Commonly located endogenous retroviruses (ERVs) prove common ancestry between different "kinds" of organisms. There are no other viable explanations for them.
New! Executive Summary. Click on this if you want the concise version.
New! Executive Summary. Click on this if you want the concise version.
from creationists about the case for common descent
from endogenous retroviruses (ERVs).
These are specific markers that establish, beyond any reasonable doubt, the truth of common descent.
Each question links to its answer.
If you baulk at my use of the "P" word, "proof", please visit https://barryhisblog.blogspot.com/p/on-proof.html, and for the "T" word, "true", see https://barryhisblog.blogspot.com/p/a-little-learning-is-dangerous-thing.html
If you wish to ask further questions or discuss any entries, post your questions
or comments in the discussion section below, or join the FaceBook group, ERV.
Please visit the Veritas YouTube channel, like, share, comment and subscribe.
See also my interview with Mark Torrender of Talk Beliefs, and do the same.
A more detailed, technical account, with references to the scientific literature, can be found @ "https://web.archive.org/web/20230531193743/http://www.evolutionarymodel.com/ervs.htm" Nov 2009,
Another good one-stop page covering the topic can be found at Jon Peters' site, TruthfulOrigins. Click on the image.
Here's a great video on the subject from "Stated Clearly".
And other vids.
0. This looks hard. Do you have a simple introduction to the subject?
1. What is the "case for common descent" from ERVs?
1.1 What are "Long Terminal Repeats" and how do they confirm common ancestry?
2. Why do virologists and geneticists conclude that ERVs come from retroviruses? Isn't that just supposition on their part?
3. Isn't this just circular reasoning, assuming evolution to "prove" evolution?
4. How many ERVs are shared, in common locations, in the genomes of humans and chimps?
5. Don't retroviruses target particular locations in the DNA? Doesn't this explain corresponding ERVs?
6. ERVs do stuff. Doesn't that prove that they didn't originate from retroviruses, but were designed?
6.1 ERVs PROTECT against viral infection. Surely, this means that they were designed to do so?
7. ERVs promote the transcription of host DNA. Doesn't this prove they are designed?
8. ERVs are essential in reproduction (syncytin and the formation of the placenta). How can this be?
9. Aren't the same ERV genetics in the same places in different species because they have to do the same job?
10. But how can you rule out design as an explanation?
11. How could a species survive a massive invasion of retroviruses into its genome?
12. How could ERVs survive programmed cell death (apoptosis)?
13. The same retrovirus or ERV has been found in two species that evolutionists say are very distantly related. How is this possible?
14. What if we find an ERV in a common location in chimpanzees and gorillas, but not in humans?
15. David DeWitt at AiG says ERVs do not line up with the expected evolutionary progression. What gives?
16. What's all this about the Phoenix Virus? Sounds like a Michael Crichton science fiction story!
17. Hasn't the evolutionist's story about ERVs been debunked by "scientists" such as Dr. Yingguang Liu and Dr. Georgia Purdom?
18. Could you have this backwards? Maybe retroviruses come from designed-in variation inducing genetic elements (VIGEs)?
19. About me.
20. Other articles on ERVs.
21. An interview with Mark Torrender of Talk Beliefs. https://youtu.be/e5sRjGng9kU
22. If anyone wants to go into more detail (a lot more detail) on the subject of virology, look into Columbia University's Virology – Biology 3310/4310 which includes a series of video lectures on YouTube.
23. Extra viewing
Footnote: I am trying to discuss ERVs with a certain Duane Cadwell at http://rationalfaith.com/2019/07/are-young-earth-evidences-needed-to-defend-christian-faith/
Articles:
Perhaps ERV-like sequences are sources of escaped genes that contribute to the genesis of retroviruses. Perhaps retroviruses precede the establishment of ERVs, as is observed today. Perhaps both are true in different instances.
ReplyDeleteRetroviruses produce ERVs, but ERVs have also (rarely) been observed to produce retroviruses. Some creationists speculate that ERVs were designed as tools of genetic engineering, to produce retroviruses and spread genetic material around, and were installed independently in different species. There are problems with this idea.
ReplyDelete1) Retroviruses are pretty indiscriminate as to where they integrate their DNA. This can cause severe problems, and this is why there is so much excitement at the moment of writing about CRISPR, which is a precise genetic engineering/therapy/research tool that does not have these problems. It's not a very good way of
2) Most ERVs are faulty. Disabled by mutation and methylation (thank goodness). The disabling mutations are largely the same in closely related species. See http://barryhisblog.blogspot.fr/p/the-natural-history-of-retroviruses.html
Oops. The editing function is on the blink. Point 1) should end, "It's not a very intelligent way of tinkering with genomes!"
DeleteBarry I've argued with creationists before who have made the same case that all retroviruses we have today came from the ERVs we were designed with.
DeleteOne of the major flaws with this argument is the fact that many of our ERVs are flanked by two near identical LTRs which conform to the pattern U3-R-U5. We know exactly how these duplicate LTRs are formed - they are formed in the reverse transcription process from RNA to DNA.
http://www.microbiologybook.org/flash/hiv-ltr-fn.html
In other words if we ever see and ERV in our DNA flanked by LTRs (and there are tens of thousands of these which are shared with chimpanzees in identical locations), then we can be absolutely sure that this sequence is foreign to our genome and came from a retroviral infection at some point in our past.
I believe the next step the Illuminati plan is to engineer a virus that will change genetics to create Nephilim for Anrichrist's World government. See my books.
DeleteI believe that you are a raving nut-case, Jeremy.
DeleteThe other point to make is that the experiments with the reconstructed Phoenix HERV-K retrovirus demonstrated that you have to remove the mutations from the ERVs in order to get functional retrovirus. If retroviruses were inserting into genomes to produce ERVs, and subsequent mutations altered the ERVs further from that original and functional retroviral genome, then a consensus sequence of different ERVs should give you the original retrovirus genome, and it should be functional. That's exactly what we see. When you line up the ERVs and use them to produce a consensus sequence, that consensus sequence produces a viable retrovirus that also inserts into the same types of genomic motifs (of which there are millions in the human genome) that we find ancient HERV-K insertions.
ReplyDeleteTo use an analogy, you don't conclude that the cars at a junkyard are on their way to becoming new cars. ERVs have all of the dents and rust that you would expect from an ancient insertion.
Here I am, Mr Barry, and so far I have seen no text of yours that accounts for the issues with the potential detrimental effects posed by uncontrolled ERV insertions and activity accumulating during millions of years prior to the evolution of the mechanisms that tightly control these retroviral elements (for example, more than 40 genes are required to properly regulate the ERV's...)
ReplyDeleteERV integrations, like mutations from other sources, are more likely to be detrimental than advantageous. The detrimental ones become extinct because their carriers fail to reproduce so well. The advantageous ones tend to tend to increase in frequency in the population, because they aid successful reproduction. Th eprocess is known as the natural selection of advantageous heritable variations.
DeleteI'm interested, Anon. Do you have an alternative explanation for correspondingly localised ERVs in different species?
Re
Deletefor example, more than 40 genes are required to properly regulate the ERV's...)
I have no idea what you are talking about here
Can you please cite the literature to supply a window into these 40 genes?
Since herv dont have that many tital it must be host genes
Afaik hosts dont have genes thst regulate rv infections
Re
Deletefor example, more than 40 genes are required to properly regulate the ERV's...)
I have no idea what you are talking about here
Can you please cite the literature to supply a window into these 40 genes?
Since herv dont have that many tital it must be host genes
Afaik hosts dont have genes thst regulate rv infections
Re
Deletefor example, more than 40 genes are required to properly regulate the ERV's...)
I have no idea what you are talking about here
Can you please cite the literature to supply a window into these 40 genes?
Since herv dont have that many tital it must be host genes
Afaik hosts dont have genes thst regulate rv infections
Barry, you have done a wonderful job here. I may have already told you this but I know Graeme Finlay personally and have co-presented with him to NZ biology teachers. I also have his book.
ReplyDeleteThank you, David! :) For other readers, Graeme Finlay's book, Human Evolution, is a great source on ERVs and other genetic markers that ceryify common descent. For those who deny common descent for "religious" reasons, Finlay happens to be a Christian.
Deletehttp://www.cambridge.org/us/academic/subjects/life-sciences/evolutionary-biology/human-evolution-genes-genealogies-and-phylogenies
Certify.
Deletehttp://www.sciencemag.org/news/2016/03/viral-fossils-our-dna-may-help-us-fight-infection?utm_source=sciencemagazine&utm_medium=facebook-text&utm_campaign=viralfossils-2747
ReplyDeleteViral ‘fossils’ in our DNA may help us fight infection
https://medicalxpress.com/news/2016-07-kinds-retroviruses-lookor-actthe.html
Traits are determined by gene sequences:
http://sciencerefutesevolution.blogspot.fi/2017/03/human-traits-and-epigenetics.html
No two kinds of retroviruses look—or act—the same
Tomi, Will you enable comments on your bog? If not, I don't see why I should allow you to comment here.
DeleteBTW, the fact that epigenetics can influence traits does not mean that genes cannot.
And also BTW, none of your material addresses the case for common descent from common ERVs!
Folks, this is someone who posts garbage on a Facebook "Intelligent Design" group. He gives the lie to the assertion that Intelligent Design enthusiasts are not just dishonest (is there any other sort?) creationists.
DeleteBarry blocked me after I showed these evidences that prove his claims pseudoscience. There are no mechanisms for large scale evolution.
ReplyDeleteI blocked you on Facebook for being a twat. I'm quite happy to let you document your twattery here. Are you going to let me comment at your blog?
DeleteHey Tomi, isn't it a sin to lie?
DeleteIn the meantime I did some real research (which scientist suppose to do, isn't it?):
ReplyDeletehttps://www.mdpi.com/2073-4409/8/2/130
It is now beyond any doubt that most retroelements serve regulatory. We found 200 million transcription factor binding sites associated with retroposons. So, this ends the junk DNA era completely. It shows that the genome is a computer, where the functional elements (the genes) sit in an ocean of regulatory elements. Every gene in every celltype has its own unique pattern of gene expression due to differential recruitment of retrolements from which the genes are initiated.
So, we are really dealing with VIGEs, not remnants of viruses. Viruses arise in a few recombinational steps from another class of VIGEs, from ERVs:
Deletehttps://creation.com/images/pdfs/tj/j23_1/j23_1_99-106.pdf
https://creation.com/images/pdfs/tj/j23_1/j23_1_107-114.pdf
https://creation.com/images/pdfs/tj/j27_3/j27_3_105-112.pdf
Unknown, you need to read the FAQ entries. You will learn that the "Junk DNA" strawman characterisation of the evidence from ERVs is just that. A strawman. And strawman arguments are fundamentally dishonest. Nobody denies that many elements of ERVs perform functions. Just read FAQ answer #1! Of course, retroviruses include promoters. How else would their genes get transcribed? If you really still think that ERVs are designed, you need to be able to answer, satisfactorily, the questions @ https://barryhisblog.blogspot.com/p/in-science-we-apply-principle-of.html
Deletea) What is reverse transcriptase designed to do?
b) What is integrase designed to do?
c) Why were ERVs designed with a viral codon bias?
d) What is the design purpose of re-transcribable promoters?
e) What were the HERVs that produced the consensus sequence that generated Phoenix designed for?
f) What is the design purpose of both exogenous and endogenous KoRV?
g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?
h) What is the design purpose of giving some people certain HERVs and not others? See also - More ancient viruses lurk in our DNA than we thought.
i) What is the design purpose of creating different syncytins in different placental lineages?
"In the meantime I did some real research"
DeleteSearching for and cherry picking something that you think somehow supports your position is not "real research".
"which scientist suppose to do, isn't it?"
You implication that some scientist has not done "real" research is a lie. Isn't that supposed to be a sin?
And research English grammar.
There are about 200,000 ERVs and ERV fragments are found in common locations in chimps and humans, not 14. Humans and chimps were separately created. The probability of 200,000 ERVs randomly landing in the same corresponding location in the genomes of both chimps and humans is 0. Therefore, ERVs are not from viruses. This means that the majority of ERVs are actually part of the original genome and have been there since the animal was created. The common ancestor of chimpanzees and humans is a mythological creature that never existed.
ReplyDeletePaul, you seem to have either not read or not understood. The ERVs have not landed randomly in corresponding locations in the two species. Each ERV "lands" in a more-or-less random location, but from then on, it is heritable. The reason it is in the same location in both species is that it has been inherited by both species. Read my FAQ further and you will see why we conclude that ERVs derive from retroviruses, and why "design" doesn't explain their existence.
DeleteYou seem to have either not read or not understood. Humans and chimpanzees were separately created, thereby proving that ERVs are not from viruses.
DeletePaul, you have a rather eccentric notion of "proof"!
DeleteThere is nothing eccentric about taking facts and drawing logical conclusions from those facts.
DeleteHey Paul, I thought lying is a sin, and yet you did it repeatedly here.
DeleteCan you explain why Alus are not merely highly functional, they seem to serve 3-D chromosomal architectural function as well A-I editing points for dsRNAs, but be highly diverse from chimps to humans (by about twice no of edits) if common ancestry is shared?
ReplyDeleteWhy do you see differing placental lineages for ERVs in differing mammals as evidence for evolution? Convergent evolution is a problem not an asset to your case. Not just one improbable miracle, but serial, parallel examples of negligible improbability,esp when procreation hinges on success.
Re. ALU elements, this blog is about ERVs. Time permitting, I will look into tem. It would be helpful if you can provide references to illustrate what you are saying.
DeleteRe. different syncytins, it is often the claim from cdesign propnentsists that the same design points to the same designer. Different syncytins in different lineages is explainable by different endogenisation and exaptation events from different retroviruses. "Design" does not explain different syncytins at all.
Dear all
ReplyDeletei hope you all doing well with this outbreak,
im wondering if some one can help me in some understanding or clear pipeline to identify ERVs in an animal genome ?
Barry is a fraud.
ReplyDeleteI'd be very interested in any attempt of yours to try and justify such a statement. Perhaps we can have a conversation, Anonymous?
DeleteHey Anonymous, I thought lying is a sin?
DeleteThis comment has been removed by a blog administrator.
ReplyDeleteHi i am new on the block
ReplyDeletei appreciate the common ancestry argument - however i still suggest that a larger question remains - namely how could the incredible genetic and biological complexity that is found in life and particularly in sophisticated organisms like man have evolved all by itself - so perhaps the retroviruses argument has proved that creation of species was by evolution from simple life forms but could this really have occurred unguided - there are huge statistical and mathematical problems in positing that random mutations brought about advantageous adaptations that were then selected and passed on to next generation - for example how many "attempts" does it require to produce a random beneficial mutation and are we talking about a significant adaptation as a result of the mutation or very minor incremental one - or a form of cumulative multi-step evolution - thanks and have a good day
Hi Daniel, and welcome on the block. :) To be honest, the "larger question" is irrelevant to the evidence for common descent from ERVs. However life and viruses came about, we still need an explanation for commonly located ERVs. I've never come across a viable one other than common inheritance. Even "intelligent design" can't cut it as an explanation. It makes no sense. Even if life and viruses arose by means other than envisaged by mainstream science, common ERVs would still need an explanation that works.
DeleteOn the subject of "random mutations", people often forget the effect of the selection of heritable variations, which affects probabilities enormously.
thanks Barry - i accepted that ERV's show common decent - my main point was that is this intended to disprove general creationism of itself or is it just to establish the fact of common decent whatever that implies for other issues
Deletere heritable variations i would be happy if you could expand on how that works - i would also be delighted if you could do so in simple first principle terms rather than a link to some article full of multisyllable biological terms which although informative doesnt often explain the basic underlying premises and axioms - i think a good theory should have basic underlying logic that can be understood by anyone with reasonable intelligence
i like to imagine an imaginary colony of say 10 rats and understanding how it might work their development of say a more sophisticated brain or other organ using this concept of "heritable variations" - thanks a lot and thanks for the warm welcome and for responding - look forward to hearing more - have a great day
Hi "Unk". ;) What this shows is that an important plank of creationism is false. What creationist claim is that different "kinds"of animals cannot derive from common ancestors, and that, for example, humans and chimps are different "kinds" (whatever that is supposed to mean) and they cannot have had any common ancestors. That is all.
DeleteA heritable variation is basically a change to the DNA which can occur when an organism reproduces. The offspring can then pass this change on to its own offspring. If one of your rats happens to reproduce and one of its pups has a change to its DNA, just by chance, that change might affect its chances of reproducing itself. If it increases its chances, that change can be inherited by its own offspring, and their offspring, and so on. This is how positive or advantageous variations can spread and increase in frequency generation by generation.
I hope this helps make it clearer.
thankyou Barry - sorry about the unk its me daniel - i have inherited this identity unwittingly repressed it as unk and it reemerges now as daniel perhaps genetically enhanced but certainly wiser for your answer
ReplyDeletei think that the main claim or challenge for evolutionaries is the maths or philosophy how could such complex order emerge from apparent chaos without some guidance from within or without - the creationist account derived from the Bible does sort of imply or can be said to imply that sophisticated forms of life "evolved" or were created from the more basic forms and thus i dont think that notion of disparate ancestors is the most major tenant of creationism that is thereby disproved - but stand to be corrected
fully accepting that changed dna can and will be passed on to subsequent generations and fully accepting for the moment that advantageous adaptations will be positively selected the basic objection still remains that the numbers dont add up since as you put it (unless we move to a more sophisticated basic premise) in order for us to arrive in the first place at an advantageous adaptation we need a fortunate but random mutation of hereditary dna that expresses itself INITIALLY in one offspring (or multiple if all in the same birth - perhaps - in mammals doesnt make much difference as they give birth typically to one or two at a time) - and so the basic question becomes can we really and mathematically ever expect a random mutation to produce a change to the biology of the offspring that will be advantageous IN A SIGNFICANT WAY -
if you take any sophisticated system and add any change randomly it will most likely have a damaging effect eg a jet engine etc - and all the more so if its a big change - only perhaps the most miniscule of changes could go unnoticed and perhaps not harmful and even beneficial but if beneficial its of a very small order - eg we cant just postulate suddenly from a random mutation that our rat adds millions of brain cells all ordered and upgrade their intelligence due to a random mutation of dna in one baby rat
Even if we establish that humans and chimps share a common ancestor how do we establish that the common ancestor wasn't a human . maybe humans evolved into all other platyrrhines and catarrhines and they get the ERVs from them . i can think of many ways to disprove this but all of them weaken the strength of the original argument .
ReplyDeleteThe nested hierarchies of ERVs, Anon. See https://www.evolutionarymodel.com/ervs.htm#The_three_layers_of_ERV_evidence_for_common_ancestry They would be different if humans were the ancestors of all platyrrhines and catarrhines, and even if they were not, they would still be evidence of what evo-phobes love to call "macro" evolution.
Deleteif orthologous retroviral insertions without common descent are extremely rare as the stated clearly video says . why is PTERV-1 found in Gorillas and Chimpanzees in the same location over 10 times like this article says https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1054887/
ReplyDelete' We unambiguously map 287 retroviral integration sites and determine that approximately 95.8% of the insertions occur at non-orthologous regions between closely related species '
4% of 287 is 11 . and the stated clearly video says that the odds of this happening without common descent is 1/the no of atoms in the universe .
by orthologous retroviral insertions i mean retroviral insertions in the same location .
DeleteIf ERV insertion points are practically random, then I would expect to possibly find an ERV inserted within another ERV. I haven't been able to find a reference about this.
ReplyDeleteHere's an example. https://pubmed.ncbi.nlm.nih.gov/10211950/
Delete"A human endogenous retrovirus-like (HERV) LTR formed more than 10 million years ago due to an insertion of HERV-H LTR into the 5' LTR of HERV-K is situated on human chromosomes 10, 19 and Y"
Thanks for the reply. That would be difficult to explain in terms of the creationist claim that ERV's are originally part of the genome.
DeleteOrthologous means deriving from a common ancestor. We can't say "same location" because different daughter species will not have 1-1 DNA base pair correspondence due to DNA insertions and deletions etc. We say orthologous or corresponding because these ERVs are found in the same positions relative to other corresponding genes.
ReplyDeletehow likely is it for an erv to infect 2 corresponding genomic locations without common descent ?
ReplyDeleteSee answer #5. "What these sorts of studies do is to survey real retroviral integration sites, using the same types of cell from the same individuals (identical DNA) in order to find any statistical 'preference' for certain types of area (in an existing gene, not in a gene, near a promoter etc.) Typically, they find some overall patterns, but no repetition of integration sites within 500 samples of the same cell type with the same retrovirus. This is not the locus specificity required to account for 200,000 integrations in precisely corresponding loci. Only common inheritance can account for them."
Delete