I’m working today, so I don’t have time to read them until later. I also think it’s really interesting, and by posting now, I’m forcing myself to have to read them later. I feel nauseous and have a headache almost all day and would prefer now to read anything that stretches my brain right now because it seems a little torturous. So it was mostly selfish. I figured someone might object that I was posting now, but I thought I’d risk it anyway because part of me does want to read this stuff. Plus if someone had specific comments on those articles then I’d have less to focus on.
Thank you for your comments. We have been studying the evidence for more than a year now with some PhD’s in the science who have been working in this area for many years.
We are interested in creating an informative video and simply breaking down the widely accepted evidence into something that a non-expert can understand.
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If it’s really interesting, why not start with the evidence?
Focusing on the evidence is better than focusing on what anyone says about what anyone says about some of the evidence.
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Yeah what many of those links can be summarized with is this: Because someone has found a piece of an ERV insertion with a function (such as a transcription factor binding somewhere within an ERV insertion), then all ERV’s (and the rest of the ERV where a transcription factor binds) are functional.
But of course, that doesn’t follow and no good evidence supports it. One does have to wonder, though, just why it is so many putative important organismal functions have to be implemented by mutationally decaying remnants of the well-known viral genes GAG, POL, and ENV.
God: “Hmm so I need to express this gene over here in this particular tissue, how to make this work? Ahh of course, let’s use another copy of a viral reverse transcriptase gene for that, for the thirtyseventhousandth time, looking exactly like it’s been accumulating mutations under prototypical transition bias.”
Go figure.
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I plan to never use the word “random” in the video. Random is a very specific term in math and the insertion loci from my research is not 100% totally random in that there are a subset of possible insertion sites where a retrovirus and insert. We plan to use the term “highly variable” in place of “random”.
Let me know if you see any issue with that.
Case in point:
First, genetic data indicate that these sequences are not millions of years old. Using the comparative tools of evolutionary genetics, secular scientists compared the gene sequences of viruses to their counterparts in animal genomes and found that, at most, the variation in these sequences indicates they can be no more than 50,000 years old.2
How ludicrous is this this claim?
The cited reference #2 has nothing to do with “these sequences” (endogenous retroviruses).
It’s entirely about infectious, not endogenous viruses. Even worse, it’s not even about retroviruses:
https://jvi.asm.org/content/77/7/3893
“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. Let’s call it less than a dozen. Given the sheer number of these retroviruses in our genome (literally tens of thousands), and accounting for the evidence of integration preferences and site biases which I have documented above, what are the odds of finding a handful of ERV elements which have independently inserted themselves into the same locus?”
Do Shared ERVs Support Common Ancestry?
https://www.google.com/url?sa=t&source=web&rct=j&url=https://evolutionnews.org/2011/05/do_shared_ervs_support_common_/&ved=2ahUKEwjktsme1ZfuAhU57HMBHQbnDrQQFjABegQIBhAJ&usg=AOvVaw2fDl102bitf0QOVbf1tEpV
Why do you think the scientifically unpublished personal opinion of a professional ID-Creationist carries any weight?
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I suggest you scroll up and read the paper I posted earlier.
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Rofl.
You (and Dr Mclatchie) are extremely wrong about “a dozen”.
We share 99.8% of ERVs with chimpanzees.
The talkorigins article is quite outdated btw.
Amount of Shared ERVs
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.
Wow. Dr McLatchie is so grossly wrong about something so basic as how many ERVs at the same loci are shared!!
https://www.evolutionarymodel.com/ervs.htm
In addition, there are three layers to the ERV argument for common descent ;
- the sharing of ERVs in identical loci among organisms of varying degrees of taxonomic separation, and the nested hierarchies that these shared ERVs are arranged in;
- the examination of shared mutagenic discrepancies between shared ERVs, so as to infer relative sequence of insertion; and
- the nested hierarchies of shared mutations among given ERVs in identical loci.
So.
Given the sheer number of these retroviruses in our genome (literally tens of thousands), and accounting for the evidence of integration preferences and site biases which you have documented above, what are the odds of finding
a handfulalmost all ERV elements which have independently inserted themselves into the same locus given a creationist model?
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Argument from ignorance is a logical fallacy. Plus many creationists are predicting that the entire genome will prove to be functional
Well, I did read through all the papers and several times they were theorizing that harmful viruses were originally part of the genome and created good. So your argument is backwards like they are saying.
One of the articles linked to an article about Ebola. This was interesting.
Much to the amazement of many researchers, the whole Ebola genome (DNA) has been found within the genomes of several animals (including guinea pigs, opossums, wallabies, and insect-eating bats).11 Understanding the origin of this particularly deadly virus helps explain parts of why it is so difficult to treat. If Darwinian evolution were true, then these elements should be considered junk DNA and eliminated from the gene pool by natural selection. However, the presence of these whole genomes in the genomes of other organisms suggests they do something under normal conditions that we have yet to observe. Does that mean that this particular outbreak of Ebola can be traced back to one of these animals? I don’t know. No one knows. It is particularly difficult to determine the exact origin of this outbreak because no one was there to observe it.
Thank you for being kind. I found the evidence for common design to be persuasive though as I read through their articles. Curious if you will try to explain why not.
Also persuasive (from the footnotes of the Beneficial Functions of Endogenous Retrovirus)
The irony to the percentages is that no one uses the ERV percentages to argue in favor of evolution. According to the neo-Darwinian tale, everything progressed from single-celled organisms into more complex multicellular organisms. If that is true, then there should be an accrual of ERV percentages over time because there has been more time for ERVs to insert. But the actual percentages tell a different tale: budding yeast (3%), mustard weed (5%), roundworm (0%), fruit fly (2.7%), mouse (10%), and human (8.5%). Instead of steadily increasing, the percentages demonstrate no cohesive pattern. Haig H. Kazazian Jr., “Mobile Elements: Drivers of Genome Evolution,” Science 303 (March 2004): 1626–1632.
One article linked to a koala paper - it was an observable case of these insertions. So an argument for common descent. But it seemed it happens frequently…and it’s the only organism it’s been observed in, unless the mainstream article was incorrect or outdated.
So…why don’t we see it happening in humans and other mammals today? It seems like the sheer % of our genome made up of ERVs requires observation.
I’m way too tired to find the koala article back right now (let me know if you want the link) and answer other replies. I’ll try to look at them sometime this week.
This has been fascinating. Again I’m overwhelmed by the number of terms to learn to fully understand these papers. Scientists are weird - how much memorization you have to suffer through. 
Any tips on learning terms besides just google for definitions?
Genetics is weird and cool, that’s for sure.
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When I explain that a conclusion (all ERVs are functional) doesn’t follow from a particular observation (this handful of ERVs have functions associated with them) then I am not making an argument from ignorance fallacy. Rather I am saying creationists are committing a hasty generalization fallacy.
I also did go on to explain why that generalization doesn’t make sense. It simply doesn’t make sense to insist, for example, that a dead virus genome made of 30 000 basepairs of DNA needs to exist in the genome of some organism just so some regulatory protein can park itself on a stretch of 8 those 30 000 basepairs. It’s nonsense. And it definitely doesn’t make sense to insist there needs to be hundreds of thousands of such virus genomes.
No, my argument isn’t backwards. It doesn’t make sense to use hundreds of thousands of mutationally decaying remnants of genes encoding GAG proteins, reverse transcriptases, or viral envelopes proteins, to use as binding spots for transcription factors, or spacer DNA, or whatever other ad-hoc rationalizations creationists can come up with.
There’s nothing about this that’s backwards. I am taking it for granted (assuming for the sake of argument) that these functions were originally created deliberately, and explaining why that is absurd. This type of argument is known as a reductio ad absurdum.
Notice this nonsense you quoted without bothering to think about whether it is consistent with other stuff you appear to have bought into:
Clearly the author of that article is not familiar at all with the history of the concept of junk DNA, or the neutral theory of molecular evolution. The idea that natural selection should get rid of nonfunctional DNA was one of the first arguments used, by some evolutionary biologists, against the concept of junk DNA. But developments in population genetics (such as neutral theory) led to the realization that excess DNA usually carries a neglible metabolic cost to species with relatively small population sizes, such as large multicellular eukaryotes, as mammals(for example) are.
Now ironically I see another contradiction here. Haven’t you been spamming this forum telling us natural selection is impotent at removing weakly deleterious mutations? Doesn’t AIG and ICR have multiple on-line articles by people like Sanford, Carter and Price telling us that natural selection doesn’t work at removing very weakly deleterious mutations? Can you do me a favor and calculate the selective cost of carrying around every basepair from the ebola genome, and then calculate how quickly it should be removed by natural selection in these different species?
Or alternatively, they are effectively neutral remnants of horizontal gene transfer from viruses, that are slowly accumulating mutations. There is no requirement that natural selection would instantly get rid of them. As explained above, such a realization is what followed developments neutral theory.
The author of that article you’re quoting appears fantastically out of the loop. Our ability to detect ancient viral infections depends on numerous factors, only one of which is the rate at which they occur. But mutations also accumulate, so eventually an ancient viral infection will have effectively mutated to become unrecognizeable(thus undetectable). If the gene is truly nonfunctional, there is almost no selection operating on the locus, and mutations can pretty much freely accumulate (barring some negative selection against whatever deleterious functions might arise from time to time). Now that is just one reason why we should not see a continuous accumulation of viruses in the genome.
The other statement there, that because some lineages evolved to become more complex over the history of life, then all lineages should be continuously accumulating retroviral insertions, is logically incoherent. It just doesn’t follow at all.
You mean like an essentially random walk in a largely neutral space of genome size and complexity?
Here’s an opportunity for you to calculate a rate given evolutionary timescales. How many independent retroviral insertions have happened since humans and chimps split from our common ancestor? Suppose it’s been 10 (just to pick a number). 10 insertions over about 6 million years amounts to us observing one such insertion every 600 000 years.
So Valerie, how long will you live? For how long have humans had the technology, and the awareness of the existence of retroviruses? Given numbers such as those above, should we really have observed more occurring inserting in the germline than we actually have? I think you could have thought about this yourself a bit more before posting.
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Viruses insert their genomes into our cells quite often.
You may have heard of cervical cancer and Human Papilloma Virus (HPV); cervical cancer can be the result of HPV inserting itself into the cervical cell’s genomes.
HPV is believed to cause cancer both by integrating into DNA and in non-integrated episomes.[40] Some of the “early genes” carried by the HPV virus, such as genes E6 and E7, act as oncogenes that promote tumor growth and malignant transformation. Furthermore, HPV can induce a tumorigenic process through integration into a host genome which is associated with alterations in DNA copy number.[41]
Also, we have experimentally observed ERV insertions occuring
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Random is still a valid term to use in that context, IMHO. I think everyone would agree that the game of craps is random, but you get a 7 much more often than you get a 2. However, you probably don’t want to spend time fighting back against misconceptions about randomness so it might be better to find a label that is more approachable.
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That paragraph demonstrates how dishonest your source is. There are just over 200,000 ERVs in the human genome, and all but ~100 of them are found at the same location in the chimp genome. We don’t share 10 or 20 ERVs. We share over 200,000, more than 99% of the ERVs found in the human genome.
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You would think Dr Jonathan Mclatchie, PhD in evolutionary biology wouldn’t make such a cookie cutter mistake too…
Oh. He got his PhD Jan 2020 and he wrote that article 10 years ago in 2011 (a very odd timeline really by all measures).
I wonder if he still thinks that today!
Then those creationists need to explain how >90% of the human genome can accumulate mutations at a rate consistent with neutral drift. Lack of sequence conservation is the big piece of evidence for a lack of function in the vast majority of the human genome, and until that evidence is addressed the ID/creationists are just whistling in the wind.
Also, no one is saying that ERVs are evidence of common ancestry because they lack function. We are saying that they evidence common ancestry because they are found at the same base in each genome.
We can observe retroviruses inserting into host genomes in the lab.
We can also create a consensus sequence of human ERV’s, construct it, and observe what it does. What happens?
ERVs are from retroviruses. We can watch retroviruses creating insertions in the lab. We can recover viral activity from ERVs. The evidence is all there.
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Interestingly, I have pointed out this mistake to two people at the DI, and they both said they would look into it. It has been over a year since I mentioned it to them, and that article is still there with the same mistake.
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DI, creation.com, AiG have always appeared to be pushing a narrative rather than pushing for truth and accuracy in their articules, so that’s unsurprising.
It looks like Dr McLatchie has changed his tune, though, and is a guided evolutionist / perhaps something like @swamidass’s GAE. (Addit: he mentions @swamidass’s GAE on his website article on A&E).
Primates are thought to have been on the scene for 50-55 million years. During that history, they have undergone many infections by retroviruses (RNA viruses that can reverse transcribe their RNA into DNA and integrate themselves into the genome of their host). Sometimes, those retroviruses infect the germ cells (those cells that are passed on to an organism’s progeny). When this happens, the retroviruses can be vertically inherited from one generation to the next, becoming permanent relics of past viral infections. These relics are referred to in the technical lingo as endogenous retroviruses (ERVs). There are literally hundreds of thousands of those endogenous retroviruses in the human genome. What evolutionary biologists have noticed is that the distribution of those retroviral sequences across the genomes of different primates forms a nested hierarchy, resembling a family tree — exactly what you would expect to observe on the hypothesis of common descent. [24]
Furthermore, in addition to the placement of ERV sequences in orthologous loci (and its pertinent nested hierarchical pattern), we must also take into consideration the shared mutations among orthologous ERVs which also fall into very similar nested hierarchies. [25] Since mutation and ERV placement are independent factors, this is again best explained by the hypothesis of descent. Moreover, the comparative degrees of divergence between the long terminal repeat sequences on both termini of the retroviral sequence (which serve as retroviral promoters) among orthologous ERVs are also implicative of the common descent model. The long-terminal-repeat (LTR) sequences, on either end of the retroviral sequence, must be identical upon insertion. Since LTRs are identical upon reverse transcription and integration, greater mutational divergence (assuming common ancestry to be true) ought to correlate with an older insertion. This is precisely what we observe. [26] Thus, this three-tiered evidence is quite surprising on the hypothesis of separate creation but not surprising at all given the truth of the scenario of common descent.
Creationists have tended to respond to this evidence in one of two ways. The first is to point to functions that have been identified for these retroviral-like sequences in the context of the human genome, which many creationists take to suggest that these sequences are not of retroviral origin at all, but rather are endemic to the human genome. [27] For example, the LTR sequences of ERVs in the human genome “have been shown to contribute promoter sequences that can initiate transcription of adjacent human genes.” [28] Another example is the fusogenic syncytin proteins that fuse placental cells together to form the syncytiotrophoblast and which are known to be essential for placental formation. These proteins are coded for by the envelope ( env ) gene of an endogenous retroviral insert. [29] However, these functions appear to have been acquired post-integration, since the evidence indicates quite strongly that these are indeed genuine inserts into the genome. The evidence for this has to do with the integrase enzyme which is responsible for integrating the viral DNA (after it has been reverse transcribed from RNA) into the host chromosome. Integrase breaks two phosphodiester bonds, one on each strand of the host DNA. Integrase does not simply break the bonds between two base pairs. Rather, it separates the breaks by several base pairs, resulting in a jagged cut. When nucleotides are added to fill in the gaps that have been created by integrase, the result is a target site duplication, which is the hallmarks of insertion by integrase. Thus, while there are plenty of examples of functions that may be identified for ERV sequences in the context of the human genome, this is of little value in responding to this argument for common descent, since those functions appear to have been acquired after integration of these retroviral-like sequences into the human genome.
The second creationist attempt to deal with this evidence is to point to target-site preferences. [30] However, while statistical biases for integration do exist (for example regions of the chromosome that are rich in expressed genes, and near transcription start sites) these biases are not anywhere close to sufficiently locus-specific to make a significant statistical difference. [31] In fact, these biases require thousands of trials just to detect. Integration of retroviruses into a host genome therefore seem to be rather random.
To recap, we have seen that, while the evidence indicates that a transition from a chimp-like ancestor to humans is unlikely to have occurred by an unguided evolutionary process, there is nonetheless genomic evidence confirmatory of common descent of primates that cannot be ignored. I do not believe evolutionists have adequately responded to the former evidence, and I do not believe creationists have adequately responded to the latter evidence.
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we can also watch the opposite when we see that a virus can take a gene from the host genome. this also explain why a virus cant surive without the host. it make sense if it evolved from host genome and not the opposite.
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