
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If you read carefully, that’s not exactly what he said:
Out of tens of thousands of ERV elements in the human genome, roughly how many are known to occupy the same sites in humans and chimpanzees? According to this Talk-Origins article , at least seven.
So look at it this way: There are tens of thousands of ERV remnants in the human and chimp genome.
Unless these were inherited from a common ancestor, it is highly unlikely to find two of them in the same location in each species’ genome.
Investigators, at the time, had looked at 7 specific ERV insertions, and found that they all fall into the pattern that would be predicted by common ancestry.
Which do you think is more likely:
That these insertions are in the same location because of common ancestry?
Or that, by some incredible stroke of bad luck, investigators, independently of each other, just happened to pick the 7 insertions that were consistent with common ancestry, out of 100,000 or so that were otherwise randomly distributed within the genomes?
Unless I just don’t understand what you are saying here, I don’t think you are referring to the same part of McLatchie’s article that Valerie was referring to.
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The answer is that the human genome has about 203,000 ERV’s, and chimps share all but 82 of those 203,000 ERV’s. Of the approximate 203,000 ERV’s in the chimp genome, humans share all but 279 of them. The info is found in the human and chimp genome papers.
Human genome paper (2001)
The human genome paper tells us that there are 203,000 ERV’s in the human genome. The chimp genome paper tells us how many ERV’s in humans and chimps are only found in those species. This means more than 99% of the 200,000+ ERV’s in the human and chimp genomes are shared between the species.
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Nothing they present puts the retroviral origin of ERV’s in doubt. Nothing they describe is inconsistent with a retroviral origin.
There are several other pieces of evidence supporting a retroviral origin. First, the sequence divergence between LTR’s within the same ERV is consistent with the expected phylogeny. Let’s break this info down into bite size chunks. The LTR’s are long tandem repeats which are stretches of repeated DNA sequence that are found at the beginning and end of the viral genome and in the inserted provirus within the host genome.
When a virus replicates it uses one of the LTR’s as a template for the other LTR. That means the LTR’s have identical sequence when they are inserted. If ERV’s are the result of a single retroviral insertion in a common ancestor then we should see the LTR’s diverge from one another over time as they are passed down to ancestors. We should also see a match between the phylogeny of ERV LTR’s and the expected phylogeny of species. That’s exactly what we see.
From the same paper that the above image is found:
The ID/creationist explanation does not explain why we see these phylogenies for LTR divergence. The common ancestry model does. In addition to LTR divergence, the distribution of shared ERV’s follows this same phylogeny. This again is not explained by the ID/creationist model. For example, why aren’t PtERV-1 insertions found at the same location in the chimp and gorilla genomes according to the ID/creationist model? The common ancestry model predicts both the pattern of orthologous and non-orthologous ERV’s while the ID/creationist model can’t explain either pattern.
That evidence alone solidifies the retroviral origin of ERV’s, besides the more obvious evidence that we can directly observe retroviruses producing insertions in a host genome both in the lab and in the wild. However, there is another piece of evidence that I haven’t researched that thoroughly and was wondering if anyone else had some good references. When retroviruses insert into the host genome they clip the host genome open in an asymmetric fashion (which is familiar to any molecular biologists out there). DNA repair fills in the asymmetric cleavage which creates repeats of the host DNA at the ends of the retrovirus. The repeated host DNA is not copied over to newly copied retroviruses, so the presence of the host DNA repeats is evidence that they ERV was produced through the process of retroviral insertion:
The picture shows the process of transposon insertion, but my understanding is that the same thing occurs during insertion of the retroviral genome. I started to search around for specific examples of sequence with these repeats, but haven’t found any good examples yet. However, I do remember someone long ago bringing it up, so I though I would mention it here.
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