A creationist vlogger, "Standing for Truth" (SFT) has finally agreed to address, in writing, some of my arguments regarding the proof of common descent from endogenous retroviruses (ERVs).
I posted a list of questions that would be raised by the hypothesis that ERVs were designed by some intelligent entity. https://barryhisblog.blogspot.com/p/in-science-we-apply-principle-of.html
My answers to the same questions appear at Endogenization as an explanation. https://barryhisblog.blogspot.com/p/endogenisation-as-explanation.html
This page is laid out in the form of numbered question, SFT's response, and my (Veritas') comments on his response.
1:) What is reverse Transcriptase designed to do?
SFT: Viral Genome Size Distribution Does not Correlate with the Antiquity of the Host Lineages; “Our results also suggest that since retroviruses appear to be restricted to plants and vertebrates, they could NOT have played a role in the evolutionary transition from primitive cellular RNA genomes to the extant DNA-based genetic systems of extant cells, nor the viral reverse transcriptase can be considered an evolutionary vestige of the polymerase that played a role in this transition.” The results presented here demonstrate that viral genome sizes are not randomly distributed, but do not appear to be correlated with the antiquity of their hosts. Therefore, viruses may be ancient, but not primitive. Link
Veritas: This is a most peculiar response. It is an interesting notion that reverse transcriptase, or some earlier, similar enzyme, played a part on transitioning from an RNA world to a DNA world, but it hardly explains its supposed design purpose . Whether designed or not, reverse transcriptase takes an RNA polymer and uses the resources of a cell to make a dual-strand DNA version of the polymer. Why a designer would design an enzyme to do this is the interesting question, and SFT fails to address it.
2:) “What is integrase designed to do?”
SFT: It was designed to be a multidomain enzyme. Here is another thing. “Most ERV copies suffer mutations over evolutionary time that prevent the normal assembly of viral particles, preventing horizontal transmission of infections between individuals.” Link
Veritas: Again, this is not an answer. What integrase actually does is to take the DNA produced by the reverse transcriptase, snip the nuclear DNA at some point, introduce the new DNA at the point of the snip and join it up again. It's a bit like copying a piece of text and pasting the copy into another piece of text at some point. What the design purpose of this would be is anyone's guess.
3:) Why are ERVs designed with a viral codon bias?”
SFT: Because Taxonomic boundaries do exist and these originally designed ERV’s were not meant to be crossed. This is why Viruses from a bat cause things like Covid in humans but bat’s remain unaffected.
Veritas: Not an answer. (There is a theme emerging here.) Retroviruses and ERVs exhibit a viral codon bias. There can be no reason for this other than viral origin. They would do exactly the same as they currently do if they were 'designed' without such a bias.
4:) “What is the design purpose of re-transcribable promoters?”
SFT: Well if these are functional DNA elements with important factors then they need to be read like other promoters. Just because viral genes are robustly transcribed during the stage of infection when host transcription is reduced doesn't mean that this was their design purpose originally.
Veritas: This makes no sense. It's like saying, "because aircraft wings allow them to fly doesn't mean that was their design purpose originally". Re-transcribable promoters, like reverse transcriptase and integrase only make sense in the context of retroviral replication.
5:) “What were the HERVs that produced the consensus sequence that generated Phoenix designed for?”
SFT: Since what I know about “the Phoenix virus”, is that French researchers resurrected a retrovirus that became trapped in the human genome. When they exposed Phoenix to cultured human and mammalian cells, they observed spiky virus particles pinching off from the cells and floating in between them. The genomes of the cells also contained new HERV-K sequences, indicating the viruses had infected them. Since this Phoenix virus belongs to the human endogenous retrovirus line only (K-type). Then it was probably an original functionally created ERV that worked in placental development like other HERV-Ks were discovered to do. This could be a reason that there’s so many fetal developmental problems today. I would imagine this died out from mutation, like most ERV’s are dying from today. Every known ERV has lethal mutations in them. What is funny is that “they” evolutionary secular sciensints, believe that this is one of the oldest ERV’s to infect humanity going back 5 million years ago. Yet, when it began to function and form particles capable of infecting mammalian cells in culture. They quickly stated that this happened because the (HML2) family is an evolutionarily "young" family of retroviral elements. The mutations in the resurrected Phoenix virus were still active even though the Phoenix virus is nearly dead. The resurrected Phoenix produced some 'genomic offspring' that may be responsible for the synthesis of the retroviral particles that can be observed in some human cancers such as germline tumors and melanomas.
Another thing, 5 million years is just an arbitrary number they pulled out of thin air. I could write an article on the Phoenix virus and say, no its 4.5 million years old and it would have just as much credibility because no one knows. But, use a date of just thousands of years ago and now all of a sudden this doesn't agree with Evolution and you are stirring the pot too much. When you see numbers tossed around like 5 million years old, you can take that with a grain of salt because they have no evidence, no proof, nothing. To show that this is true. Pure assumption, mixed in as truth, and sold to the public as fact. The story they wield is just retrofitted to fit the evolutionary model. They didn't predict that any ERV would have any function, let alone so many of them with vital functions! Their ad hoc rescue device about them gaining function has no evidence whatsoever. They just needed to say something about it because it was devastating to the theory.
Veritas: Um - syncytin1 is encoded in the ERVW-1 env gene, and syncytin-2 in the ERVFRD-1 env gene. HERV-Ks are young, but in the real worlds of virology, genetics and evolution, millions of years is indeed young. HERV-Ks are implicated in cancers, notably testicular cancers. It's a relatively new field, but ERVs and retroviruses are increasingly being found to be implicated in many cancers. But this is not the function of retroviruses (to induce cancers), but clearly to induce host cells to produce copies of themselves. This is what the reconstructed 'Phoenix' virus did. Why, again, a 'designer' would have designed it to do what it does is anyone's guess.
6:) What is the design purpose of BOTH Exogenous and Endogenous KoRV?
SFT: Weird question, ERVs do not constitute a separate taxonomic division from exogenous retroviruses. Here we find this comment “(This refers to ERVs as a whole; any individual ERV locus or family may still represent a novel (and possibly extinct) retroviral genus). Link So I will just say for example that their functions work in conjunction with one another, they have discovered “many ERVs is interrupted by termination codons, deletions or frameshift mutations, some ERVs are transcriptionally active and recent studies reveal protein expression or particle formation by human ERVs.”
Veritas: If KoRV was designed, it was either designed as an exogenous retrovirus that would infect their hosts and thus make more virions, or it was designed into koala genomes in order to make exogenous copies. What they do, other than getting themselves replicated, is to cause cancers. The fact that the endogenous form is only found in sub-populations, and in different loci in different groups, is proof that they are not there as an originally designed feature of the koala genome. We are left with the inevitable conclusion that the KoRV ERVs derive from the exogenous form, and we are left wondering why any supposed 'designer' designed them.
7:) “If Chimp and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?”
SFT: For the same reason similar genes break in unrelated species and related species. Some genes are just weaker than others. The more important, the more conserved. It must be noted that evolutionists believe that for each virus there are many thousands of sites at which it could insert. Thus the odds that they became inserted in the same region in primates and humans is proof of ancient common ancestor relation, but here is the thing. This is not true, that is an assumption. How can I say that? Easy! Observable evidence tells us this. Different types of regions literally show us that specific viruses favor insertion into a particular spot in the genome. For example, HIV (human immunodeficiency virus) tended to insert in gene-rich regions only. MLV (murine leukemia virus ) favored integration near transcription starts, while ASLV (avian sarcoma-leukosis virus) showed only a weak preference for active genes. So clearly when some viruses enter into the system they are attracted to similar places. So this is even more evidence that if these were not all created elements at the start, that their location inside similar species is not evidence of a common ancestor but similar reaction by the virus to bind at similar spots.
Over 100 LTRs have been demonstrated to help control transcription of human genes Link and several thousand other LTRs could potentially have that function as well. ERVs and other transposable elements are known to play roles in the three-dimensional organization of the genome by functioning as ‘anchors’ that serve to isolate regions of active transcription and by modifying the structure of chromatin. Link
Veritas: "Some genes are weaker than others". This is an extraordinary claim, not backed up by any evidence. Sure, some genes are not so well conserved because they are or become relatively unimportant. This is simple natural selection, but they are not like chains, where a weak link is likely to snap under strain! We see a similar pattern with pseudogenes, where a specific disabling mutation can be found in one lineage, but a different one in another. Shared ancestry explains this. "Weak links" do not. And please, if you ever want to talk about ERVs again and wish to be taken seriously, study my FAQ. It goes into how and why we know that integrase cannot target specific DNA loci down to individual base-pair resolution, which is what would be required to dismiss the proof of common ancestry. You have again failed to come up with a 'design' explanation.
8:) “What is the design purpose of giving some people certain HERV’s and others not?”
SFT: Well you have to remember that humans originally did and that over time mutations and Polymorphism occurred in them and they are no longer shared in all people or they are missing all together because of it. For example, when it comes to HERV’s specifically “there are at least 8, and perhaps 11, of these elements are insertionally polymorphic, meaning, some human individuals have the insertion while other individuals have the empty, pre-insertion site. This shows that this virus family has been transcriptionally active within the age span of the human race.” Link
Veritas: So they are not a necessary part of any original human genome 'design'.
9:) What is the design purpose of creating different syncytins in different placental lineages?
SFT: Well the ERVW-1 gene is EXTREMELY VITAL since it is required during placenta morphogenesis. The fact that there are different created syncytins in different placental lineages is just more proof that it was designed and created because what are the odds that different placental lineages all obtained an ERV that just happened to all “retain its original fusogenic properties and participates in trophoblast fusion and the formation of a syncytium during placenta morphogenesis.” Let that sink in. Link
Veritas: Creationists/cdesign proponentsists like to answer, "Same design same designer" when confronted by phylogenetic similarities. Just like the viral codon bias in all ERVs, there was no design necessity for different syncytins in different ERVs in different chromosomes. The same designer could have used the same design in every case, just as he supposedly did in that vast majority of the genes used to 'design' all of life. There is evidence that different lineages have exapted different env genes from different retroviruses. You have no explanation as to why a 'designer' would have embedded syncytins in different retroviral structures, each in the position of a retroviral env gene, in different chromosomes when the vast majority of life's 'design' is the same.
Note: SFT's responses to my questions are posted at https://www.facebook.com/barry.desborough/posts/4251737618177006:126 where I link to this reply.
SFT's responses to my questions are also at "Creationist clothing" https://creationistclothing.com/blogs/articles/refuting-the-critics-endogenous-retroviruses-ancient-viral-infections-or-created-units-of-dna-function but it appears that I am blocked from commenting there when I give my regular email address!
https://barryhisblog.blogspot.com/p/standing-for-truth-attempts-to-reply-to.html
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