ERV's Part 2
Featured in 100 FALSIFICATIONS by Rawmatt
Evolutionists discovered ERV’s and immediately tossed them in the Junk bin, calling them 100% worthless and regarded them as “deleterious genomic parasites”. They predicted that ERVs would never be found to have function as they are just leftover fossil footprint remnants of long dead viruses. They even said that “If ERVs are found to have function, they would be highly unlikely to have come from retroviruses.” BAD NEWS EVOLUTION = Many ERVs (complete and also fragmented) are functional DNA elements! Without ERVs located at the 2 cell level, embryogenesis can't even occur!
Also; “We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1,743 cases whereopii transcription is initiated from ERV sequences that are located in gene proximal promoter or 5’ untranslated regions (UTRs).” https://www.ncbi.nlm.nih.gov/pubmed/18535086 It’s Codon redundancy that plays multiple functional roles. Abstract Endogenous retroviruses (ERVs), which are regarded as “deleterious genomic parasites”, were previously considered to be “junk DNA”. However, it is now known that ERVs, with limited conservatism across species, mediate conserved developmental processes (e.g., ZGA). Transcriptional activation of ERVs occurs during the transition from maternal control to zygotic genome control, signifying ZGA. ERVs are versatile participants in rewiring gene expression networks during epigenetic reprogramming. Particularly, a subtle balance exists between ERV activation and ERV repression in host–virus interplay, which leads to stage-specific ERV expression during pre-implantation embryo development. A large portion of somatic cell nuclear transfer (SCNT) embryos display developmental arrest and ZGA failure during pre-implantation embryo development. Furthermore, because of the close relationship between ERV activation and ZGA, exploring the regulatory mechanism underlying ERV activation may also shed more light on the enigma of SCNT embryo development in modern animals” https://www.mdpi.com/1422-0067/20/3/790 Learn even more here; genetic-degeneracy-goes-way-junk-dna/
That's right everyone! These supposed ancient dead junk viral proteins actually affect gene expression in the developing embryo by protecting the cells from infection by other viruses. Some ERVs found in humans are full-length and called (HERVKs) they are still functional as you have seen in embryogenesis. They also increase IFITM1 levels (a Protein Coding gene) on the cell surface and inhibit viral infection. While the smaller bits and pieces of ERVs (supposedly broken ERVs) also have crucial functions as well. Such as helping regulate genes, transcription, they play an important role in pluripotent stem cells and even determine cell types. So for them claiming they are all “co-opted” is nothing but pure assumption.
In 1999 Barbulescu, et al. showed that, of ten HERV-K proviruses cloned, eight were unique to humans, while only one was shared with chimpanzees and bonobos.
Another study here; “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.” http://bit.ly/3bccb5F
ERV’s and most viruses are supposedly hundreds of millions of years old if not older. This is pure speculation as no one has ever seen an ERV do this and because what we see in the world today is how fast viruses change. That’s why people get a new flu shot every year. Viruses mutate so fast, that after only a few hundred years, basically nothing of the original genome may be left. See the contrast between reality and Darwinian theory?
ERV’s are actually vital to the placenta as well. ERVs also aid transcription in one-fifth of the human genome. Then they found that ERV’s are vital for the gene p53 “The ancient retroviruses … helped a gene called p53 become an important “master gene regulator” p53 was crowned “guardian of the genome,” as biologists now call it. Its job is to coordinate the surveillance system that monitors the well-being of cells. Indeed, p53 is so important that when it fails, cancer often results. About half of all human tumors contain a mutated or defective p53 gene.” Another study revealed they activate in gene dense regions to control gene expression. They are not spread randomly throughout the genome as previously thought. So DNA isn't full of parasites at all, but rather many sophisticated ways to control gene expression. An Evolutionists might ask why the positioning of human ERVs are so similar to the positioning of chimp ERVs if viruses didn’t put them in the common ancestor? There are many Similar ERVs in Unrelated Organisms; This study = talks about the brushtail possum http://jvi.asm.org/cgi/content/full/75/5/249 This study shows cat genus, Felis has the baboon RD114 virus http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120 How could it be that unrelated ERVs in different species created essentially the same gene? “ERVWE1/Syncytin-1 and ERVFRDE1/Syncytin-2 are specific to primates and thus do not exist in other placenta. However, this apparent endogenous retrovirus hijacking for placentation use is not restricted to the primates. Indeed two unique endogenous envelope genes of retroviral origin have been found in the mouse, i.e. Syncytin-A and –B …” http://AtlasGeneticsOncology.org/Genes/ERVWE1ID40497ch7q21.html The rescue device for this? You guessed it “Convergent evolution” LOL. One may try to argue that convergent evolution is the answer they want or need, One may try and argue that convergent evolution is the answer, as the author of the quote did, but this explanation has no real scientific basis. Convergent evolution is only ever used to explain similarities between organisms that are otherwise unrelated. It’s a rescue device you see all the time used by evolutionists.
Are ERVs dormant viruses today? That’s the real question… No. They tell us these (supposed) viral invaders populating our genome have mutated to the point that they no longer lead to active infections. So why think they ever were? Besides the obvious visible gag, pol & env we see looking at them. However, When they mutate today they lead to disease! You see, scientists assume that if a sequence of a viral DNA is found in two different animal species then they probably are related and must have had a common ancestor. We know this is wrong because circoviruses, for example, are a group of viruses that are known to cause stomach problems in dogs. But upon closer investigation, these viruses have been found in the genomes of dogs, cats and panda bears. Since we now know none of these had a common ancestor then that lends more credence to the fact ERV placement sequences in common species have no validity. https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1001191
The matter of fact there are multiple theories and models for where these viruses came from and they’re still debated today. One is the virus-first model, another is the Escape hypothesis, and even another is called Giant (mimivirus) viruses theory. https://www.nature.com/news/giant-viruses-open-pandora-s-box-1.13410 / The Regressive model combats these as well especially the mimivirus theory.
It is interesting to note that ERVs are different from the retroviral genomes from which they are supposed to have originated from. Evolutionists usually explain this away by claiming that the ERV sequences have evolved to the point where they are quite different from their ancestral genomes. If this is so, then there is consequently very little to lead us to the conclusion that ERVs are derived from retroviruses.
If ERVs really are a product of retroviruses, how could they have been inserted into reproductive cells thousands of times, without fatal damage to the host then turn out to not only be beneficial but essential in our survival? Having healthy and strong reproductive cells is mandatory to produce a viable zygote, so why would viral-infected reproductive cells be considered more fit than ones without ERVs? Furthermore, how could they survive for hundreds of thousands of years in two different species? Now imagine every species on Earth/
Changes to the reproductive cells are rare and often harm the animal. So why should we believe that ERVs were inserted many thousands of times and no real problems arose back then but do now? It’s not logical.“In short, the notion that molecules of germ cells … are in states of perpetual change is not, in our present understanding of cell biology, tenable. This doesn’t mean that “molecular change does not occur; only that mechanisms provoking such change in germ cells are likely instantaneous and stochastic and probably often lethal (Maresca and Schwartz 2006) — which will preclude their persistence into future generations.” http://www.mitpressjournals.org/doi/abs/10.1162/biot.2006.1.4.357
ERV’s play an important role in pluripotent stem cells. Which may help explain how these cells maintain a state of pluripotency and are able to differentiate into many types of cells, could have profound implications for therapies that would use pluripotent stem cells to treat a range of human diseases. https://www.sciencedaily.com/releases/2013/01/130123133930.htm Do evolutionists really think an old dead virus can just mutate and then play such a crucial role as the ability of a cell to develop into the three primary germ cell layers of the early embryo then mutate again into all cells of the adult body? That without ERVs life could not even exist because there could be no offspring!!! They are illogical. These cells basically assign cell types to cells. Stem cells are vital for life.
The word ‘virus’ means toxic or poison, and that is how most evolutionists perceive them. However, if 50% of our DNA is made up of viral elements, wouldn’t that indicate that they might be essential genetic elements and that these viral elements just might be another regulatory network in organisms? This is just another case why evolutionary-based science is a menace to scientific research, discovery, and progress.
1.Retrovirus HERV-H was highly associated with epigenetic markers
- It's also associated with inducing pluripotency
- the HERV-H was also strongly associated with binding sites
So here we have VIRUSES or what you would call them. That normally would ravish its host, especially at that frequency! But instead its inducing pluripotency. It evolved in factors that bind to transcription binding sites (something viruses never do). And it is involved in chromatin and epigenetic markers.
You see, scientists assume that if a sequence of a viral DNA is found in two different animal species then they probably are related and must have had a common ancestor. We know this is wrong because circoviruses, for example, are a group of viruses that are known to cause stomach problems in dogs. But upon closer investigation, these viruses have been found in the genomes of dogs, cats and panda bears. Since we now know none of these had a common ancestor then that leads more credence to the fact ERV placement sequences in common species have no validity. https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1001191
The matter of fact there are multiple theories and models for where these viruses came from and they’re still debated today. One is the virus-first model, another is the Escape hypothesis, and even another is called Giant (mimivirus) viruses theory. https://www.nature.com/news/giant-viruses-open-pandora-s-box-1.13410 / The Regressive model combats these as well, especially the mimivirus theory. We found ERVs that contradict the animal phylogeny. Experts in the field claim this with their evidence: https://link.springer.com/chapter/10.1007%2F978-94-007-4899-6_3
Here we see ERV’s do not help them either
ERVs are required by the body and do not do the same thing in apes as they do in humans, so that's destroyed real easy.
When evolutionists actually compare the gene sequences of RNA viruses that exist today and make their typical assumptions about mutation rates and evolutionary dynamics, they come to the conclusion that the RNA viruses we see today originated, at most, 50,000 years ago according to the evolutionist's timescale. Why is this a paradox? Well, remember that retroviruses are RNA viruses, and they are supposed to have been infecting primates long before humans evolved. Thus, in evolutionary terms, they need to be much older than 50,000 years old.
"Yet a very different picture of RNA virus origins is painted if their gene sequences are compared; by using the best estimates for rates of evolutionary change (nucleotide substitution) and assuming an approximate molecular clock (21, 33), it can be inferred that the families of RNA viruses circulating today could only have appeared very recently, probably not more than about 50,000 years ago. Hence, if evolutionary rates are accurate and relatively constant, present-day RNA viruses may have originated more recently than our own species." - Molecular Clocks and the Puzzle of RNA Virus Origins, Edward C. Holmes, American Society for Microbiology Journal of Virology https://jvi.asm.org/content/77/7/3893.full
So, in humans, ERVs are necessary for many things; we have almost 98,000 bits and pieces of ERVs. What they are: are Broken DNA elements left over from our pristine state of creation Most are solo LTRs (retroviral promoters) initiate transcription. But today only a handful (50-60 HERVKs--youngest family of ERVs) are recognizably complete ERVs.
So humans have 50-60 complete HERVKs to compare. But, chimpanzees only have ~20 of the same family. 13 of these are not orthologous with humans at all, so they just tell the public that these were inserted after the human/chimp split. Just another rescue device for evidence that counters their story. ONLY a few complete ERVs are found in the same location!!
Overall it doest matter if ERVs are in the same place or not because it comes down to function. So any alignment is just pointless for proving evolutionary relation.
It's all about function, if ERV’s “are” or “were'' functional, then the entire argument falls apart and creation is vindicated. Lets recap on specific ERV’s and their function… Do these shared ERVs have function? YES THEY DO!
Regarding the HERV-E Family; “While both LTRs were shown to promote transcription in vivo and in vitro, their respective activity and tissue specificity appeared to differ even though they shared a high degree of sequence identity … The results from this study illustrate how slight variations in transcriptional regulatory sequences can have a profound effect on promoter activity and demonstrate the complex regulatory effects of human endogenous retrovirus elements on human gene expression.” Study Think about that for just a second, the same ERV in the same location in a primate does something totally different. And also consider “no infectious counterparts of human endogenous retroviruses (HERVs) are known to exist today” Study
Below is a picture of KAP1, a master gene regulator. You will notice an ERV attached to it! So without ERV’s no regulation of the KAP1 gene. This is utter proof of design, not evolution. The matter of fact, the ERV had to be present from the beginning and this is proof. So this alone destroys an insertion at a later time.
If ERV Elements Deteriorate Rapidly, Why Did Only One ERV Remain Active and Continue to Infect All Placental Mammals Over a 70 Million Year Period?
Evolutionists point to “lack of selection pressure” to explain why ERVs deteriorate rapidly, but then point to “bursts” of copy numbers when they need ERVs to be conserved: “Southern blot analysis of a large series of mammalian genomic DNAs shows that HERV-L-related elements—so-called ERV-L—are present among all placental mammals, suggesting that ERV-L elements were already present at least 70 million years ago. … Phylogenetic analyses allowed the establishment of a plausible evolutionary scheme for ERV-L elements, which accounts for the high level of sequence conservation and the widespread dispersion among mammals … One rather striking feature of our results is the observation of a high level of sequence conservation among ERV-L elements. It is generally admitted that such sequence conservation is a common feature of functional genes, whereas noncoding sequences as well as pseudogenes diverge more rapidly, due to the lack of any selection pressure …
Rather, a scheme in which sequence conservation is the unnecessary consequence of the transpositional activity of the transposable element itself (which requires both transcription activity and coding capacity), independent of any possible selective pressure imposed by the host, appears more plausible and would account for the data. According to this scheme, a functional sequence present in an ancestor of mammalian species would survive only if active, simply by generating a sufficiently high number of copies, so that despite the fact that such elements are submitted to genetic drift, as any pseudogene-like sequence, and also to elimination through transposon excision, there still remain functional copies of the founder element. Evidence for the transpositional activity of ERV-L elements is provided by the occurrence of bursts in both the primate and mouse branches, which resulted in large increases in ERV-L copy numbers.” http://jvi.asm.org/cgi/content/full/73/4/3301
“endogenous retroviruses in neural progenitor cells. Another intriguing finding in human brain cells and mouse models was that endogenous retrovirus HERV-K’s (complete ERVs) appears to be protective against neurotoxins.” This study even states that because they believe these are nothing but evolutionary leftovers and Despite their prevalence, the function of human endogenous retroviruses (HERVs) in humans is largely unknown. https://pubmed.ncbi.nlm.nih.gov/26818265/
Remember Members of the HERV-K family are typically found in areas near genes [which code for proteins]. The regulatory role of HERVs has been demonstrated in the liver, placenta, colon, and other locations. Source: Norbert Bannert and Reinhard Kurth, “Retroelements and the human genome: New perspectives on an old relation” [PDF], Proceedings of the National Academy of Sciences, 101:14572–14579, 2004.
HERV-K(HML-2), termed HK2, codes for all viral proteins and produce virus-like particles, it is not known if these virus particles package and transmit HK2-related sequences.”
HERV-H is a class of primate-specific endogenous retrotransposons. It is transcriptionally active in both human preimplantation embryos and PSCs, and plays a critical role in pluripotency, stem cell maintenance and somatic cell reprogramming. HERV-H is also epigenetically regulated and is associated with binding sites.
HERV-W The cytotrophoblast cells produced by HERV-W proliferate and invade maternal endometrium, which is key to implantation and placental development.
HERV-R aka (ERV3) is expressed in syncytiotrophoblasts not only in the placenta but also in hydatidiform moles and choriocarcinomas. It seems to be related to cell fusion. ERV3 env is expressed in certain embryonic tissues such as the adrenal gland and nervous tissues. Perhaps this will help explain the Nervous system, as of now. No such luck for evolutionists and we know they are not looking at ERVs for function,
- “Surprisingly little is known about the evolutionary origin of the central nervous system.” Secular scientists are unaware of the evolutionary origin of the nervous system to which they belong.
- “Despite the new genomic data from the diverse animal phyla and improved resolution of the animal tree of life, the field has failed to reach agreement on the nature and timing of the early evolution of neurons.” https://cichlid.biosci.utexas.edu/sites/default/files/evoneuro/files/liebeskind_et_al._2017.pdf
“There is no evolutionary record of nervous systems...”
- “The origins of neural systems remain unresolved.”
HERV-F HERV-F(XA34) Analyses of expressed sequence tags (ESTs) have identified the expression of HERV-F(XA34) sequences in placental tissue, fetal liver/spleen, and olfactory tissue.
HERV-Fb The analyses indicate that the 5'-LTR of HERV-Fb functions as an alternative poly A site of a Krüppel related zinc finger gene (ZNF195).
HERV-p53 shapes and controls the p53 or TP53 gene that codes for a protein that regulates the cell cycle. crowned “guardian of the genome,” Its job is to coordinate the surveillance system that monitors the well-being of cells as well as being a human tumor suppressor. Indeed, p53 is so important that when it fails, cancer results. About half of all human tumors contain a mutated or defective p53 gene.”
Erv-9 controls the ERV9-1 gene (Endogenous Retrovirus Group 9 Member 1) an Uncategorized gene in the database system. So who knows what it does for now.
Overall the HERV-E, HERV-F, and HERV-W families, were found to be active in all tissues with the exception of the rectum and ovary; and the HERV-FRD family, which is inactive only in PBMCs, stomach, and prostate.
ERV3 high expression was found in the following locations: Adrenal glands, Rathke's pouch and (probably) the pituitary gland, nerve roots, primitive glomeruli, peripheral ganglia and structures of the primitive skin. Study
“The majority of HERV elements are riddled with deleterious mutations, large deletions, and insertions of other repetitive elements https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1456821/ the accumulate of random mutations destroy a once complete HERVK making it eventually an inactive fossilized proviruses remnant. Because of this the vast majority of endogenous retroviruses are inactive. All ERVs have lethal mutations. They believe that HERVs play a multifactorial role based purely as a consequence of their abundance in the genome.
Molecular analysis (PCR and Southern hybridization) of CERV 2 elements demonstrates that this family is present in chimpanzees, bonobo, gorilla and old-world monkeys but absent in humans, the matter of fact they still cannot even find correlation between disease and ERVs. “Despite major interest in the link between HERV-W expression and human pathogenesis, no conclusive correlation has been demonstrated so far.”
So, according to them, after monkeys surfed to America from Africa, which all evolutionists believe happened. They are assumed to have brought ERVs with them according to the theory. When they started to split off these supposedly dead junk functionless ERVs got passed on because they are no longer viral invaders that caused harm. So if they have any function then they are not from a virus. Guess what? They do, end of story. The ERV argument is as dead as evolutionism.
“The HERV-W env gene product has also been shown to block infection by an exogenous retrovirus, suggesting that the expressed HERV-W env gene could have a beneficial function to the host (Ponferrada et al., 2003Down).” http://vir.sgmjournals.org/cgi/content/full/85/5/1203
“Thus, HERV-W Env confers host cell resistance to infection by SNV. This is the first report of a human endogenous retrovirus gene product blocking infection by any exogenous retrovirus.”http://www.ncbi.nlm.nih.gov/pubmed/12664292 So wait, a virus produced a gene to block viral infection! There is more evidence, “some avian and murine ERVs can block infection of related exogenous retroviruses at entry by receptor interference; mouse Fv-1 blocks infection at a preintegration step, also can be viewed as an ERV.” http://www.pnas.org/cgi/content/full/101/30/11117
And “in the case of both Fv4 and Rmcf, the mode of defense is by the domesticated env gene blocking the receptor required for retrovirus entry.” Study It gets even more crazy ! “These results suggest that the loss of ERV3 mRNA expression is associated with susceptibility to choriocarcinoma.”
http://www3.interscience.wiley.com/cgi-bin/abstract/112716625/ABSTRACT Now they just admitted that ERVs are beneficaly in preventing trophoblastic cancer!
What does evolution have to say about this? Well they had to say “We propose a model in which Iris has “switched sides,” having been recruited by host genomes to combate baculoviruses and retroviruses, which employ homologous envelope genes to mediate infection.” study That's right everyone, ERV’s infected us, then switched sides and turned on their own virus kind. LOL
Evolutionists might ask why the positioning of human ERVs are so similar to the positioning of chimp ERVs if viruses didn’t put them in the common ancestor? This becomes a pointless question when they realize that there are many Similar ERVs in Unrelated Organisms; “… and two closely related ERV genomes are found in a carnivore (fox) and a ruminant (sheep).”
This study = talks about the brushtail possum http://jvi.asm.org/cgi/content/full/75/5/249
This study shows cat genus, Felis has the baboon RD114 virus http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120
“For instance gamma-retrovirus was isolated from trophoblastic cells of the baboon placenta. This virus was found to be very closely related antigenically and by sequence homology to the endogenous RD114 virus in cats (which is itself unrelated to endogenous FeLV). http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120
How could it be that unrelated ERVs in different species created essentially the exact same gene? “ERVWE1/Syncytin-1 and ERVFRDE1/Syncytin-2 are specific to primates and thus do not exist in other placentae. However, this apparent endogenous retrovirus hijacking for placentation use is not restricted to the primates. Indeed two unique endogenous envelope genes of retroviral origin have been found in the mouse, i.e. Syncytin-A and –B ….” http://AtlasGeneticsOncology.org/Genes/ERVWE1ID40497ch7q21.html
The rescue device for this? You guessed it “Convergent evolution” LOL.
Now look at this….
“Now it appears that another level of evolution occurs that is not driven by point mutations. Instead, retroviruses insert DNA sequences and rearrange the genome, which leads to changes in gene regulation and expression. If such a change in gene regulation is beneficial, it is passed onto future generations.” http://www.physorg.com/news114266805.html
Wait a minute... Did you see what they just said! LOL
That quote is very telling. There are tens of thousands of ERVs in human and chimp genomes. Yet they tell us they mostly are NOT beneficial, yet this article tells us the exact opposite and they will ONLY be passed on IF THEY ARE Beneficial!
So what if ERV’s are in the same spot. It's all about function! “Taken together, our findings suggest that HERVs behave like normal cellular genes and are a permanent component of the transcriptome of a cell.” http://jvi.asm.org/cgi/content/full/79/1/341
They admit they do not know anything here = “The question arises as to whether HERV elements can continue to change our genomic landscape through active retrotransposition or recombination events. While no direct evidence indicates that such events are ongoing in the human genome, members of the HERV-K family appear to be the most likely candidates for playing such a role.” [http://www.genetics.org/cgi/content/full/171/3/1183
Considering Viruses are tested to be young, it's over for them, ERV’s are not old either….
This study is awesome as well and shows viruses are young = https://jvi.asm.org/content/77/7/3893 “While the RNA viruses we see today may not date back quite this far, the evidence that some DNA viruses have evolved with their vertebrate hosts over many millions of years (24) makes an equally ancient history for RNA viruses a natural expectation. Yet a very different picture of RNA virus origins is painted if their gene sequences are compared; by using the best estimates for rates of evolutionary change (nucleotide substitution) and assuming an approximate molecular clock (21, 33), it can be inferred that the families of RNA viruses circulating today could only have appeared very recently, probably not more than about 50,000 years ago.” Hence, if evolutionary rates are accurate and relatively constant, present-day RNA viruses may have originated more recently than our own species.
Before discussing the solutions to this apparent paradox, it is important to determine exactly why the molecular clock estimates of RNA virus origins are so recent.
The data even shows viruses are young. But of course, the writers have to explain this phenomenon by creating Ad Hoc excuses as to why this clock is so young. Remember if a paper isn't worded correctly. It's a great possibility that it won't be published. Grant funding will be stopped and maybe your job will be lost if they are not going along with the paradigm.
It's simple people, ERV's are only about 500 to 600 bases in length. The genome is multilayered. You can just dump vital information into the genome and expect it to function . You can just co-opt hostile RNA sequences from viruses and expect them to play a large role in regulating a genome . Viruses were one functional element of the genome. Now they are corrupt. They have similar features but ERV's perform vital functions and viruses destroy the genome.
ERV’s cannot be from viruses. It's one assumption after another which disregards a plethora of data. The fact that these transposable elements code for regulatory factors that are critical for the regulation of gene expression that produces various organs verifies this. It's nonsense to believe the DNA of a virus could possess the information to regulate genes to produce organs in vastly more complex organisms, especially if one believes the nonsensical idea that they became co-opted for this function since the organ already existed prior to the imagined introduction of the viral DNA!
Humans and chimps were created separately. The matter of fact there are multiple theories and models for where these viruses came from and they’re still debated today. One is the virus-first model, another is the Escape hypothesis, and even another is called Giant (mimivirus) viruses theory. https://www.nature.com/news/giant-viruses-open-pandora-s-box-1.13410 / The Regressive model combats these as well, especially the mimivirus theory. We have also found ERVs that contradict the animal’s phylogeny. Experts in the field claim this with their evidence: https://link.springer.com/chapter/10.1007%2F978-94-007-4899-6_3 If ERVs are from viruses then the probability of this occurring is 0. Therefore, ERVs are not from viruses. Also, ERVs have the exact same mutations in completely separate organisms making it even more unlikely that ERVs are from viruses. There is no proof whatsoever in any study, laboratory or observation that these sequences are from viruses, just hypothetical theories of ERV insertions that supposedly took place millions of years ago because all their prior theories are dying. These sequences of nucleotide bases are part of the original genome.
Also consider this, in order for you to be immune to a virus you would have to be lacking the portion of DNA that the virus is going to affect. There are whole segments that are shared by multiple animals in common with humans and they have solely selected the segments from certain apes and assumed that because they are affected by the virus DNA wise, that we somehow have to be descended instead of realising that this is the same across any animal that has common segments of DNA. Either way, this just points out that the virus just distorts the DNA portion it is designed too and this is as far as it can go. Segments that are similar do not prove ancestry. They prove commonality in segments of DNA based on created functions. The whole point breaks down when you realize how viruses work and that the ERVs are present in all common DNA segments if function is required, revealing a created hierarchical pattern of design. It makes clearly no sense to assume when you realize the sheer number of mutations that would have been required for the vast differences between humans and apes.
If you are really into the technical papers on ERV’s I placed it here; https://docs.google.com/document/d/19K0QmvbtkTikp0uRq3ZzKKcLyO2Qtdfg5DZZNIvb1tc/edit?usp=sharing
As to not bore my readers to death with the details.
When secular science decides to be open minded and look specifically at all ERV’s for function, they will quickly realize the full role they served and still do serve and we will have even more evidence to vindicate creation. Until that time we just have to wait. The question that remains that most important is, were these created elements or later additions to the genome. Given their absolute necessity for life, it seems obvious. Until it's observed and proven that foregn viral invaders can assimilate the genome and turn from disease causing viruses into beneficial DNA elements, the secular camp will be nothing but pure storytelling regarding ERVs.