“Yes, evolution by descent from a common ancestor is clearly true. If there was any lingering doubt about the evidence from the fossil record, the study of DNA provides the strongest possible proof of our relatedness to all other living things”
~ Francis Collins, 4/6/2007, CNN
"The new DNA evidence has a very important role beyond illuminating the process of evolution. It could be decisive in the ongoing struggle over the teaching of evolution in schools and the acceptance of evolution in society at large. It is beyond ironic to ask juries to rely on human genetic variation and DNA evidence in determining the life and liberty of suspects, but to neglect or to undermine the teaching of the basic principles upon which such evidence, and all of biology, is founded."
~ Sean Carroll, "The Making Of The Fittest: DNA And The Ultimate Forensic Record of Evolution". 2006.
What are these ERVs?
The abbreviation stands for Endogenous Retro Viruses. Let’s take each word separately starting from the right.
A virus is a very small entity that must use a host cell to reproduce. They must hijack a cell and can’t reproduce by themselves. They are basically tiny infectious parasites; thousands can fit inside of a cell. They use genetic material, either DNA or RNA, that they inject into host cells to use the host resources to make more of themselves. The DNA or RNA is carried from cell to cell by a protein capsule. Because they can’t replicate without hijacking a cell and have no significant structures compared to cells biologists still don’t know whether to call them living or not.
Retro refers to some viruses that use RNA instead of DNA as their genetic material and must do a conversion to DNA to use the host machinery. The host cell’s primary instructions are DNA, so this category of virus needs to convert its RNA to DNA before it can be inserted into host DNA to trick the host cell into making viral products instead of normal cell substances. Normally, RNA comes from DNA. Thus this is “retro” going backwards from RNA to DNA. Most viruses just use the cellular machinery outside the nucleus to make more viruses without inserting into the cell’s DNA. Viruses then bud off having their genetic material inside their protein and lipid capsules to infect other cells. But these viruses, called retroviruses, directly infect the host DNA in the nucleus. Often, the infection kills the cell. Also, the body can detect the infection and the immune system attacks the cell or the cell realizing it is infected, commits suicide, a process called apoptosis. Many retroviruses cause cancer and disease.
If a cell is infected successfully by a retrovirus the body can fight it off but often the genetic instructions can be left behind or become silent, called being latent to awaken later - thus passing them along to offspring if the retrovirus infects a sperm or egg cell (gametes). Over time these spread throughout the population and because they pick up mutations they eventually are genetic fossils of past infections. Since they now pass onto all the offspring in the population each generation, the old degraded retroviruses are now endogenized; they now become part of the genome although originally they came from outside their ancestors. If the ERV is only found in humans, it’s called a HERV.
Retroviral lifecycle and components.
We need to get into some details here, but it’s very important. It will be important to evaluate anti-evolution objections especially in the light of how scientists know what ERVs are and what they mean to evolution. Please take 5 minutes and watch a short video of a retroviral life cycle below after reading this section.
In this case the prestigious Howard Hughes Medical Institute is looking at HIV, but all retroviruses have the same life cycle and the same basic genetic components. Notice that the retroviral genome is spliced into the host DNA by cutting it in using an enzyme called integrase and then sealing the ends of the retroviral and host DNA.
The viral RNA has been converted to DNA by another enzyme the virus brought with it called reverse transcriptase. This produces two cut ends on either side called Target Site Duplications (TSDs). Think of these as knots on each end of a section of rope if you were splicing it in. The cut ends can be identified by their DNA sequence. In the example below ATTAT is the target sequence where in insertion took place. Also note that the retroviral lifecycle is complex, which will be an important issue when looking at objections put forward to the ERV evidence.
The end result of the retroviral genome insertion in this sequence of genes is shown in orange in the diagram below:
LTR-gag-pro-pol-env-LTR
In order to get the provirus read, the virus uses a host enzyme called RNA polymerase II. This enzyme is normally used to transcribe mRNA for use into later translation of peptides (making proteins, especially enzymes to make other products), so although it uses a promoter to start transcription, since the promoters don’t code for amino acids that make up proteins, the host enzyme doesn’t transcribe them. Promoters are needed to start copying the DNA. With only one set of promoters in the provirus, the copied provirus would have no promoters at all for the next generation of virions and they would not be able to activate after being inserted into another cell. The retrovirus “solves” this problem by polymerizing lots of promoters during reverse transcription.
Due to the copying system it turns out that these promoter copies all must be identical. These are called Long Terminal Repeats, or LTRs. These promoter copies are in the hundreds in LTRs and will be critical to our discussion shortly. Note: the host cell already has it's own promoters. The LTRs are a collection of promoters from the virus so it can continue to infect other cells when copied. The LTRs are not original to the cell line but have been passed down after the original infection.
Retroviral Lifecycle: HIV as an example
The gag genes code for capsid proteins, the pol for reverse transcriptase and other enzymes, and env into molecules for the envelope. As noted, intact ERVs are dead old retroviral insertions and are mutated to the point of being non-functional. However, the host cells have been able to use some of the viral genes for themselves. The most famous is probably the placental formation in mammals that is dependent on an old proviral env gene. So although there are no functional ERVs, parts can be used by the cells. An ERV gag gene has also been identified as being used by host cells (Arc gene). The process whereby cells use old retroviral genes for their own use is called exaptation or co-option.
Summary. Retroviruses are different from most other viruses in that they have RNA that must be converted to DNA so they can insert their DNA into host chromosomes/DNA to trick the cell into making viral products instead of host products. They are DNA parasites. This process of producing a DNA copy of their RNA is done by one of their enzymes they bring with them called reverse transcriptase. Another enzyme the virus also brings in, integrase, is used to cut the host DNA to finish the insertion. We know this occurs because both ends that are sealed back together with the viral DNA between them leave marks called TSDs on each end. The virus then uses a host enzyme to read it’s three genes (gag-pol-env) to make viral proteins. But this enzyme, host RNA polymerase II usually reads mRNA to make RNA products and will not read a promoter needed to start the copying, so the virus’ “offspring” upon infecting another cell will have no way to start reading its DNA. To get around this problem the retrovirus makes a bunch of promoters and puts them on either side of the provirion genes. These are called LTRs because the promoters are copied many times over. Importantly, unlike reverse transcriptase, the copying of the LTRs is very exact and all the LTRs for that particular insertion have no errors or mutations. The end result is TSD-LTR-gag-pol-env-LTR-TSD. Some authors include an additional coding domain called “pro” that codes for protease before the “pol” coding domain.
ERVs - function, and creationist confusion
The parts of the ERV that cells especially love to co-opt for their own use are the LTRs because they are rich in promoters. The LTRs are central in the attempts to discredit this evidence for human evolution which I will discuss shortly. It turns out that about 8% of the human genome is made up of ERVs. That’s 8% of about 3 billion nucleotide pairs in the DNA “rungs of the ladder” - a huge part of human genomes and 440,000 ERVs are present in our genome. Most of these by far are single LTRs since it's common for the two LTRs to loop back on one another to fuse into a single solo LTR. There are however, some fully sequenced ERVs with all the genes present. When reading the literature, it is often written that ERVs have functions, but note that they are talking about only LTRs nearly all the time, or a gag or env viral gene. A fully functional ERV is not present because if it was it would be called a provirus; an active retrovirus in the host DNA. And ERVs are dead retroviruses by definition that have been endogenized, or spread throughout the population most often after millions of years. Most of the 8% are LTR-retrotransposons. These can no longer make new infectious retroviruses and have the sequence LTR-gag-pol-LTR. As you can see they lack the env gene. But they can jump around in and out of the host genome and are a type of transposon. Thus, when an article notes that an ERV has function, they are usually referring to only an LTR component, a part left over from an ERV, and not the entire ERV. Same with co-opted env or gag genes.
Stop - Let Me Up For Air!
Let’s summarize some points so far.
1. When a retrovirus infects a cell it inserts its genome into the cell’s DNA to parasitize the cell, hijacking the cell’s machinery to make new viruses. We can see that happening today.
2. These retroviral genomes are identified as LTR-gag-pol-env-LTR DNA sequences. We know the lifecycle of retroviruses and know where and how these components are made. There are retroviral infections right now that we can see and study in humans like HIV and even currently in a retroviral epidemic in Koala bears; this current retrovirus has not become fully endogenized. When we find ERVs throughout a population or just their LTRs we know sometime in the past the species had a retroviral infection in the sex cells.
3. Where the retrovirus inserted its genes into the host DNA at a target site there are two areas on each end of the splice as a result with the target site duplicated, called TSDs or Target Site Duplications. The ERVs, mostly LTRs, are not original to the host DNA. They were cut in.
4. Many ERVs are just remnants of the original provirus. Most are mutated and degraded down to their LTRs only or the LTR ends loop back and join making a solo LTR. Some gag and env genes are left for example, still functional, and are used and co-opted by the host cell - turning the tables on the virus. This is called exaptation. Similar to you using a large wrench as a hammer if needed. Not the original function, but a new function that can work. The irony of turning a parasite’s corpse to good use should not be lost. LTRs are rich in promoters and cells love to use them for their own functions. Scientists are finding functional parts for some ERVs all the time but so far it represents a very small percentage of the total.
5. ERVs are old retroviral infections. Their genomes, when intact, match retroviral genomes (called proviruses) that make new retroviral particles to infect new cells. Their DNA is not original to the host DNA. In the literature, ERVs are often mentioned as functional but what the authors are referring to most often are the left-over LTRs alone.
6. Recall from your biology courses that mRNA reads the DNA, and it in turn is read by tRNAs that have certain amino acids attached. As the string of amino acids grows in length to becomes a peptide they can become large enough to be called proteins. The four bases (ATCG) are actually read in 3s which are called codons. There are thus 64 possible combinations of three bases to specify a codon. Some of the codons specify STOP and not an amino acid. 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. 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 Cystine 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 should have the same codon bias. They don't.
From: University of Leicester. Fair use attribution
So - What’s the big deal?
Well, here’s the big deal. First, it turns out that when a retrovirus inserts its genome into the host DNA it does so randomly. There are preferred areas that pick up more than others such as chromosome 19, and they often insert into transposons called LINEs. But the actual insertion is random to locus (like a specific address). A locus (loci, plural) is the exact DNA location looking at the A,T,C,G sequence. Secondly, after the human genome was sequenced it was noted that a huge percentage of our DNA is made up of ERVs - 8%. What do you do if you’re a scientist? You sequence other great ape genomes, like chimp, gorilla and orangutan and compare them.
What did they find? Turns out that 200,000 ERVs are shared by chimps and humans alone and we have 440,000 ERVs in our genome. Remember, these are the result of random insertions down to the genetic code level. About 200,000 are in the exact homologous locations between chimps and humans despite knowing they insert randomly to DNA sequence (but some broad genetic areas can be preferred, just like some intersections tend to have more accidents but do not involve the same vehicles and the exact same areas within the intersections). We can know this by looking at the DNA sequences and nearby DNA sections. Many have the exact same mutations. It’s like two students writing papers on the same topic thousands of miles apart and claiming that they shared nothing between them, no communication, etc. But when you look at their papers written at different schools with different authors and in different states, what do you do if the papers have the same exact sentences? You know what happened. They both went on the Internet and copied from the same source material. They were not independent but share the same source material, the same origin. They were not produced independently of one another. It is mathematically impossible that 200,000 randomly inserted retroviruses happen to be in the exact same locations between two different species. There is only one rational conclusion - those retroviruses had to have inserted in a common ancestor before they split to become different species. This is solid proof of a shared ancestry between chimp and humans and we know we split from a shared ancestor with chimps about 6 million years ago. We did not evolve from modern chimps but with a shared primate ancestor in the distant past.
The only rational explanation, for example, for finding 200,000 shared ERVs between chimps and humans that insert randomly and are found in the same locations between species, often with the same mutations, is that the ERVs must have been inserted before the species split. That is the summary for this entire evolution section on ERVs, or to be exact, shared ERVs. It rules out common design and rises to the level of proof for common ancestry. Human evolution and most would argue macroevolution is true based on shared ERVs in the great apes alone. Paleontologists long ago constructed phylogenetic trees showing that humans and chimps shared a common ancestor at one time, about 6 million years ago due to the fossil evidence. The DNA in our own cells when compared to chimps and the other great apes shows evolution and confirms the fossil evidence.
The only rational explanation, for example, for finding 200,000 shared ERVs between chimps and humans that insert randomly and are found in the same locations between species, often with the same mutations, is that the ERVs must have been inserted before the species split.
Phylogenic Trees; their importance to species' origin debates
If you recall I mentioned that scientists also sequenced other great ape’s genomes and compared them for ERVs. As expected, as one moved away evolutionarily from humans and chimps the number of shared ERVs decreased between the species. Also, because ERVs had inserted over many millions of years the ones more distantly related had fewer and fewer ERVs that were the same in terms of mutations. Evolutionary trees can be constructed just looking at ERVs and LTRs that confirm the fossil record for great ape evolution produced by paleontologists.
Below is an ERV that was found in three species. Notice the TSDs on either side.
From: Finlay, G. 2021. Human Evolution: genes, genealogies and phylogenies. Paperback ed. Page 39. Cambridge University Press. 283 pg. without Ref and Index. Fair Use Attribution
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 phylogenic tree confirming evolution and common ancestry. Recall there have been hundreds 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 phylogenic 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.
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
Lastly, below is a phylogenic 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.
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
Many others have noted this incredible evidence for human evolution and macroevolution. Graeme Finlay wrote the definitive book on DNA findings rising to the level of proof of human evolution (6). It's an amazing book for the lay person. Jon Perry and Stated Clearly produced a video about ERVs. Barry Desborough has dedicated an entire web site to ERVs and has a FAQ section that covers just about every question or objection. Actually, Perry’s entire Stated Clearly series detailing other science and evolution topics is excellent. Please watch his short video below on shared ERVs; it may also help to crystalize my presentation here in video form. So, it’s not about ERVs actually, its about shared ERVs that insert randomly and are found in the same locations between species. It’s not about functions, because no fully ERVs have functions; just parts do and they are co-opted functions.
Again, Barry’s site as a great resource for all your shared ERV questions:
Turning the Tables on viruses: using past infections
Over millions of years as species were invaded by retroviruses, the host species were often successful in using the viral parts for it's own use. Previously mentioned have been all the LTRs rich in promoters that many species including us use for transcription to make DNA products. An env gene has been co-opted in humans to use in building the placenta is another example.
But 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. “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). 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 previous retroviral infections which has been shown to be random insertions. And those shared locations still mean support common ancestry.
Common Objections
If you’re satisfied with the above reasons why shared ERVs among the great apes is slam dunk evidence for human evolution and macroevolution you can probably skip this part. But anti-evolutionists, mostly religious creationists, will still try to find something wrong with the science and conclusions here because in their minds evolution can’t be true no matter how solid the evidence. For that, read on my intrepid follower. Remember, Barry’s site (an Englishman living in France) has just about any objection that can be made answered on his site.
In my experience, below are the most common objections put forward for shared ERVs and evolution.
1. An early one was that the ERVs don’t insert randomly. Yes they do - by locus.
2. ERVs have functions. No they don’t, but parts (gag, env ) do, especially the LTRs as detailed above.
3. ERVs are not old retroviral insertions. They have functions (referring probably to the LTRs only). The reason they are in the same spots between species is because of common design and that the great apes are very similar. Nope. We have research and present day retroviral examples showing how they insert and cause disease. The retroviral proviral genomes match exactly the ERV genomes, including the LTRs. We have the TSDs at each end where they were spliced into the host DNA. They are not original to the host DNA. Scientists have reconstituted a retrovirus from a family of HERVs and it produced infective parasitic retroviruses, not host DNA functions.
4. The VIGE myth. ERVs and LTRs that are shared by so many species are original and designed it is claimed. They perform functions (recall that ERVs don't - just parts stolen by the host after the retrovirus becomes an ERV). This resistance to shared ERVs proclaiming loudly human evolution and evolution in general eventually leads to the manufactured idea of the "VIGE", so called "variation-inducing genetic elements". These are like unicorns and leprechauns; VIGEs don't exist except in the minds of anti-evolutionists. In their view all the ERVs have functions and that's why they are shared across so many species' lines.
This attempt of salvaging common design fails. Why? Because of phylogenetic trees. ERVs nest in a way that proves evolution. If ERVs were originally native to the host and later became defective as a result of a "Fall", they could not be put in a diagram that shows evolution. The broken down gene sequences and mutations in LTRs would not show a pattern of common ancestry. In addition, we are told over and over that evolution can't produce new genes and new information (not true) and yet if these ERVs were original and then became parasites and retroviruses later, that means complex new life cycles and viral entities had to form at "The Fall", thus violating the anti-evolutionist claims about new forms never evolving, or "de-evolving". Before this "Fall", they jumped around but did not cause disease by breaking genes like they often do now? Where and how did the retrovirus get integrase and reverse transcriptase from? You can’t have your retrovirus/ERV cake and eat it too. They are forcing a theological concept (VIGE mythology really masquerades for another myth) into a science discussion, because they have no real science to back up their last attempt to salvage common design, which with nested ERVs and phylogenetic trees is disproven.
Barry Desborough writes why the fanticiful "VIGEs" are not a viable creationist answer: https://barryhisblog.blogspot.com/p/could-you-have-this-backwards.html?m=1
The human population never went below 10,000 by DNA analysis. There never was a global flood nor an ark as detailed in the Bible. There was never a bottle neck of 2, or 8 coming off a boat to found the human race (reboot). Even William Lane Craig and Joshua Swamidass in their 2021 and 2018 books admit to human evolution but have convoluted rationalizations to still have a historical Adam. Modern humans evolved about 300,000 years ago and the population never went below 10,000. https://socratic.org/questions/what-is-the-lowest-number-of-human-population-in-history
"In other words, yes, it is a theoretical possibility that quite a bit of human genetic variation was created in a primordial couple, but the genetic evidence does not look that way. Instead, it looks very much like all of our variants come from mutation. And as we noted earlier, if the variation represents accumulated mutation, that accumulation has been going on for a very long time, on the order of a million years." "In other words, the answer to our original question is no: genetic data does not provide evidence that our ancestral population ever consisted of a single couple. A straightforward interpretation of that data is that our ancestors were part of a population in the thousands as far back as we can see... Every indication we currently have from this kind of analysis, then, is that genetic data do in fact rule out a single pair of ancestors within the last 500,000 years. Such a date would put Adam and Eve well before the appearance of Homo sapiens, making them members of an earlier Homo species... What are Christians to do with Adam and Eve, then, given this evidence? That is not really something for me to say: I study genetics, not theology. For those of us who never thought Adam and Eve were recent historical figures and also our sole genetic ancestors, these findings don’t matter much". https://biologos.org/articles/what-genetics-say-about-adam-and-eve "While this quantitative data is not as easy to appreciate as other sorts of evidence we have examined, it nonetheless is compelling: humans, chimpanzees, and gorillas have, within their genomes, the exact pattern of incomplete lineage sorting predicted by (a) relatedness as evidenced by all other lines of genomic evidence (such as shared mutations in individual genes) and (b) large ancestral population sizes throughout the speciation process... The actual result is about 30%, suggesting a population of about 62,000 individuals. This result adds further support to the prior evidence that the common ancestral population of humans and chimpanzees was large."
https://biologos.org/series/genetics-and-the-historical-adam-responses-to-popular-arguments/articles/adam-eve-and-human-population-genetics
5. Perhaps you are thinking that one way to test these two competing ideas that ERVs are old retroviral infections vs. they were originally part of the genome and after the “Fall” somehow changed and evolved into complex infectious retroviruses (never mind that this is an increase in information and complexity post Fall) would be to resurrect an old HERV and see what it did. If it made retroviruses that went on to infect other cells would not that be great evidence to the objective reader that ERVs are old retroviral infections? I think the creationists are focusing on LTRs and not the 10% of ERVs that have the entire genome sequence or all the retrotransposons that have all the genes and LTRs except the env gene. I don’t see how their VIGE idea fits because of these exceptions to their “model”.
That’s what the scientists did. It turns out trying to repair a single human ERV was not feasible, but knowing that a certain family of HERVs had evolved from an ancestor HERV as it jumped around and mutated they could by overlapping and comparing several, work backwards to reconstruct what the original ancestor HERV was. Guess what? It produced viable retroviruses that went on to infect other mammalian cells. And of course, if evolution were not true, they would not have been able to reconstruct the ancestral retrovirus from its evolved downstream ERVs. They called this ancestral retroviral progenitor that became an active retrovirus "Phoenix".
Conclusion: ERVs including their LTRs are not original to the host genomes.
https://www.scientificamerican.com/article/how-to-resurrect-an-extin/ https://www.nature.com/news/2006/061030/full/news061030-4.html
Here is the actual publication: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665638/
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." https://digitalcommons.rockefeller.edu/cgi/viewcontent.cgi?referer=&httpsredir=1&article=1077&context=student_theses_and_dissertations
A mouse ERV reverted to a fully functional retrovirus provirus able to produce retroviruses with only 1 mutation. The defect in Emv-3 is caused by a single base substitution in codon 3 of p15gag.
6. Jon Perry got so much push back against his video on shared ERVs from creationists that he made another video to answer their objections and rationalizations. This is a superb video detailing why their objections fail.
Other videos Perry made in response to creationist objections can be found here:
Creationists are angry with Jon Perry: Endogenous Retroviruses - Part 1 https://www.youtube.com/watch?v=B75lH9FeYiM
Creationists are angry with Jon Perry: Endogenous Retroviruses - Part 2 https://www.youtube.com/watch?v=Ox2-BXTfKss
7. Usually, nearly all creationist objections will contain some kind of assertion that the ERVs (really fragments; only solo LTRs are left most often. See above) are vital for functions (functions, functions, and more functions!!!) and that is why chimps and humans (and the other great apes) share them in the same homologous locations. But not all humans have some LTRs, so that is a difficulty for creationists. They must admit SOME of them must have been from retroviruses. In addition, the host already has it's own promoters and enhancers - why also have them from viruses? And of course why do the ERVs we find nest in a way that shows evolution? We can use these observations to evaluate the creationist attempt to discount shared ERVs as great evidence for common ancestry in the great apes as is done in this 20 minute video:
8. In June, 2023 a fascinating report was published that detailed a type of cellular survival of the fittest that occurs in every early embryo - "An Ancient Battle Is Playing Out in the DNA of Every Embryo" Millions of years ago, retroviruses invaded the human genome. Today some of these viral remnants threaten the developing embryo while others fight to defend it."
9. In January, 2024 researchers identified a viral gag gene that produces the viral protein MERVL-gag which is necessary in very early embryonic and modulates our URI gene.
Summary
I have chosen shared ERVs between humans and the other great apes because I think that this observation represents some of the best evidence for evolution. That it also satisfies desires for “macroevolution” and human evolution evidence is a special bonus.
The concept of shared ERVs is deceptively simple. Let me try another analogy in addition to the plagiarized papers I already gave. Let’s say we have two persons living in different states or countries. They are each instructed to take identical pistols and bullets and fire 100 shots at a paper target 50 yards away. When you compare the two targets all the holes line up. That of course is mathematically impossible. Somehow the targets were copied either from one of them or a third master target - but the targets somehow trace back to the same ultimate origin. The bullets are like the retroviruses targeting the host DNA. The bullet hole edges are ragged like the cut-ins in the host DNA with flanking TSDs at either end. What we know is that these were not independently created. Most importantly, there are 200,000 shared exact homologous “holes” (ERVs) between chimps and humans in their genomes. The ONLY rational explanation is that chimps and humans share the same origin and that these insertions could only have happened before the species split. To invoke a “Fall” that originally these were designed for something else and somehow jumped out of the cell after evolving all kinds of enzymes and a multilayered space capsule to go between cells now as a parasitic virus stretches the imagination beyond breaking points. Of course, the fact that the ERVs can be nested in a phylogenic tree showing evolution invalidates VIGEs and "The Fall" mythologies as just ad hoc rationalizations.
Are there more examples of evolution from comparative DNA findings in the great apes? Absolutely.
A. Human chromosome 2 is a fusion of two chromosomes and if one lines up chimp chromosomes 12 and 13 end to end to our HC2, they match (called 2a and 2b when comparing all of the chromosomes between us and chimps). See my discussion of HC2 fusion here. After our ancestors split from a common ancestor we shared with chimps, we went from 48 chromosomes to 46 sometime 1- 3 million years ago. For individuals this only takes two generations in a population. The reason I don’t list this as the best evidence for evolution is that it could still be claimed that a creator/designer just made humans that way after creating the other great apes. To my astonishment however many creationists are actually arguing that HC2 is not a fusion.
B. It turns out that our DNA breaks frequently and we have emergency repair mechanisms that quickly patch them, grabbing any DNA close by. This produces unique scars that can be identified and compared across species. As with shared ERVs, they also show common descent and ancestry and also will independently nest in evolutionary phylogenic trees, proving evolution. See DNA repairs, this site.
C. Another DNA finding is similar to shared ERVs. It turns out that we have about 20,000 pseudogenes - old mutated genes that no longer function. And we share many of them in the same locations often with the same mutations as chimps and less so with the other great apes who are more distantly related to us. This also is great evidence that we share a common ancestor with chimps, and evolution explains the similarities in our looks (phenotypes) and at the genetic level (genotypes) while common design is ruled out. Evolution is demonstrated to a very high level of confidence when looking at our genomes and comparing them to other animals, especially chimps and the other great apes.
Let alone that we carry pseudogenes for making egg yolk, chickens carry old non- functioning genes for making teeth and tails, and of course even whales will on occasion grow hind legs from old DNA they possess, called an atavism. See my discussion about pseudogenes. See my whale evolution videos about atavisms. Anti-evolutionists must stop denying our biological histories. As one person wrote, the newer DNA findings result in a second Galileo moment for creationists. The DNA findings cry out common descent, common ancestry. Evolution, “macroevolution” is true not only from the fossils, biogeography, developmental biology, etc. but confirmed by DNA findings.
References
1. How the Placenta evolved and why https://whyy.org/segments/the-placenta-went-viral-and-protomammals-were-born/?fbclid=IwAR1xG6y3zP3NOOMWbOKW17ikvBUvgnY9nIOtpjaPxWbRECbdwnfsnzO8myI
2. Endogenous retroviruses - increasing genomic plasticity [functions for parts of ERVs]
3. Essential role of endogenous retroviruses in evolution
4. The Case For Junk DNA [with comments about ENCODE] https://journals.plos.org/plosgenetics/article?id=10.1371%2Fjournal.pgen.1004351&fbclid=IwAR0Sih-kUTid35xGiASCeg8veWc4u871lPJQCKjXACubtSNHQ7tFe2v0BwQ
5. Three layers of evidence for evolution from ERVs
The above has site has been removed. Google docs copy: https://docs.google.com/document/d/17KaYjZ9zM7e8zkG2y9udqVG-NQJx-QP_Gjz1xzyt5Fk/edit?fbclid=IwAR0OUCVejbJ7Xbqz0Cl0hjRAasAi90sVv8y-ppLAv2e67AVy_ctKlROIHA8&pli=1#heading=h.lb8ebmgum4wx
His YouTube explanation: https://www.youtube.com/watch?v=_kfLo4Wd6cc
6. Finlay, G. 2021. Human Evolution: genes, genealogies and phylogenies.
Paperback ed. Cambridge University Press. 283 pg. without Ref and Index
7. Origin and Deep Evolution of Human Endogenous Retroviruses in Pan-Primates. 2022, June 23. Viruses. 2022, 14(7), 1370; https://doi.org/10.3390/v14071370
8. The Evolution of the HERV-W group.
HERV-W Group Evolutionary History in Non-human primates: : characterization of ERV-W orthologs in Catarrhini and related ERV groups in Platyrrhini. 2018.
9. Hunting Fossil Viruses in Human DNA https://www.nytimes.com/2010/01/12/science/12paleo.html#:~:text=In%20the%20latest%20issue%20of,viruses%20lurking%20in%20our%20genome.
9. Ancient Viruses in Your DNA Fight Off New Viruses https://www.wired.com/2016/03/ancient-viruses-hidden-human-dna-fight-off-new-viruses/
10. Million Year-old viruses help fight cancer, say scientists
11. Ancient Viral DNA may help humans fight infections
12. New study reveals an innate genome response to retroviruses in kolas.
