The Beavis and Butthead of Creationism Ride Again

My comments in red, links in blue, responding to an article in black.

An article by "Donny B." or "Donny Burdinsky" and "Mattman" (AKA "Standing For Truth" or SFT), discussing my work has just come to my attention. It's taken nearly three years to do so, which gives an indication of their reach on the internet, where i am very active, but such behaviour as they exhibit should not go unpunished nevertheless.

A little background. They "challenged" me, a long time ago, to come on their YooToob channel, to discuss my favourite special topic, endogenous retroviruses, or ERVs. See my FAQ,  https://barryhisblog.blogspot.com/p/endogenous-retroviruses-frequently.html
 
Having seen the atrocious way they treat their invitees on their channel, I declined, offering the more mature choice of a written discussion. They continued to jeer and snigger like a couple of spotty adolescents, calling me a coward for not wanting to step into their trap. Eventually, I got pissed off enough with this that I relented. I told them that I would do an opening section on video that they could respond to, and if the discussion continued, we could stitch our presentations together, to present a to-and-fro discussion. They said, "OK", so I produced an opener on a topic that they had claimed they wanted to discuss, the creationist notion of "VIGEs", which you can view here, @ https://youtu.be/VOZ2NPO2XhA

They immediately became "too busy" with other things to reply to it, and they have blocked me from any means of access to them, their site, and any of their other internet outlets. They have apparently done this with other people too, whenever they have painted themselves into a corner.

Bringing up my name and my work without even informing me, let alone giving me the opportunity to respond, and hiding behind their blocks, is totally unacceptable behaviour. They display no moral or intellectual courage or decency. But then, they are creationists.

The article I comment on here shows that all they have is empty rhetorical strutting and posturing.

Refuting the Critics: Endogenous Retroviruses

by Standing for Truth December 16, 2020

ANCIENT VIRAL INFECTIONS OR CREATED UNITS OF DNA FUNCTION?

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:

https://barryhisblog.blogspot.com/p/in-science-we-apply-principle-of.html

This "militant critic" is on the side of every virologist, geneticist, researcher and serious student of biology, who recognise that commonly DNA located ERVs are slam-dunk evidence for common ancestry between the species that possess them. Not "universal common ancestry". That is concluded from other forms of evidence. And I am not so much a critic, but a defender of science and reason from your sort of nonsense. I happen to be an educator, a formally qualified, experienced and successful teacher, who trained for his profession at a Christian-founded college.

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.”

The link is https://barryhisblog.blogspot.com/p/whats-all-this-about-phoenix-virus.html. You obviously haven't read or taken in my articles on Phoenix, or even what you yourself have just written! Again, this is not evidence for "universal common ancestry", but clear evidence that ERVs derive from exogenous 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:

This is where we came in. If you read this, I repeat my invitation to you to make a video presentation rebutting what I say about creo "VIGEs".

Are these DNA elements really evidence for universal common ancestry? 

Will it ever go in with you? This is NOT "evidence for "universal common ancestry", put proof that certain species, for example, humans and chimps, must have had common ancestors who bequeathed to us our commonly located ERVs. 

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.

Bringng up Tomkins is a big mistake. See
https://barryhisblog.blogspot.com/p/viral-genome-s-bunk.html
https://freethoughtblogs.com/pharyngula/2012/03/11/a-tiny-bit-of-knowledge-is-a-dangerous-thing/
and
https://barryhisblog.blogspot.com/p/viral-genome-junk-hits-trash.html

“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.”

The usual desperate bleat of the creationists. "Look! these elements have function, so they must be designed!" They forget that this argument went out with Paley. If it has a function and looks, superficially, that it was designed, it must have been. No. Yes, some (but definitely not all) elements have a function. Real scientists found all this out and told us. See https://barryhisblog.blogspot.com/p/the-not-junk-efence.html

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...

...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.  

A bare-faced lie. Why am I still shocked by creationists lying for Jesus? It's their common M.O. after all. Let's take a favourite topic they bring up, a class of functional, nay, now vital genes, syncytins. These are genes that appear in the genomes of placental mammals, and help form syncytial layers in the development of placentae, essential in gestation. You can find the full details easily. We've all got Google. Anyway, briefly, what syncytins do is to fuse cells together to make multi-nucleated tissue that forms a part of the placenta. Guess what? HIV, a retrovirus does exactly the same thing, fusing immune system T-cells into multi-nucleated tissue in order to fight them. But HIV has never been known to endogenise. It is a retroviral trick, not an exclusively ERV trick. Guess what? it's 'env' gene' a standard, recognised, retroviral gene, is what causes the immune system cells to be fused together. And guess what? The genes for syncytins are in exactly the same loci, in ERVs, where, in a functional retrovirus like HIV, you will find their env genes. And guess what else? Syncytin-bearing ERVs, different ones, are found in different lineages, in different chromosomes. The co-option, ('exaptation', in the jargon), has occurred many times in many species. So much for "same design, same designer". The argument that it couldn't have happened so many times is a perfect example of the argument from personal incredulity. It clearly has. Deal with it.

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:

Here's what I think of Doyle's article. https://barryhisblog.blogspot.com/p/on-doyles-large-scale-function-for.html

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

And of Luskin's. https://barryhisblog.blogspot.com/p/skip-to-content-es-evolution-news.html

SFT then plugs Peer Terborg, AKA, Peter Borger, AKA Pieter Borger some more. Already dismissed.

PART TWO: 

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

(My answers to the following questions can be found here, @ https://barryhisblog.blogspot.com/p/endogenisation-as-explanation.html)

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. 

This is not an answer. The question was, "What is reverse Transcriptase designed to do?"

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.” 

This is not an answer. The question was, “What is integrase designed to do?”

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. 

This is not an answer. The question was, "Why are ERVs designed with a viral codon bias?”

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.

So LTRs need to be re-transcribable because they are a vital part of the RNA->DNA->RNA retroviral replication cycle. Thank you.

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.

So endogenization IS a thing. Thank you.

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.

No evidence is offered to support these assertions.

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.

This is rather muddled. HERV-Ks are considered to be relatively young ERVs because they have fewer mutations and are more complete than other ERVs. I have explained the experiment to you, including what is meant by a "consensus sequence", here, @ https://barryhisblog.blogspot.com/p/the-phoenix-virus-explanation-of.html. Yes, ERVs have mutations in them. They are lethal, not necessarily to their hosts, although there are indications that they can be. They are "dead" proviruses because their mutations prevent them from being replicated as normal, full proviruses do. The hypothesis was that HERV-Ks are very similar, but with differing mutations, and that they descended from a single source retrovirus. The consensus sequence allowed each ERV to have a "vote" on what base should be in each location, thinking that the "majority vote" at each location would yield an original working retrovirus. Not a "VIGE". Not a designed in functional element useful to a host organism such a syncytin gene, but a fully functional retrovirus, capable of getting replicated by hijacking host cells. It did.

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.”

You have completely missed the point again. KoRV is endogenized in different DNA loci in different sub-populations of koalas. It is not present at all in some sub-populations. Therefore it cannot be a component of any original koala genome design. The existence of exogenous KoRV confirms that it is a retrovirus currently endogenizing in kolas.

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. 

We've been through this. Firstly, there is no evidence that genes have "weak spots" where they tend to "break" more often. You are just pulling that out of your orifice.
Secondly, it is a lie to say that "evolutionists" "believe" that for each virus there are many thousands of sites at which it could insert. It's virologists, and they don't "believe" this, they know it. Again, you have been shown surveys of integration loci. I report on them here, @ https://barryhisblog.blogspot.com/p/relationship-between-integration-sites.html. From that page, "Yes, we know that ERVs can integrate in certain areas with a statistical preference. But this is not the base-level resolution targeting which would be required to question the endogenization hypothesis. I liken the issue to road traffic accident statistics. Yes, certain stretches of road are more prone to accident than others, but it is extremely rare for a road traffic accident to involve a collision in exactly the same spot and even more rare for them to involve exactly the same vehicles and the same occupants. It's far more likely that you are looking at duplicates of reports of the same accident.You could decide that these accidents were intelligently designed by some malicious supernatural force, or you could decide that the accident statistics are due to the particular road layouts, traffic patterns etc."

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.” 

So ERVs derive from retroviruses, and are not part of a supposed "design" of an original genome. Thank you.

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 

What happened to the same design, same designer? As I remark above, this is purely an argument from personal incredulity - "I can't understand it so it must be false. A well - known form of fallacy. The reasons why syncytins are concluded to have retroviral origins is also given above.

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Your site does not accept my email address when it asks me for one before I can leave a comment. Big surprise.

Here are a couple more of my articles dealing with "SFT" and their antics.

https://barryhisblog.blogspot.com/p/standing-for-truth-attempts-to-reply-to.html
https://barryhisblog.blogspot.com/p/did-team-sft-really-debunk-stated.html

https://www.amazon.co.uk/product-reviews/B08H6NM8SP/ref=acr_dp_hist_1?ie=UTF8&filterByStar=one_star&reviewerType=all_reviews#reviews-filter-bar

Again, my answers to my own questions can be found @ https://barryhisblog.blogspot.com/p/endogenisation-as-explanation.html