Refuting the Critics: Endogenous Retroviruses

Ancient viral infections or created units of DNA function?


Featured in: SPECIAL CREATION (Upcoming book Dec 2020)

We have covered endogenous retroviruses in great deal throughout all of our books and videos. There are still some very militant critics who refuse to admit that ERV’s are not evidence for universal common ancestry. One of these critics is named Barry Desborough and this is his blog that we will be debunking in this article:

Mr. Desborough has also attempted to assert ERV’s are evidence for universal common ancestry by looking to the “Phoenix Virus” Experiment. This can be found at his blog titled “ERV FAQ: What’s all this about the Phoenix Virus? Sounds like a Michael Crichton science fiction story! This experiment proves that ERVs originated as retroviruses.”

This critic completely misunderstands the point of dispute. The question is not whether ERV-like sequences can form viruses (in fact, one creationist hypothesis for the origin of viruses post-Fall is that they arose from ERV-like sequences in our genome--For example: instead of coming into our genome from the outside, they may have originated from within our genomes--More on this in the video). The more important question is: are ERV-like sequences functional units of DNA? The "Phoenix virus" experiment does not answer this question. The data strongly supports the VIGE model (Variation Inducing Genetic Elements). Dr. Peer Terborg points out why mainstream scientists are backwards in their thinking when it comes to these functional DNA elements all throughout the genomes of living organisms:

“The findings of the new biology demonstrate that mainstream scientists are wrong regarding the idea that transposable elements are the selfish remnants of ancient invasions by RNA viruses. Instead, RNA viruses originate from transposable elements that were designed as variation inducing genetic elements (VIGEs). Created kinds were deliberately frontloaded with several types of controlled and regulated transposable elements to allow them to rapidly invade and adapt to all corners and crevices of the earth. Due to the redundant character of VIGEs, their controlled regulation may have readily deteriorated and some of them may now merely cause havoc. The VIGE hypothesis provides elegant explanations for several biological observations that may otherwise be difficult to interpret within the creationist framework, including the origin of diseases (RNA viruses) and chromosome rearrangements. The VIGE hypothesis may be a framework for extended creationist research programs.” Source:  Terborg, P., The design of life: part 4—variation inducing genetic elements and their function, Journal of Creation 23(1):107–114, 2009.


Are these DNA elements really evidence for universal common ancestry? Or are they evidence for God’s amazing design. The created heterozygosity and front-loading of DNA elements model best explains the data. Dr. Peer Terborg continues in the next sentence answering a number of important questions as to why these variety of DNA elements are created units of DNA function:

Some intriguing questions can already be raised. 1. Were VIGEs intentionally designed to cause diseases? No, they were not. It is conceivable that the transposition and integration of VIGEs is not entirely random. The transposition of VIGEs may have been originally present in the baranome as controlled and regulated elements and activated upon intrinsic or external triggers. To induce variation in offspring, triggers for the transposition of VIGEs could be released during meiosis, when the reproductive cells are being produced. The emergence of RNA viruses from VIGEs may be a result of the Fall, when we were cut off from the regenerating healing power of the Creator.

2. Why are some VIGEs located in the exact same position in primates and humans? Each original baranome must have had a limited number of VIGEs, some of which we still find on the same location in distinct species. In distinct baranomes, VIGEs may have been located on the exact same positions (the T-zero location), which then explains why some VIGEs such as ERVs, can be found in the same location in, for instance, primates and humans. In addition, sequence-dependent integration of VIGEs may also contribute to this observation.

3. How could Bdelloid rotifers, a group of strictly asexually reproducing aquatic invertebrates, rapidly form novel species? Asexual production of progeny, as observed in Bdelloids, is found in over one half of all eukaryotic phyla and is likely to contribute to adaptive changes, as suggested by recent evidence from both animals and plants. The Bdelloids may have been derived from pluripotent baranomes containing numerous DNA transposons and retro elements, including active LTR retrotransposons containing gag, pol, and env-like open reading frames. These elements are able to reshuffle the genomes and facilitate instant variation and speciation.

4. Do we also observe remnants of DNA viruses in the mammalian genomes? If not, this advocates my idea that RNA viruses emerged from VIGEs, and implies DNA viruses have a different origin; probably, as with the Mimi-virus40, they originated from degenerated bacteria. 5. Why was a class of VIGEs designed with information for protein capsids? The capsid may have been acquired from the host’s genome or it may have been designed to prevent the RNA molecules from attaching themselves to, or finding, integration sites. A very speculative idea may be that these VIGEs were designed to shuttle information from the soma to the germ-line. One thing is clear, however: creation researchers have loads of work to do.”

         In my book “The First Couple-Independent Origins”, I reference Dr. Jeffrey Tomkins who has examined the function of these front-loaded DNA elements in great detail.

         “When it comes Transposable Elements (TEs), Dr. Jeffrey Tomkins in his review of Dr. Jonathan Well’s book The Myth of Junk DNA, points out that in every identified class of Transposable Elements, function has been identified:

One class of DNA that has also been the target of evolutionary propagandists is the diverse group of DNA features called transposable elements (TEs), sometimes referred to as “jumping genes”. Many scientists have stated that all of the subclasses in this diverse group were merely genomic baggage conferred by ancient ancestral viruses that infested our DNA and have served no other purpose than to bloat and expand the genome with meaningless DNA fragments. However, the past several decades of research now show that every identified class of TEs (LINEs, SINEs, ERVs and DNA-transposons) all have important roles in the function of the genome during development, growth, and day-to-day physiological activity. Wells discusses the history of these discoveries along with detailed information about each sub-class of TE and its currently known functional characteristics. Interestingly, all of these TEs are now known to have multiple functions depending on the type of cell and its activity. Rather than cryptic viral genome contaminants, it is now clear that TEs are absolutely critical to genome function and survival. TEs apparently also play important roles in cell stress responses and other protective measures. The Myth of Junk DNA clearly shows how the various classes of TEs present in the genome are not useless trash, but indispensable functional factors.” Please see: Tomkins, J., The junk DNA myth takes a well-deserved hit, Journal of Creation 25(3):23-27, 2011. Also see: The Myth of Junk DNA by Jonathan Wells.”

In the next paragraph of my book cited above, I debunk the claim that these incredibly important functional roles could have been co-opted through evolutionary processes.

“Critics of biblical creation have attempted to say that the various functional roles discovered in Transposable Elements were co-opted. They have invented a fancy story to explain away the data that is contradictory to their evolutionary story. They have also attempted to downplay the evidence for function by asserting these functions are rare and only few. Is this really the case? I address these objections in my book “Why Human Evolution Is False: The Scientific Case For Independent Origins”. 

The evidence is irrefutable. The data is unquestionable. We can see a multitude of peer reviewed technical papers validating the remarkable functionality of these Endogenous Retroviruses. And not only the ERVs, but incredible functions for the other various classes of retrotransposons. Guardians of evolution will habitually downplay the function and say it's only a few trivial functional roles discovered in these retrotransposons. 

Evolutionists once again are hopeless in their struggle to hold onto what they once claimed was the absolute best evidence for human evolution. These ERVs and other classes of retrotransposons are not just “kind of '' functional, they are extraordinarily functional to the point that they are critical to the health of living organisms. Then the evolutionist will try to say these functions were co-opted, when in fact, there is absolutely no evidence for this so-called co-option.  

Anytime a proponent of evolution tries to say these functions, such as regulating genes and determining cell types, or even important in development, were co-opted, just know that it is a clear confession that they have no genuine empirical answer. This answer to the function of retrotransposons is a rescue device employed to desperately hang on to this last piece of evidence for human evolution. Declaring they were co-opted is nothing but fancy storytelling void of any real empirical data and real scientific substance. It is time for the evolutionists to tap out and accept the truth of Biblical creation and independent origins.” (pages 76-77)

In the same article, Dr. Jeffrey Tomkins explains why ENCODE has been so important in overturning the junk DNA paradigm:

During the course of explaining these concepts, the publicly-funded ENCODE project (Encyclopedia of DNA Elements) is mentioned. ENCODE was a critical public research effort that discovered how much of the genome, even the parts that do not directly code for protein, is regulatory in some way. In fact, the regulation of gene expression by the wide variety of RNAs produced from non–protein-coding DNA sequence are now being perceived as more important targets of study than the actual protein-coding sections of the genome. The wide diversity of noncoding RNAs (ncRNAs) in a cell affects virtually all aspects of growth, development and physiology. The protein-coding sections of the human genome, comprising less than 3% of the whole, are somewhat analogous to the raw materials (bricks, boards, wire, etc.) one would use in a building construction project. It is the intelligent oversight, implementation and usage of these raw materials that makes the building take shape and function, and that seems to be what ncRNAs are used for.”

The evidence for genome-wide functionality is overwhelming.Source: Standing For Truth. The First Couple: Adam and Eve – Independent Origins.

         In his article titled “Large scale function for ‘endogenous retroviruses’”, Shaun Doyle points out that it is not just 1 or 2 functional roles found in these ERV’s as the proponents of ape-to-man evolution like to assert as a counter argument to the data:

         “Moreover, researchers have recently identified an important function for a large proportion of the human genome that has been labelled as ERVs. They act as promoters, starting transcription at alternative starting points, which enables different RNA transcripts to be formed from the same DNA sequence.

‘We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1,743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5’ untranslated regions (UTRs).’


‘Our analysis revealed that retroviral sequences in the human genome encode tens-of-thousands of active promoters; transcribed ERV sequences correspond to 1.16% of the human genome sequence and PET tags that capture transcripts initiated from ERVs cover 22.4% of the genome.’

So we’re not just talking about a small scale phenomenon. These ERVs aid transcription in over one fifth of the human genome! ‘These data illustrate the potential of retroviral sequences to regulate human transcription on a large scale consistent with a substantial effect of ERVs on the function and evolution of the human genome.’3 This again debunks the idea that 98% of the human genome is junk, and it makes the inserted evolutionary spin look like a tacked-on nod to the evolutionary establishment. These results support the conclusions of the ENCODE project, which found that at least 93% of DNA was transcribed into RNA.” Source: Doyle, Shaun., Large scale function for “endogenous retroviruses’, Journal of Creation 22(3):3, 16, December, 2008.

The empirical data is exactly what a biblical creationist would expect—Why would God design life that is composed of mostly junk, evolutionary leftovers, ancient viral infections, and genomic fossils? Based on the design hypothesis, we would expect genomes of function and functional DNA elements.

Also—Please read these technical articles on this important topic (if the critics think they have any rebuttal at all—they have a lot of work to do):

Luskin, C., ‘Large Scale’ function for endogenous retroviruses: Intelligent Design prediction fulfilled while another Darwinist argument bites the dust, Discovery Institute, 21 August 2008,

Evidence for the design of life: part 1—genetic redundancy

Evidence for the design of life: part 2— Baranomes - Terborg, P., The design of life: Part 2—Baranomes, J. Creation 22(3):68–76, 2008.

The design of life: part 3—an introduction to variation-inducing genetic elements - Terborg, P., The design of life: Part 3—an introduction to variation-inducing genetic elements, J. Creation 23(1): 99–106, 2009.

The design of life: part 4—variation-inducing genetic elements and their function - . Terborg, P., The design of life: Part 4—variation inducing genetic elements and their function, J. Creation 23(1):107–114, 2009.

The ‘VIGE-first hypothesis’—how easy it is to swap cause and effect

(Search for these 5 must-read articles for further understanding on this topic)

Also—Please see:


Answering Barry Desborough’s specific questions in his blog cited at the beginning of this article:

1:) What is reverse Transcriptase designed to do? Viral Genome Size Distribution Does not Correlate with the Antiquity of the Host Lineages; “Our results also suggest that since retroviruses appear to be restricted to plants and vertebrates, they could NOT have played a role in the evolutionary transition from primitive cellular RNA genomes to the extant DNA-based genetic systems of extant cells, nor the viral reverse transcriptase can be considered an evolutionary vestige of the polymerase that played a role in this transition.” The results presented here demonstrate that viral genome sizes are not randomly distributed, but do not appear to be correlated with the antiquity of their hosts. Therefore, viruses may be ancient, but not primitive. Link 


2:) “What is integrase designed to do?” It was designed to be a multidomain enzyme. Here is another thing. “Most ERV copies suffer mutations over evolutionary time that prevent the normal assembly of viral particles, preventing horizontal transmission of infections between individuals.” Link 

3:) Why are ERVs designed with a viral codon bias?” Because Taxonomic boundaries do exist and these originally designed ERV’s were not meant to be crossed. This is why Viruses from a bat cause things like Covid in humans but bat’s remain unaffected. 

4:) “What is the design purpose of re-transcribable promoters?” Well if these are functional DNA elements with important factors then they need to be read like other promoters. Just because viral genes are robustly transcribed during the stage of infection when host transcription is reduced doesn't mean that this was their design purpose originally.

5:) “What were the HERVs that produced the consensus sequence that generated Phoenix designed for?” Since what I know about “the Phoenix virus”, is that French researchers resurrected a retrovirus that became trapped in the human genome. When they exposed Phoenix to cultured human and mammalian cells, they observed spiky virus particles pinching off from the cells and floating in between them. The genomes of the cells also contained new HERV-K sequences, indicating the viruses had infected them. Since this Phoenix virus belongs to the human endogenous retrovirus line only (K-type). Then it was probably an original functionally created ERV that worked in placental development like other HERV-Ks were discovered to do. This could be a reason that there’s so many fetal developmental problems today. I would imagine this died out from mutation, like most ERV’s are dying from today. Every known ERV has lethal mutations in them. What is funny is that “they” evolutionary secular sciensints, believe that this is one of the oldest ERV’s to infect humanity going back 5 million years ago. Yet, when it began to function and form particles capable of infecting mammalian cells in culture. They quickly stated that this happened because the (HML2) family is an evolutionarily "young" family of retroviral elements. The mutations in the resurrected Phoenix virus were still active even though the Phoenix virus is nearly dead. The resurrected Phoenix produced some 'genomic offspring' that may be responsible for the synthesis of the retroviral particles that can be observed in some human cancers such as germline tumors and melanomas.

Another thing, 5 million years is just an arbitrary number they pulled out of thin air. I could write an article on the Phoenix virus and say, no its 4.5 million years old and it would have just as much credibility because no one knows. But, use a date of just thousands of years ago and now all of a sudden this doesn't agree with Evolution and you are stirring the pot too much. When you see numbers tossed around like 5 million years old, you can take that with a grain of salt because they have no evidence, no proof, nothing. To show that this is true. Pure assumption, mixed in as truth, and sold to the public as fact. The story they wield is just retrofitted to fit the evolutionary model. They didn't predict that any ERV would have any function, let alone so many of them with vital functions! Their ad hoc rescue device about them gaining function has no evidence whatsoever. They just needed to say something about it because it was devastating to the theory. 

6:) What is the design purpose of BOTH Exogenous and Endogenous KoRV? Weird question, ERVs do not constitute a separate taxonomic division from exogenous retroviruses. Here we find this comment “(This refers to ERVs as a whole; any individual ERV locus or family may still represent a novel (and possibly extinct) retroviral genus). Link So I will just say for example that their functions work in conjunction with one another, they have discovered “many ERVs is interrupted by termination codons, deletions or frameshift mutations, some ERVs are transcriptionally active and recent studies reveal protein expression or particle formation by human ERVs.”

7:) “If Chimp and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?” For the same reason similar genes break in unrelated species and related species. Some genes are just weaker than others. The more important, the more conserved. It must be noted that evolutionists believe that for each virus there are many thousands of sites at which it could insert. Thus the odds that they became inserted in the same region in primates and humans is proof of ancient common ancestor relation, but here is the thing. This is not true, that is an assumption. How can I say that? Easy! Observable evidence tells us this. Different types of regions literally show us that specific viruses favor insertion into a particular spot in the genome. For example, HIV (human immunodeficiency virus) tended to insert in gene-rich regions only. MLV (murine leukemia virus ) favored integration near transcription starts, while ASLV (avian sarcoma-leukosis virus) showed only a weak preference for active genes. So clearly when some viruses enter into the system they are attracted to similar places. So this is even more evidence that if these were not all created elements at the start, that their location inside similar species is not evidence of a common ancestor but similar reaction by the virus to bind at similar spots. 

  Over 100 LTRs have been demonstrated to help control transcription of human genes Link and several thousand other LTRs could potentially have that function as well. ERVs and other transposable elements are known to play roles in the three-dimensional organization of the genome by functioning as ‘anchors’ that serve to isolate regions of active transcription and by modifying the structure of chromatin. Link 

8:) “What is the design purpose of giving some people certain HERV’s and others not?” Well you have to remember that humans originally did and that over time mutations and Polymorphism occurred in them and they are no longer shared in all people or they are missing all together because of it. For example, when it comes to HERV’s specifically “there are at least 8, and perhaps 11, of these elements are insertionally polymorphic, meaning, some human individuals have the insertion while other individuals have the empty, pre-insertion site. This shows that this virus family has been transcriptionally active within the age span of the human race.” Link 

9:) What is the design purpose of creating different syncytins in different placental lineages? Well the ERVW-1 gene is EXTREMELY VITAL since it is required during placenta morphogenesis. The fact that there are different created syncytins in different placental lineages is just more proof that it was designed and created because what are the odds that different  placental lineages all obtained an ERV that just happened to all retain its original fusogenic properties and participates in trophoblast fusion and the formation of a syncytium during placenta morphogenesis.” Let that sink in. Link 

Think about this everyone. Are bacteria important? Are they good for you? You bet they are. You couldn't even live without them. So of course they were created within us. The same applies with ERV’s. Are they important? Are they good for you? You bet they are. Life could not exist without them. Now, does this mean that some are not harmful to us in today's world? Of course not. But Genetic Entropy explains this.

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