ERVs 2.0 - a response to Budinsky and SFT
- Jon Peters
- 5 days ago
- 33 min read
Updated: 2 days ago
Why the Standing For Truth (SFT) attack against randomly inserted retroviruses producing shared ERVs in different species that basically proves human evolution fails. ERVs are still the best evidence for human evolution and "macroevolution".
Introduction
Several people in addition to myself have noted that the random insertions of retroviruses producing dead viral genomes called ERVs that are shared exactly between species offers the best evidence for evolution, human evolution, and “macroevolution” that science has discovered. Barry Desborough has dedicated over a decade to this claim and produced a massive FAQ section and website defending the assertion. Jon Perry of Stated Clearly produced an excellent short video about ERVs and then created an ERV video for objections. That produced more attacks and so he made two more short videos (angry creationists Part 1 and, angry creationists Part 2) defeating the numerous objections he received from fundamentalists. In my 50 years of intermittently debating evolution most people in my opinion are mainly concerned about two major subjects: human evolution and “macroevolution”, commonly defined by creationists as speciation above the taxonomic Family level of “kinds”.
I have created a website that discusses only two examples for macroevolution and avoids my views on worldviews; one in my opinion rises to the level of proof of what people are usually most interested in. All references to my blogs are best not read on just a cell phone. This example, shared random ERVs, I have settled on for debate purposes because it ends the continued unwarranted onslaught against science. In part because it accomplishes all three objectives - basically proving evolution, human evolution and “macroevolution” through not only the identification of shared random retroviral insertions but also because they produce an evolutionary phylogenetic tree that can only be rationally explained by evolution and is confirmed by other random changes to original genomes. Various creationists have pushed back against the ERV findings and have written articles and produced videos to try and undermine the scientific consensus. In my blog on ERVs as the best evidence for evolution and “macroevolution” nearly every anti-evolutionist attempted objection is addressed and defeated.
However, one very active apologist for Young Earth Creationism (YEC) has been so active in trying to discount ERVs that he has produced a book addressing his creationist views, numerous videos, and several articles arguing that nearly all ERVs are instead original to the host and not the result of parasitic retroviruses. He really is fighting the conclusions that ERVs provide for us near proof of evolution and I respect him for at least realizing he must vigorously battle the science since it would kill his YEC species origin beliefs.
Fortunately and mercifully for us Donny Budinsky of Standing For Truth, has released a short video (7:45 min) and article summarizing his major points from his copious anti-ERV writings enabling us to examine his major claims without putting in days or weeks investigating his views. It would be very beneficial to Budinsky's manufactured controversy if persons read my ERV blog before reading this blog on why he is so completely wrong. Please note that as a defender of YECism Mr. Budinsky most assuredly holds the usual YEC tenets that the entire universe and earth were created about 6,000 years ago, there was a global flood around 2300 BC wiping out all land animals including humans except 8, and those selected animal “kinds” on a supposed ark. He probably holds also that a historical Adam several thousands years ago created out of dirt founded the entire human race up to the ark genocide about 4,000 years ago and not that humans have absolutely evolved by ERV data - except of course those 8 on the ark. It is no wonder that he would strenuously attack the ERV findings since once he understood them, they would indeed completely destroy all creationism types that deny human evolution, and the narrative that he has fabricated for himself and shared with anyone that would listen.
Purpose of This Blog Entry
As the saying goes, all swans are white until you find a black one. It is my contention that we don’t need to study in detail all of Mr. Budinsky’s ERV misunderstandings. Nor engage in ERV creationist wack-a-mole. We just need to identify a few false foundational critical assertions or interpretations, show why they are wrong, and then the entire rationalized manufactured house of creationist ERV cards will fall. This approach will reward attempted brevity (you may disagree about that!) and appeal to all who are interested in ruling out his ERV narrative. I have linked to his recent summary video and blog so I cannot be accused of straw manning his views. If one really wants to understand his mistaken, erroneous ERV story, please read my ERV blog first or consult Barry's FAQ ERV section or Jon Perry's ERV videos before reading this blog although it is not strictly necessary. Actually, in terms of basic ERV biology, Mr. Budinsky does a pretty good job in his summary video with some basics, so even the first two minutes may help you if you can ignore the pejorative and occasional descriptions of evolution and science (“so called”, “evolutionary stories”, share sequence “similarities” to retroviruses, etc.) in the first 2 minutes of his video referenced above.
Two other non scientific topics that apply here will be addressed in the Appendix for those interested. First will be the 2024 new word Dan Barker coined called contraduction. Barker repeatedly encountered this problem in his debates and it is rampant in creationist apologetics. This is what Mr. Budinsky has done by trying to take the truths about ERVs and turn them around 180 degrees to fit his presuppositions. As will be discussed it is similar to thinking that the nose was made to hold glasses and the crowing of the rooster brings the sun up rather than the other way around.
The second entry will involve how one goes about searching for truths, called epistemology. Mr. Budinsky has fallen victim to using a method similar to that common in religions which involves searching for “evidence” to support beliefs and presuppositions rather than the successful and opposite method science usually uses. The former results in a chaos of thousands of different and often mutually exclusive religious beliefs. The latter coalesces on single truths.
Why SFT’s attempts at contraduction fail.
1. He repeatedly claims that ERVs only resemble retroviruses. They do not; they have the exact same genes as retroviruses that insert their DNA to parasitize the host DNA to reproduce more retroviruses. The key is his assertion that the majority of ERVs are *** original designed elements *** and not introduced as an infection. He is probably referring to solo LTRs. This one claim if not true completely causes all the rest of his story telling to implode. One of the things creationists rarely do is put their rationalizations into a hypothesis that can be tested and falsified. From his summary slick video and article (please read that and his short video referenced above) we can see that he never asks as scientists do, "what would disprove my views"?
Please watch this 5 min video of a typical retroviral life cycle produced by HHMI, one of the most prestigious medical organizations in the world. Notice how medical researchers have worked out the various steps so they could produce drugs to block the replication of the virus at several points in its life cycle. I will refer to this 5 min video later also as a testament against another part of his fabricated story.
The 3 viral gene groups or domains (sometimes authors will pull protease out of the pol genes separately, making it 4 viral gene groups) if inserted without promoters would not be read by the host enzyme because there would be no promoters to start the transcription (copying) step and the host enzyme would not make mRNA of the provirus genes. So right before the virus inserts its DNA into the cell it makes a bunch of identical promoters, in the hundreds and attaches them at each end of the 3 genes. These viral promoters are called LTRs or Long Terminal Repeats. When the LTR-gag-pol-env-LTR viral DNA package (provirus DNA - active infective retrovirus) is introduced the virus can now make copies and often destroy the cell. We know that the viral DNA including the LTRs are not original to the host cell because:
(A) Where the host DNA is cut and the viral DNA is inserted, the ends are repaired and sealed by copying DNA at the splice site and placing copies of them attached to the ends of the LTRs, producing something called Target Site Duplications, or TSDs. So scientists can find this foreign DNA by finding TSDs. See below Figure 1. Budinsky's attempt to explain ERVs with "fixed" vs. "unfixed" ERVs will be discussed shortly. ERVs and ERV LTRs are not "originally created functional units" as Budinsky claims. We know they are inserted.
Figure 1. Insertion of identical ERV found in homologous locations between chimps (CERV 30) and humans (HERVK10). Notice the TSDs on either side sealing the break point for the insertion. These ERVs cannot be original to the genomes.
Although complete ERVs contain the full TSD-LTR-gag-pol-env-LTR-TSD sequence, for several reasons including mutations and looping most of what we see are degraded proviruses to the point that only LTRs remain. Non functional provirus genomes are called ERVs if they are able to get into gametic cells and spread to all the individuals of the population a process called endogenation. About 8% of our entire 3.1 billion nucleotide genome is made up of ERVs = nearly 250,000 and 90% of those are just the LTRs left over. But 10 % are mostly intact, inactive and cannot make new infective retroviruses. This lets us know that LTRs indeed come from retroviral genome insertions. Some have the complete complement of parts and some for example are just lacking the env viral gene. See Figure 2.
Figure 2. Retroelements showing the loss of various parts from a full ERV to various retrotransposons to retroposons. Note that the viral enzyme necessary to convert RNA to DNA to accomplish parasitic insertion comes in with the viral genome (RT=reverse transcriptase) but is lost in SINEs and processed pseudogenes. RT is not original to the host but is viral in origin as we will see. Some comments about transposons will be discussed later in the text. From:
Virology - Retroviral Derivations
Vincent Racaniello, Lecture #9, 2013. Columbia University. Course: Virology
No copyright infringement intended. Fair Use Permitted
It is very common for people to not realize that left over LTRs represent one form of HERVs. Budinsky wants to deny this and claim solo LTRs are original to the genome because they are all functional and present in all humans, so he uses their other property calling them "fixed" in his writings which are just endogenized, the "E" in ERVs (Endogenized Retroviruses). And "unfixed" ERVs to him are recent true infections that have not spread to everyone in the population, which science calls polymorphisms. More on his claim later but it all goes back to trying to apply contraduction and flipping the truth and view that according to him ERVs are mostly LTRs as original by a creator and not infectious rather than the other way around. Got it? When scientists are referring to human ERVs (HERVs) they are often pointing to just the left over LTRs, and LTRs as discussed are full of promoters. But ERVs can also obviously contain much more than just the LTRs - like about 10% of the HERVs have the full complement of the provirus although inactive due to mutations. Important - no ERVs are functional, just parts of them. LTRs are from ERVs as we have seen and they are missing all the viral genes. If the spliced-in viral DNA was functional it would produce infectious viruses, and would be called a provirus, not an inactive fossilized ERV much later or parts of them, the result of random retroviral insertions. ERVs by definition are not fully functional. The LTRs are missing all the viral genes. The cell has its own promoters but if you had "safe money" dropping on you without consequences would you not use it? This co-option by the host cell of promoters or in some instances even some viral genes for its own use is called exaptation and is well known in virology.
B) Solo LTRs. Budinsky is enamored with solo LTRs because he wants them to be originally created and not derived from retroviruses. He notes that "solo LTRs [the many HERVs without gag, pol and env] "are assumed by apologists of ape-man evolution to be degenerated ERVs because they are broken fossils"[but actually according to him they lack these genes because they were created to not need those genes to perform their functions. Solo LTRs never had viral genes according to his story]. Since they are full of promoters they of course have functions. To this he asserts that because their function does not require viral replication and they were created that way, this is why the viral genes are missing in solo LTRs. See the contraduction and in this case the circular reasoning? But we have already seen where in the HHMI retroviral life cycle video that they are made before insertion and why the virus makes them - the provirus viral genome would not be read by the host enzyme to make mRNA without a promoter. It is incredible he reverses the reality and makes this claim. There is no evidence they are original to the host genomes and as we will see, reasons they are not. He just needs them to be original for his fabricated contraduction creationist story. Furthermore, scientists have worked out that the LTRs naturally loop back to form a solo LTR which is stable and why we find nearly all old LTRs in us solo. Newer studies show the looping is common and occurs relatively early. Solo LTRs are not original to the genome as Budinsky wants us to believe. See Figure 3.
Figure 3. Formation of Solo LTRs, retrotransposons and LINE-1 transposons. Trying to claim that since LTRs are endogenized and fixed means they can be host in origin and not of viral origin, and only "unfixed" LTRs (polymorphic) are of viral origin is not true. All full ERVs and parts of ERVs like all LTRs are derived from retroviruses. None are original to the host DNA. From: https://link.springer.com/article/10.1186/s12977-018-0442-1
Explanation of components from source: "Genomic structure of ERV sequences. Panel a shows a schematic representation of a generalised retroviral provirus. The four coding domains found in all exogenous retroviruses are indicated. The precise organization of these domains varies among retrovirus lineages, and some viruses also encode additional genes. The long terminal repeat (LTR) sequences are comprised of three distinct subregions that are named according to their organization in the genomic RNA: unique 3′ region (U3), repeat region (R), and unique 5′ region (U5). Panel b shows a schematic representation of processes that modify ERV sequences. (1) Recombination between the two LTRs of a single provirus resulting in the formation of a solo LTR. (2) Recombination between the 3′ and 5′ LTRs of a given provirus leading to a tandem duplicated provirus. (3) Adaptation to intracellular retrotransposition, resulting in the loss of the envelope gene. (4) LINE1-mediated retrotransposition, resulting in loss of the 5′ U3 sequence, and the 3′ U5 sequence. Variants with larger 5′ truncations may also occur. Poly-A tails at the 3′ end and L1-typical target site duplications flanking the retrotransposed sequence are usually found for these forms.
2. Codon bias in the ERV DNA coding genes shows that full or partial genome ERVs are not original to the host genome and DNA. The gag, pol and env genes exhibit a viral bias and reveal their viral origin, programmed to hijack the host machinery to make more viruses. The four bases (ATCG) in DNA to make proteins are actually read in 3s from the DNA, called codons. There are thus 64 possible combinations of three bases to specify a mRNA codon. Some of the codons specify STOP and not an amino acid to be added to make the protein. But since life tends to use only 20 amino acids, there is a lot of duplication and this is called Codon Degeneration. Note in the table below for example the amino acid Serine can be specified by tRNAs using UCU, UCC, UCA, or UCG for codons (RNA uses U instead of T in DNA). Why is this being discussed here? Because different living species often have a codon bias for using different codons. One way we know ERVs are not native is that they have a different bias from native host DNA when specifying amino acids. For example in humans Cysteine is specified by UGC but in a yeast species (S. cerevisiae) it is UGU. Glutamine is GAG in humans but GAA in this yeast (Wikipedia). It's like you can tell an English accent from different parts of the world - England, Scotland, Ireland, Australia, or America (also Boston and southern accents in America). If the ERVs were native to our DNA they would have the same codon bias. They don't. See Figure 4 for possible codon configurations assigned to different amino acids.
Figure 4. Table of mRNA codons showing variety in possible amino acid designations. See text for explanation how this demonstrates gag, pol, and env genes are not \host derived. From: University of Leicester. Fair use attribution. For educational purposes only. What this means: The viral reverse transcriptase (RT) that comes in with the virus that converts the viral RNA to viral DNA produces a codon bias in the viral genome. Proteins are made of amino acids and they have a different set of codons by the mRNA making amino acids that we can tell are from retroviruses and not ones produced by the host. Often AI works well in areas of science that are not controversial: AI Overview
"Yes, viral proteins and products exhibit a distinct codon usage bias (CUB), which is the non-random, unequal use of synonymous codons to encode amino acids. This bias is not merely a reflection of the host's codon usage but is shaped by a complex interplay of forces, including mutation pressure, natural selection for efficient translation, genome architecture, and the need to evade host immune responses.
Key findings regarding viral codon bias include:
Host-Specific Adaptation: Viruses often adapt their codon usage to match the tRNA availability of the specific host or tissue they infect (e.g., respiratory viruses show high U/C usage, matching the respiratory tract).
Suboptimal Usage: Surprisingly, many human-infecting viruses, particularly RNA viruses, use "suboptimal" codons (rare in humans). This is believed to:
Slow Down Translation: This may allow for proper protein folding, especially for large, complex viral proteins.
Evade Immune Recognition: Reduced use of CpG dinucleotides (a type of codon bias) helps viruses avoid detection by the host's innate immune system, such as ZAP (zinc finger antiviral protein).
Driving Forces: While mutational pressure (e.g., APOBEC/ADAR enzymes causing C-to-U or A-to-G changes) often shapes viral genomes, natural selection also plays a significant role, particularly in maximizing fitness.
Variation Among Viruses: The extent of codon bias varies; for instance, some large DNA viruses show higher optimal codon usage, whereas many RNA viruses show higher bias toward A/U-ending codons.
Codon Pair Bias: In addition to single codon bias, viruses show "codon pair bias" (the preference for certain combinations of adjacent codons), which can significantly affect translation elongation rates and viral fitness.
Applications: Understanding viral codon bias is crucial for vaccine design, where "deoptimizing" a virus (using rare codons) can attenuate it, while optimizing a gene (using common codons) can increase protein production for vaccines." Bottom line - the protein coding genes gag, pol, env cannot be host genes; they demonstrate a viral codon bias unlike their host DNA. This is important when Budinsky spends much time touting functions of parts of ERVs. Indeed, gag genes for neural development and the famous env gene for placental formation definitely came in as retroviral genes in the past and NOT original because of codon bias. They were co-opted by the host to use - exaptation.
3. LTR DNA bias does not match host DNA, confirming they are all exogenous derived. Again, the LTRs retain differences compared to the host DNA that mark their origin as viral and NOT created with the host DNA for specific functions as Budinsky claims. Since according to Budinsky solo LTRs are "fixed" and originally supposedly created with Adam at the beginning of humans this is falsified. His ad hoc crucial assumption alone is falsified by DNA LTR bias and completely undermines his entire fabricated contraduction. We could be done now showing his entire narrative is wrong since 90% of HERVs are solo LTRs and he failed to test his proposals. Again, AI in this case summarizes nicely the evidence: AI Overview
"Yes, Long Terminal Repeats (LTRs) derived from endogenous retroviruses (ERVs) exhibit distinct biases that reflect their viral origin, primarily through, and as a result of, their interaction with the host genome over millions of years
These biases, which highlight their viral history, include:
Orientation Bias (Antisense Bias): The largest proportion of older retroelements/LTRs shows a significant orientation bias opposite to that of nearby genes (antisense).This is likely because antisense insertions are less disruptive to host gene expression than sense-oriented insertions, allowing them to persist.
Structural Conservation: LTRs act as the regulatory machinery for retroviral expression (promoters, enhancers, polyadenylation signals). Because this functionality is necessary for their initial, parasitic replication, these sequences are conserved, and LTRs are easily identified as viral.
Sequence Homology and Divergence: While newly integrated LTRs are identical at both ends (5' and 3'), older "solo" LTRs (formed by recombination) show accumulation of mutations, yet still retain signature sequences that allow identification of their ancestral viral families.
Target Site Duplications (TSDs): Similar to retroviruses, LTR retrotransposons create short, 4- to 6-bp duplications of host DNA at the site of integration, a hallmark of viral integrase activity.
Integration Site Bias: Some LTR retrotransposons exhibit a preference for specific genomic regions (e.g., rDNA loci), a characteristic that helps them survive in the host genome, similar to how viruses maintain specific infection tropisms.
Evolutionary Context:
While early in their integration, LTRs behave strictly as viruses, over time, the selective pressure from the host leads to mutations that often make them inactive (defective). However, the "bias" or "signature" of their viral origin remains, and they can sometimes be "co-opted" to serve new regulatory functions for the host."
4.The enzyme that converts the retroviral RNA to DNA so it can be inserted into the host DNA is reverse transcriptase (RT). In Budinsky's wishful narrative and concocted story he claims it to be a host enzyme. He writes, "ERVs did not invent reverse transcriptase. It is host machinery, designed for legitimate genome functions". That is patently untrue and falsifiable. We know it comes in from the retrovirus because it does not match other host RNA polymerases. When posting a story in science beware of making claims out of thin air that can be falsified. Like his entire ERV fabricated narrative of rationalizations he is just generating assertions due to presuppositions driven by his religious beliefs. AI Overview
Yes, reverse transcriptase (RT) (from retroviruses) differs significantly from typical host cell enzymes like RNA polymerase, primarily because it synthesizes DNA from an RNA template..., uses a primer, lacks proofreading, and has unique multi-domain functions (RNA-dependent DNA pol, DNA-dependent DNA pol, RNase H), allowing high error rates crucial for viral evolution, unlike host enzymes that maintain genome stability.
Key Differences from Host Enzymes (like RNA Polymerase)
Template & Product: RT uses an RNA template to make DNA; host RNA polymerase uses a DNA template to make RNA.
Primer Requirement: RT needs a primer (like a tRNA) to start synthesis, whereas host RNA polymerase can initiate without one.
Proofreading: Most viral RTs lack 3'-to-5' exonuclease (proofreading) activity, leading to frequent errors, while host DNA polymerases have proofreading for accuracy.
Multiple Activities: RT has three activities (RNA-dependent DNA pol, RNase H, DNA-dependent DNA pol) within one enzyme complex, whereas host enzymes are typically specialized.
Unique Characteristics of RT
High Error Rate: The lack of proofreading allows high mutation rates, essential for retroviruses to adapt and evade host defenses.
Multi-functional Domains: It possesses distinct domains for RNA-dependent DNA synthesis, RNA degradation (RNase H), and DNA-dependent DNA synthesis to complete the viral genome conversion.
Template Switching: RT can switch templates during synthesis, contributing to genetic diversity and the creation of novel transcripts.
In essence, RT is a specialized viral enzyme [not original to the host DNA] with unique biochemical activities and error-prone nature that contrasts sharply with the high-fidelity, template-specific enzymes found in host cells.
Retroviruses insert their viral genome into the host DNA randomly to a specific locus. There are so called hot spots like their tendency to insert in chromosome 19 and LINEs. Hower for example Chromosome 19 has about 60 million specific loci that could be the site of an insertion so hot spots have no effect on the specific pattern that is observed when multiple species have ERVs exact to ATCG sequences AND specific locus locations. We find that the EXACT same ERV can be found in the EXACT same homologous locations between species. Since there are 250,000 HERVs, when we find the same exact ones in other species the only rational conclusion is the retrovirus had to have inserted in a shared ancestor of the species being compared. There is no other rational explanation. But there is more. Not all the ERVs are shared by all the related species. If all we do is survey great apes we find a pattern is revealed. And it's the same pattern we see with fossils. A hierarchical phylogenetic evolutionary ERV tree is produced. This kills allanti-evolution rationalizations and is a key reason why so many of us when seeing this realized that all anti-evolution objections are now dead. This is our Galileo Moment, our 1633. Many people on both sides of the debate do not know of these DNA findings but Barry, I , Biologos, Jon Perry and others are trying to get the word out. What a time to be alive regarding anti-evolution attacks since 1859 and especially in America since the 1950s with YECism. From my ERV blog, The best evidence for human evolution: See Figure 6 below "The next diagram below shows many ERVs that were identified. Some are shared by nearly all, some only found in fewer species. They nest in a hierarchy that produces a phylogenetic tree confirming evolution and common ancestry. Recall there have been thousands of ERVs discovered and finding the exact same ones in different species that can be nested like this is only explained by evolution. Also remember that phylogenetic trees can be produced independently by many areas of origin research including fossils, gene sequences (see DNA evidence in whales), DNA repair, pseudogenes, etc. This coming together of multiple independent evolutionary lines of confirmation is known as consilience.
Notice that some ERVs like ERV-KC4 are found in most species tested whereas others such as ERV K-18 are found in fewer species. White and black boxes refer to two different sources.
Shared ERVs from random retroviral insertions Figure 6. Various ERVs found in different species producing an evolutionary tree that match other trees using different independent data. From: Finlay, G. 2021. Human Evolution: genes, genealogies and phylogenies. Paperback ed. Page 36. Cambridge University Press. 283 pg. without Ref and Index. Fair Use Attribution. For educational purposes only.
In the evolutionary tree below researchers found the same pattern even if limited to just one family of ERVs. See Figure 7. Again from my ERV blog, "below is a phylogenetic tree using ERVs that were found just from one family of ERVs, ERV-K. Notice again that some are shared by some groups and not others. If evolution were not true, this nested grouping would be impossible. For example, 30 were found just in humans, whereas 10 were found in all groups except New World Monkeys. Recall these insertions are random and represent hits to DNA that can only be explained if the retroviruses inserted before the species split off."
Figure 7. Full length ERV-K (HML-2) inserts in the human genome showing the number arising (ovals) at each branch leading to humans. Data for solo LTRs are from chromosomes 7, 19, and 21. From: Finlay, G. 2021. Human Evolution: genes, genealogies and phylogenies. Paperback ed. Page 40. Cambridge University Press. 283 pg. without Ref and Index. Fair Use Attribution
6.But wait, there is even still more.
It turns out that the random insertion of retroviruses that produce ERV changes in original genomes and nest in phylogenetic evolutionary trees in the DNA data when species are compared are just one of several independent categories of DNA raw data without presuppositions. There are about 250,000 HERVs and 200,000 of them are found in chimps.
Also producing random changes in our DNA besides 250,000 ERVs from retroviral insertions are random DNA breaks/repairs, random segmental duplications, random transposons also called jumping genes and pseudogenes. These all produce the same evolutionary trees independently with different DNA findings. We are talking about 600,000 LINE-1s, over a million Alus, hundreds of DNA repaired breaks, thousands of segmental duplications, and 20,000 pseudogenes that are shared exactly between species. The slam dunk DNA basically proof of human evolution, macroevolution is overwhelming.
Let me show you one of my favorites. It turns out that DNA is rather fragile, breaks frequently and randomly, and must be repaired quickly. The cell grabs any DNA lying around to make a patch that becomes a unique "band-aid" and scar. If you guessed that there are TSDs on either side of the repaired break pat yourself on the back. Note that these findings are independent of the origin of DNA, functions of DNA, complexity, or the fact that all life on earth uses the same 5 nucleotide bases. They are just raw data without presuppositions that basically prove evolution, macroevolution.
An excerpt from my blog on DNA repairs. Only an 8 min read. An actual repair is shown in the blog. These shared random breaks, shared unique repairs, and the fact they nest in evolutionary trees provides not one but three seperate layers of evidence for macroevolution, human evolution in only one category. See Figure 8.
"DNA breaks are random and potentially catastrophic. The molecular details... are yielding to stringent molecular analysis, which have revealed that the telltale messiness of the repair patch is inherent to the repair system. Random breaks are fixed by the desperate co-option of any available DNA... Such patches are sufficient evidence of great ape monophylicity." ~ Graeme Finlay.
“These represent a relatively well-preserved selection of sites that have survived vast tracts of time since the Euarchontoglires and Boreoeutheria ancestors lived… The distribution of shared repair patches generates a phylogenetic tree that is congruent with that generated from ERV and retrotransposon insertions. NEHEJ and retrotransposition are wholly independent processes…” .(Finlay)
Figure 8. Identical DNA repairs compared between species. They nest in a hierarchical pattern demonstrating shared ancestry. OWM = Old World Monkeys. NWM = New World Monkeys. From: Finlay, Graeme. 2013. Human Evolution: genes, genealogies and phylogenies. p 140. Figure 3.3. Cambridge University Press. Social sharing and Fair dealing applied per publisher's web instructions. Because even considering that this is true about this DNA data produces instant denial in creationists without looking at the findings. I wrote an introduction to all these DNA findings with links to the various categories to actually see the DNA evidence. If interested, just pick a link to the blog that discusses it. The continued denial of human evolution, macroevolution, is just perverse. Link #1 in the introduction goes to the discussion and examples of DNA repairs. Link #5 goes to transposons (jumping genes). The central principle is the same in all categories so once you understand it, all the different examples are easy to understand. A common attempted creationist objection is to note that some shared changes in these nested evolutionary trees skip a group. For example in Figure 6 what if ERV-H10 was found in Gorillas and humans but not chimps? Would this not be a problem for all the other hundreds of shared nested DNA findings? This does happen, even in a relatively high percentage in some examples. Not at all. This is explained by incomplete lineage sorting, which biologists have known for some time. I have written a smaller entry about it in this blog Evolutionary Musings #14
7.The Creationist chant: functions, functions, functions
For most of the rest of his video and article he spends a tremendous amount of digital ink and video photons (now made more slick with newer techniques) parading out all the functions that have been found for ERVs. The placenta formation from an env gene but fails to tell us that there are nearby viral gag and pol genes indicating not a host source but a complete retroviral source if there was any doubt. Immune system regulation, a gag gene important in neuron function, tumor suppression (p53 cancer suppressor gene - and yet he fails to mention why the Creator gave us only one copy and elephants got 20. Guess what species has few cancers?), and of course all those promoters & enhancers in the viral produced LTRs. Finding co-opted ERV parts that the host is using out of 500,000 retroelements in no way undermines the shared random pattern in nested evolutionary trees. Presupposition arguments against the DNA findings are just hollow projections. The logical fallacy of incredulity often comes out at this time. If you recall in the HHMI 5 min video you can see that the env gene allows the forming viron to fuse with the cell surface membrane before budding off. That of course is exactly how the early placenta forms as a mass of fused cells to invade the wall of the uterus, a syncytium.
8.Repaired ERVs
It may have occurred to some, what if the mutations in ERVs were repaired, would that be a test to see if the ERVs were from retroviral infections or part of a Creator's original "design" in the genome? If the ERVs went on to become active proviruses again to produce infectious virions and not normal host products, would that not be fantastic evidence for a viral origin to ERVs? Scientists have done that at least twice. Most ERVs are so degraded and impossible to repair them singly using known principles of ERV family relationships and grouping and working backwards to know what to repair can test this prediction. They had to use more recent HERVs that had fewer mutations. (a). Here is the original publication. An infective virus producing pro-virion from repaired related non functioning HERVs. "Human Endogenous Retroviruses are expected to be the remnants of ancestral infections of primates by active retroviruses that have thereafter been transmitted in a Mendelian fashion. Here, we derived in silico the sequence of the putative ancestral “progenitor” element of one of the most recently amplified family—the HERV-K family—and constructed it. This element, Phoenix, produces viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny." They could do this by using mutations like Russian nested dolls. (b) Interestingly, a PhD student also resurrected a functional retrovirus [Derivation of HERV-KCON] from a family of ERVs, and published his dissertation in 2010. "Here, a HERV-K provirus whose sequence resembles that of an ancestral human-specific HERV-K(HML-2) was constructed. All viral proteins encoded by this provirus were demonstrated to be capable of functioning in the context of a retroviral replication cycle. While some recent studies have reconstituted “live” viruses from synthetic DNA (Cello et al., 2002; Tumpey et al., 2005), this and a similar study of HERV-K published nearly simultaneously (Dewannieux et al., 2006) are the first examples in which the replication cycle of a virus has been reconstituted using a group of sequences that represent ancient fossils and are demonstrably defective." Source here. (c) A mouse ERV reverted to a fully functional retrovirus provirus able to produce retroviruses with only 1 mutation change. The defect in Emv-3 is caused by a single base substitution in codon 3 of p15gag.
9.The creationist attempt at diversion to mechanisms, "how". The "wellexpldainthis" or "whataboutthisthen" at the end of his article is a way to divert from what we DO know and what basically proves human evolution and macroevolution. None of the DNA random shared changes to genomes that nest in evolutionary trees is affected by the origin of DNA, the origin of retroviruses or not knowing how all the steps in retroviral evolution occurred. God? Aliens? All natural? The evolutionary trees still are a product of evolution. For example, with bullet forensics we can show the same gun, the same origin. However, who fired the gun, where and when it was bought or who owns the gun changes nothing about the conclusion that when two fired bullets have the same scratches they MUST have had the same origin. This is such a common problem when creationists are losing debates I wrote a blog about it. How vs What.
10.Retroviruses evolved from ERVs? The ultimate contraduction rationalization pulled out of thin air? We are told by creationists that life (and viruses) is too complex to have arisen through natural evolution. Please watch the HHMI 5 min video again. The retrovirus is not a simple product of nature. He expects us to believe that complex ERVs and their life cycle evolved from simple LTRs and other simple ERVs? Really? After Adam or at his creation? How? When? Over what period of time? This is unicorn level hail Mary belief.
11.ERVs help protect against viral infections. Of course they do. Viruses do this all the time. If they get in to parasitize a host, they don't want competition from other viruses. They close the door behind them. This is not a created "design". It's evolution. Lots of animals will mark their territories to warn other members of its species to "keep out". It is well studied in virology and called viral interference. Just another example of his contraduction. From my blog on ERVs: "But [host] genomes also contain a history of using viral DNA to fight off future retroviral infections. Similar to an army capturing opposing canons and turning them on their enemy. A virus called MER41 infected a monkey-like ancestor about 45 - 60 million years ago and is now used to switch nearby cells to fight pathogens (9). Sometimes dormant remnants of past retroviral infections become expressed when a cell goes rogue and becomes cancerous. The immune system can detect what it thinks is a retroviral infection and attack the cancer cells. This has been observed in lung cancer (10). Researchers in 2022 noted that a retroviral derived env gene produced a product called Suppressyn that was found to block a cell surface receptor ASCT2. This receptor is used by type D retroviruses to gain entrance to cells during infections. "The study provides proof of principle that an ERV-derived envelope protein can protect against infection in human cells." (11).
Currently koala bears are suffering from an epidemic retroviral infection that causes many to die through horizontal transmission. “What we are seeing with koalas is something that every organism on the planet has gone through. Animals get infected by retroviruses that enter the germline cells. These viruses multiply and insert themselves into the germline genome, altering host genome organization and function, and the process continues until the invader is tamed by the host. At the end of this infection cycle, the host has changed,” (12). The virus, KoRV, comes in several subtypes and some are infectious and others are endogenized. Koalas have been infected by retroviruses in the past and researchers discovered that previous infection offered some protection from current infections. A special class of small RNAs (anti-sense piRNAs) function like genome antibodies attacking viruses that in general resemble past viral infections. During infection the virus produces intron unspliced RNAs that can be recognized by the cells as viral in origin and chopped up producing "sense piRNAs", to disrupt viral replication. These then become the target of the anti-sense piRNAs, a type of innate genome defense mechanism (12). Of course the host had to be infected before with all the problems including death that would be possible. The competition between viruses to infect the same host is well known and is called viral interference. It makes sense in an evolutionary view that viruses would not want to share "the spoils" and would also like to "close the door" so other viruses could not gain entrance to the host it has invaded. Again, it's a function yes, but only in context of evolution and previous retroviral infections which has been shown to be random insertions anyway. And those exact shared locations still mean support common ancestry." Summary
1 All ERVs including solo LTRs are viral in origin. None are specially created. 1a. TSDs show they were inserted. LTRs and viral domains are not original 1b. Solo LTRs are formed by looping of the previous single viral DNA LTRs ends and
are missing the middle viral genes. Of course they are not original to the host
2. ERV coding domains show codon bias; the codons are different from the host DNA & RNA. The viral gag-pol-env genes can only be viral in origin. Viral products exhibit distinct codon bias different from the host DNA.
3. LTR non coding DNA including solo LTRs show distinct biases from the original host DNA. They are not created original as part of the host DNA as Budinsky had hoped.
4. We can currently watch retroviral infections insert their full provirus infective genome of LTR-gag-pol-env-LTR. LTRs are viral in origin made before the insertions so to provide promoters for viral reproduction. We know why and when the virus makes the LTRs.
5. More recent retroviral infections in human populations often produce ERVs not spread to all individuals in the population. These are called polymorphic HERVs and often have fewer mutations present since they have spent less time in the population. The endogenized ("fixed") retroelements are no different in terms of origins; all ERVs are viral derived as evidenced in this blog. Budinsky's attempt to admit that polymorphic HERVs are from retroviruses and fixed HERVs are non viral by a creator fails because of 1,2,3, and 4 above.
6. We can currently watch retroviruses invade individuals (HIV eg) and insert their full proviruse genome of LTR-gag-pol-env-LTR. LTRs are viral in origin and are made right before insertion of the provirus genome to provide promoters for viral replication. Genetically they show differences from normal host promoters.
7. Reverse Transcriptase is of viral origin as detailed with evidence in this blog. Bundsky's claim that it is a "design element" by a Creator and not of viral etiology is disproven.
8. Millions of raw DNA findings without presuppositions show random changes to original genomes that nest in phylogenetic evolutionary trees when found in other species. They come from at least 4 different independent categories and make it mathematically impossible that these DNA findings don't rise to the level of proof of human evolution, "macroevolution". Besides ERVs, they include DNA repairs, segmental duplications, pseudogenes, and transposons by the millions. A blog introduction was supplied with the links to actually show the raw DNA findings
9. Scientists on two occasions tested the hypothesis that if non-solo LTR ERVs could be made functional again they would "come alive" and do their original functions. This was accomplished and the resulting functional provirus from the ERVs did not do host functions but assembled infectious virions that went on to infect other cells. All ERVs are thus former retroviral infections and are not originally created as part of host DNA. Recall that HERVs are 90% LTRs and 10% are the full mutated and non functional provirus of LTR-gag-pol-env-LTR.
Appendix
"All things being equal, the simplist explanation tends to be the right one"
~ Sir William of Ockham (1287–1347)
Contraduction - This is a term Dan Barker popularized in his 2024 book of the same title. He defines it as "an informal fallacy that occurs before reasoning begins... a hidden fallacy". It is a "backward-leading premise that can sabotage logic without the reasoner knowing why". It is an unrecognized presupposition that has it's owner finding many false reasons why something appears true. He gives several examples of flipping thinking and explanations exactly backwards. "A contraduction, specifically, is a 180-degree mirroring of reality that can be blamed on a self-centric or self-selected point of view." Examples include the nose was created to hold glasses. The crowing of the rooster brings up the sun. Rivers have their courses to fit state borders instead of the reverse. And in the analysis of Mr. Budinsky's writings and productions trying to rationalize away the overwhelming evidence that shared random ERVs are not original to genomes and nest in evolutionary trees, it is obvious that he uses contraductions profusely. We know ERVs like HERVs and LTRs evolved from old retroviruses; it is not the other way around as he imagines. Claiming retroviruses evolved from LTRs and HERVs is clearly absurd. I have shown in this blog why we can test his contraductions and find them falsified. He is married to his contraduction ERV views because to admit the truth would mean his acceptance of human evolution. Rather, he has chosen to go to war with science because his religious views have been elevated to sacred beliefs, above reproach, and merged with his core identities. To reverse or correct them would feel like a death.
I have encountered this level of denial in debates and often underneath are reasons to hold onto a faith narrative no matter how absurd and falsified. In one instance (JA) his religious beliefs saved him from drugs and saved his marriage. Or perhaps someone's "coming to Jesus or Allah" saved them from divorce or gambling. Or maybe they had a near death experience that was so emotional that they cannot give up certain beliefs. In all these cases no amount of evidence will change minds. Like when Ken Ham was asked during a debate what would change his mind and his answer was "nothing". Does Mr. Budinsky have strong reasons why he has dedicated much time and resources to ERV denial? A slick website and now improved videos shows his dedication to his faith beliefs. Are his previous occupations of a registered practical nurse (one of the least educated medical positions) and possible car salesman(?) now second to any online income, so he cannot afford to change his views on evolution and Young Earth Creationism? I know of one YEC FB site where the husband has died but the widow is keeping the website going and merchandise selling because of a need for income despite numerous people pointing out complete absurd YEC claims. Barker notes that Charles Darwin basically reversed a false contraduction, and the puddle quote of Douglas Adams basically did the same regarding the design inference for the Fine Tuning Argument. Contraductions among apologists are everywhere once we know how to recognize them. Who hasn't experienced one personally sitting in a train, looking out the window next to a "stationary train" and thinking that we were now beginning to move when it was really the train next to us?
There is a philosophical principle at play here with the ERV writings and productions by Mr. Budinsky. The study of knowledge acquisition in philosophy is called epistemology. The approach of theology and science in my opinion are directly opposite. One searches for "evidence" to prove views where the other generally tries to disprove (the one used by science) rather than prove (theology and apologetics). One leads to thousands of "supported" beliefs, often mutually exclusive, while the other tends to coalesce into single verified truths. Apologists, especially human evolution denying creationists including Mr. Bundisky, usually think and apply the poorly producing epistemology of finding "evidence" to support views that are often presuppositional. They are only interested in finding observations that support views they already have. Mr. Budinsky either did not know or care about all the ways his ERV fabricated views could be disproven as demonstrated in this blog. Rather than discuss this in detail further, I have presented my views on this assertion in a 13 min short blog. As usual, best not read on a cell phone. Another interesting observation is the apologist embrace of any "possibility" no matter how improbable or absurd to avoid a conclusion that is so well supported that to deny it would be perverse. And yet they never sell all they own and purchase lottery tickets since it's "possible" that they could win the lottery.
A creationist PhD reverses his opinion about ERVs as evidence for human evolution. Jonathan McLatchie is a Fellow at the Intelligent Design Discovery Institute in Seattle. Previously, he was an assistant professor at Sattler College, Boston, where he lectured in biology for four years. He holds a Bachelor’s degree (with Honors) in Forensic Biology, a Masters (M.Res) degree in Evolutionary Biology, a second Master’s degree in Medical and Molecular Bioscience, and a PhD in Evolutionary Biology.
In early writings about ERVs he pushed back about them being excellent evidence for human evolution. However, even he can't avoid the conclusion of common ancestry from ERVs. "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."
He details the two most common creationist objections - functions and target site preferences which he appropriately dismisses from the evidence. He ends by admitting human evolution from the shared random ERVs is the best conclusion but appeals to his incredulity (a logical fallacy) that it could have happened without God guiding it. "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." https://jonathanmclatchie.com/the-search-for-adam-and-eve-human-origins-according-to-scripture-and-science/
As a reminder, my website is funded by me alone and for educational purposes only. I derive no financial reimbursement from it, and there is no clickbait issues I am aware of.
Comments