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  #1  
Old 12th June 2013, 03:36 PM
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ERVs put chimp/human common ancestry beyond any reasonable doubt.

Opening statement in support of the proposition that, “ERVs put chimp/human common ancestry beyond any reasonable doubt.”

This is a debate between myself and Mark Kennedy. Other posters - please do not post to this debate thread. There is a commentary thread here, http://www.christianforums.com/t7751...6417/#poststop

I shall demonstrate, beyond all reasonable doubt, that ERVs (endogenous retroviruses) are the inherited remnants of retroviral integrations with ancestral gamete DNA, or the inherited remains of retrotranspositions of the same, which also integrated with ancestral gamete DNA.

I shall show why it is unreasonable to suppose that apparently orthologous ERVs are there by design.

I shall show, by estimating from survey data, that the probability that all the apparently orthologous ERVs common to chimps and humans beings are where they are by coincidence is so vanishingly small that it reasonably dismissable.

I shall show why it is unreasonable to suppose that apparently orthologous ERVs common to chimps and humans are where they are due to deterministic necessity.

I shall deal with the common objections to the evidence from orthologous ERVs, namely, the significance of the existence of an ERV fixed in chimps and gorillas but not in humans, ERVs that are functional, useful or even essential for the creatures that possess them, and the fact that ERVs are a source of variation or horizontal gene transfer for evolution to act upon.

If my opponent has any other objections, I shall respond to them as they arise.

Citations of research documents will be provided for each of the points gone into.

Last edited by BarryDesborough; 12th June 2013 at 11:20 PM.
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  #2  
Old 13th June 2013, 12:23 PM
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BarryDesborough has challenged me to a formal debate on a pretty easy argument to deal with, the homology arguments related to ERVs. The logic goes that since ERVs are exclusively the result of germline invasions that the only way they can be in both genomes (chimpanzee and human) is a common ancestor. Most ERV invasions are somatic (not inherited by offspring), that is they don't effect the cells that produce eggs and sperm. What is truly astonishing with Darwinian logic is that it is so dramatic in it's scope, with little proof they make universal applications. They do this with beneficial mutations, because there are rare, but multiple examples, it becomes the explanation for any requisite change in the DNA during a major evolutionary change throughout natural history. This would never be allowed in any of the sciences but with Darwinian logic it is not only permissible, it's required.

I will demand only one thing from my opponent and it's non-negotiable. If the homology argument (things alike) is an argument for common ancestry then the inverse logic being intuitively obvious, is proof of independent lineage, thus creation. For this I do not need his permission.

ERVs account for 8% of the human and chimpanzee genomes and we are supposed to accept that all of these permanently fixed features of the genomic landscape are the result of these rare germline invasions. I have already addressed this subject at length and the debate I had with LM was focused almost exclusively on the ERVs. I doubt I will need to find any further resources to handle the arguments I will encounter in this debate. Here are my primary sources:


PtERV1-like elements are present in the rhesus monkey, olive baboon and African great apes but not in human, orang-utan or gibbon, suggesting separate germline invasions in these species. (Initial Sequence of the Chimpanzee Genome, Nature 2005 available online)

Instead of demonstrating how this is remotely possible given the known mutation rate evolutionists would rather talk about this: Phylogenies of seven HERV loci. When 8% of the human genome is made up of ERVs with a 94% nucleotide sequence identity should we really be supprised the seven loci are the same? For HERV-K JML 6.17 they identified 5 substitutions, a couple of them had as many as 10. This is supposed to be some kind of proof?

Here they discuss the probability of the 11 substitutions, assuming they happened by chance:

Fig. 1. Classification of transposable elements. The percentage of each element in the genome and the estimated number of the elements of the main groups are indicated. PNAS 2004


Two CERV families have no human orthologues

CERV 1/PTERV1
With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. CERV 1/PTERV1 elements range in size from 5 to 8.8 kb in length, are bordered by inverted terminal repeats (TG and CA) and are characterized by 4 bp TSDs...Phylogenetic analysis of the LTRs from full-length elements of CERV 1/PTERV1 members indicated that this family of LTRs can be grouped into at least two subfamilies (bootstrap value of 99; Figure 3). The age of each subfamily was estimated by calculating the average of the pairwise distances between all sequences in a given subfamily. The estimated ages of the two subfamilies are 5 MY and 7.8 MY, respectively, suggesting that at least one subfamily was present in the lineage prior to the time chimpanzees and humans diverged from a common ancestor (about 6 MYA). This conclusion, however, is inconsistent with the fact that no CERV 1/PTERV1 orthologues were detected in the sequenced human genome.

Retroelements and the human genome: New perspectives on an old relation

I expect that will be sufficient, since my opponents OP was remarkably short and identified no source material I will wait to see what he comes up with. I have fielded homology arguments from fossil evidence, these I have learned to refute with ease. I have encountered arguments regarding beneficial mutations but the Darwinian has no answer for how the human brain could have evolved from the ape. I encountered a number of homology arguments regarding pseudo genes, particularly the GULO gene and it is now defunct on these boards. Homology arguments from comparative genomics are all but extinct now except for these ERV arguments and they are weak at best.

Like all Darwinian homology arguments the first order of business is to neutralize the false assumptions. Then isolate the fallacious logic, ad hominem and circular arguments being the easiest to nail down. Then when you have reduced the argument to the actual empirical evidence sorting through the terminology and identifying the relevant source material is a challenge. Once that is accomplished and I expect it will be all too easy here, refuting the baseless assertions of your opponent is little more then emphasizing the available proofs.

Comparative genomics can only yield a definitive proof for common ancestry if, and only if, it can provide insights into the emergence of adaptive traits. Failing this burden of proof homology arguments are little more then dramatic theater which is performed for other Darwinians and the uninformed. The stage is set, the dwindling audiences in the Darwinian theater of the mind have taken their seats. BarryDesborough will be your narrator, the lights go down, the curtain is raised.

It's showtime.

May the truth prevail,

Mark Kennedy
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Last edited by mark kennedy; 14th June 2013 at 07:34 PM.
  #3  
Old 14th June 2013, 09:11 AM
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Positive case, post 1.

Preliminary remarks

Thank you for your opening statement, Mark. I have a few observations.

I have included a “Terms” section to help us avoid confusion over exactly what certain terms mean.

The case for common ancestry from orthologous ERVs is not a mere homology argument. Read my post carefully, and you will see that it rests upon the probability of multiple separate coincidental integrations to corresponding DNA loci in different species being vanishingly small. I do not require your permission to disregard non-orthologous ERVs. They are essentially irrelevant.

I note that you cite certain items, but are inconsistent with citations and links. Links to tables and diagrams without an indication of the source documents are of little value, and you made an error with your link regarding CERV1 and PTERV1. You should have cited (Polavarapu 2006) and not (Bannert 2004). Please take a little more care with citations and links. On the subject of the suggestion that “at least one subfamily was present in the lineage prior to the time chimpanzees and humans diverged from a common ancestor”, three points: 1) This was based on estimated ages. 2) It is now recognized that the chimp/human split probably occurred over an extended period of time, and 3) these ERVs were not necessarily fixed (ubiquitous) in ancestral species. There are many other cases of genetic material “making it” into one lineage and not into a related lineage.

Terms

Exogenous retroviruses (XRVs) are infectious virus particles.

Endogenous retroviruses (ERVs) are reasoned to be exclusively the result of exogenous retroviral integrations with germ-line DNA (endogenizations). Exogenous retroviral integrations with somatic cell DNA are not endogenous. Their integrations are normally called proviruses.

When we examine ERVs in different species, we may find them in corresponding locations in the DNA of those species. These are usually called orthologous ERVs, orthologous meaning equivalent by way of being derived by common ancestry. As this is the question under discussion, I shall not use the word orthologous, so as not to beg the question. Instead, I will say “corresponding” or "shared”, and will then proceed to prove that corresponding ERVs are indeed orthologous.

Fixed ERVs are ERVs that are present in all individuals of a species.

Non-orthologous ERVs indicate separate endogenizations in different species, or the failure of an ERV to become fixed in one daughter species of a common ancestor, while becoming fixed, or at least represented in another daughter species. Non-corresponding (non-orthologous) ERVs are not evidence for common ancestry. Neither are they evidence for uncommon ancestry. They are essentially irrelevant to the case for common ancestry from corresponding ERVs. Perhaps an analogy will help here. Bill Bloggs is recorded on video, waving a gun around and stuffing dollar bills into his swag-bag at a branch of Wells Fargo. This is evidence that he is a bank robber. He is not recorded waving a gun around and stuffing dollar bills into his swag-bag at a branch of Citigroup, but this is not evidence that he is not a bank robber!.

Exogenous Retroviruses

Retroviruses enter host cells, “reverse” transcribe their RNA genomes into DNA, and integrate the resulting DNA with the host cell’s nuclear DNA. (Temin, 1970), (Baltimore, 1970), (Coffin, 1979).

Although there are general statistical trends the locus of the integration is highly variable. Retroviruses tend to target particular cell types, but do not infect all of them. (Taruscio 1991), (Skinner et al., 2001), (Mitchell, 2004), (Wang et al., 2007).

The Wang study showed that the probability of a retrovirus endogenizing in the same location twice is no greater than 1/500.


Endogenous Retroviruses.

The structure of a provirus and a complete* ERV are essentially the same. Most ERVs, however, are not fully functional proviruses. (Coffin, 1979), (Weiss, 2006)

* There are many fragments of ERVs in our DNA, and in that of chimpanzees.

An example of a retrovirus in the process of becoming endogenized is the koala virus KoRV. (Tarlinton, 2006). A functional retrovirus, the “Phoenix Virus” has been resurrected from dormant ERVs. (Dewannieux 2006). These studies confirm the retroviral origins of ERVs.

In contrast with provirus integrations in somatic cells, ERVs are found in the DNA of all nuclear cells, Each ERV being found in exactly the same location, going from cell to cell. This is why they are regarded as being endogenous. All the cells of the body are daughter cells of the zygote, formed by the fusion of the sex gametes. Going back through our ancestry, for each type of ERV, there has to have been a single ancestral gamete or zygote that an exogenous retrovirus endogenized. (International Human Genome Sequencing Consortium, 2001). ERVs may multiply further in the DNA by retrotransposition, but these may also be regarded as additional instances of endogenization - they have to have occurred in germline cells in order to be endogenous.

There are some 200,000 ERVs and ERV fragments in the human and the chimpanzee genomes. Less than 1% of these are lineage-specific (no corresponding ERV in the other species).
(International Human Genome Sequencing Consortium, 2001), (Chimpanzee Sequencing and Analysis Consortium, 2005).

For all these ERVs and ERV fragments to have endogenized separately in each species, but for their locations to correspond as they do, would be a coincidence of truly staggering unlikelihood. For one pair of endogenizations to correspond by coincidence, the probability would be 1/500. For two, it would be 1/500 x 1/500 = 1/250,000. For three, 1/500 x 1/500 x 1/500 = 1/12,500,000 or 1/5003. For 200,000, the probability of coincidence is 1/500200,000. For all intents and purposes, it is impossible for chimps and humans not to have had common ancestors.

References

Baltimore, D. “Viral RNA-dependent DNA Polymerase” Nature vol 226, p1209 June 27 1970. http://tamu.edu/faculty/kunkel/Baltimore.pdf

The Chimpanzee Sequencing and Analysis Consortium, “Initial sequence of the chimpanzee genome and comparison with the human genome“, Nature 437, 69-87 (1 September 2005), Initial sequence of the chimpanzee genome and comparison with the human genome : Article : Nature

Coffin, J. M. “Structure, Replication, and Recombination of Retrovirus Genomes: Some Unifying Hypotheses”, J. gen. Virol 1979, 42, 1-26. http://jgv.sgmjournals.org/content/42/1/1.full.pdf

Dewannieux, M., Harper, F., Richaud, A., Letzelter, C., Ribet, D., Pierron, G., Heidmann, T., “Identification of an infectious progenitor for the multiple-copy HERV-K human endogenous retroelements”, Genome Res. 2006, 16: gr.5565706. Identification of an infectious progenitor for the multiple-copy HERV-K human endogenous retroelements

International Human Genome Sequencing Consortium, “Initial sequencing and analysis of the human genome”, Nature 409, 860-921 (15 February 2001). Initial sequencing and analysis of the human genome : Article : Nature

Mitchell, R.S., Beitzel, B.F., Bushman, F.D., “Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences”, PLoS Biol. 2004 August 2(8): e234. Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

Skinner, L. M., Sudol, M., Harper, A. L., Katzman, M., “Nucleophile Selection for the Endonuclease Activities of Human, Ovine, and Avian Retroviral Integrases” The Journal of Biological Chemistry, January 5, 2001 276, 114-124. Nucleophile Selection for the Endonuclease Activities of Human, Ovine, and Avian Retroviral Integrases

Tarlinton R.E., Meers, K., Young, P. R. “Retroviral invasion of the koala genome“ Nature 442, 79-81 (6 July 2006). http://www.nature.com/nature/journal...ture04841.html

Taruscio, D., Manuelidis, L., “Integration site preferences of endogenous retroviruses.“ PubMed Chromosoma. 1991 Dec;101(3):141-56. Integration site preferences of endogenous retrov... [Chromosoma. 1991] - PubMed - NCBI

Temin H.M. and Mizutani, S. “RNA-Dependent DNA Polymerase in Virions of Rous Sarcoma Virus”, Nature vol. 226 p1211 June 27 1970. http://tamu.edu/faculty/kunkel/Temin.pdf

Wang, G. P., Ciuffi, A., Bushman, F. D., “HIV integration site selection: Analysis by massively parallel pyrosequencing reveals association with epigenetic modifications”, Genome Res. 2007 August; 17(8): 1186-1194. HIV integration site selection: Analysis by massively parallel pyrosequencing reveals association with epigenetic modifications

Weiss, R. A., “The Discovery of Endogenous Retroviruses”, Retrovirologt 2006 3:67. http://link.springer.com/content/pdf...-4690-3-67.pdf

Last edited by BarryDesborough; 14th June 2013 at 09:40 AM.
  #4  
Old 15th June 2013, 01:29 AM
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Originally Posted by BarryDesborough View Post
I do not require your permission to disregard non-orthologous ERVs. They are essentially irrelevant.
Which means you ignore the differences and overstate things in common. What you are attempting to do is evade in the inverse logic. Orthologs assume a common ancestor, they do not prove one. It really is nothing more the another homology argument known as, 'Sequence homology' which includes Paralogy, Ohnology, Xenology, Gametology. (see Homology) If we are going to be using terms like orthologous then it should be understood that it is a homology argument used in comparative biology. It is orthologous if and only if two species share a common ancestor. Currently I am aware of only a handful of orthologous ERVs in the human and chimpanzee genomes. It's just another homology argument and a poor one at that. Just like all Darwinian theater if it's something in common is proves common ancestry and if it's not it's called natural selection. The inverse logic is never considered because common ancestry was already assumed a priori.

you made an error with your link regarding CERV1 and PTERV1.
Forgot the link and the citation for the table, sorry about that.

On the subject of the suggestion that “at least one subfamily was present in the lineage prior to the time chimpanzees and humans diverged from a common ancestor”, three points: 1) This was based on estimated ages. 2) It is now recognized that the chimp/human split probably occurred over an extended period of time, and 3) these ERVs were not necessarily fixed (ubiquitous) in ancestral species. There are many other cases of genetic material “making it” into one lineage and not into a related lineage.
1) Ages of CERV1 and PTERV1 are estimated to be right around the time of or previous to the split.
2) We have no idea when the split was because the Chimpanzee lineage is not represented in the fossil record.
3) That's called horizontal transfer and it's rare, just like ERV germline invasions themselves.

Terms

Exogenous retroviruses
Endogenous Retrovirus is one retrovirus transmitted in germ-line DNA from an infected parent to offspring.
Exogenous Retrovirus one transmitted horizontally. (Retrovirus)

Instead, I will say “corresponding” or "shared”, and will then proceed to prove that corresponding ERVs are indeed orthologous.
If you could characterize their sequence, location and the loci it would be helpful. You cite three papers from the 70s in one paragraph (Temin, 1970, Baltimore, 1970, Coffin, 1979). Then three more current in the next. (Taruscio 1991, Skinner et al., 2001, Mitchell, 2004, Wang et al., 2007). All you really have to say about this is:

The Wang study showed that the probability of a retrovirus endogenizing in the same location twice is no greater than 1/500.
I have yet to see the relevance of HIV DNA integration sites to a supposed germline invasions some 25 my ago. Isn't HIV a somatic infection? We seem to have skipped over the part where massive germline invasions are possible without resulting in the extinction of the species. I understand that they happen but we are talking about 8% of the human genome here.

There are many fragments of ERVs in our DNA, and in that of chimpanzees.
With 96% of the respective genomes being the same that comes as no big surprise. Comparative sequence identity does not demonstrate that 8% of the human genome is the result of germline invasions. To elaborate on how ERVs work you discuss briefly ERVs that supposedly happened 25 my ago and then compare it to HIV as an example of how a retrovirus works. So far I'm a little underwhelmed.

An example of a retrovirus in the process of becoming endogenized is the koala virus KoRV. (Tarlinton, 2006). A functional retrovirus, the “Phoenix Virus” has been resurrected from dormant ERVs. (Dewannieux 2006). These studies confirm the retroviral origins of ERVs.
I was wondering when we would get to this. They take all of the complete copies of the 9.4-kb HERV-K(HML2) provirus. Reconstruct 20 amino acid sequences with only one frameshift in the original reading frame. 'Phoenix Virus', the first infectious HERV available at the date of the publication Oct. 31, 2006. 293T cells were infected. I read through the paper a couple of times and saw nothing all that spectacular in the results. All it really demonstrates is that this HERV if reconstructed can go viral, so what?

We are talking about 8% of the human genome, supposedly being the result of a massive germline invasion. The first actual infectious HERV unleashed on T cells and what did it actually prove?

There are some 200,000 ERVs and ERV fragments in the human and the chimpanzee genomes. Less than 1% of these are lineage-specific (no corresponding ERV in the other species).
(International Human Genome Sequencing Consortium, 2001), (Chimpanzee Sequencing and Analysis Consortium, 2005).
That's right, they found:
112,000 ERV class 1 79.2 Mb 3.69% of the genome
8 ERV class II 8,9 Mb .31%
83,000 ERV class III 39.5 Mb 1.44%
Table 11. Number of copies and fraction of genome for classes of interspersed repeat.

These would not be compared to the chimpanzee genome until 2005. They found 73 human-specific insertions of the HERV-K and 45 chimpanzee-specific insertions, leaving ~9 human-specific insertions before dying out.

Against this background, it was surprising to find:


Notice the ERV class I has over 200 elements closely related to a baboon endogenous retrovirus, with 88% product identity and a feline endogenous virus, 86% product identity. PtERV1-like elements are present in the rhesus monkey, olive baboon and African great apes but not in human. (Initial Sequence of the Chimpanzee Genome, 2005)

It's no wonder evolutionists don't want to talk about them, it makes a lot more sense to talk in circles around what, a couple dozen orthologous sites? I say talk in circle around them because what I know about them I learned years ago from fielding that old Talk Origins probability argument so many times.

For all these ERVs and ERV fragments to have endogenized separately in each species, but for their locations to correspond as they do, would be a coincidence of truly staggering unlikelihood. For one pair of endogenizations to correspond by coincidence, the probability would be 1/500. For two, it would be 1/500 x 1/500 = 1/250,000. For three, 1/500 x 1/500 x 1/500 = 1/12,500,000 or 1/5003. For 200,000, the probability of coincidence is 1/500200,000. For all intents and purposes, it is impossible for chimps and humans not to have had common ancestors.
So far no one has demonstrated that it's even possible for there to be a germline invasion on that scale. With very little proof and without identifying a single direct ERV comparison you fabricate this pointless probability argument. As with all homology arguments the requisite null hypothesis is abandoned, never to be considered. Still waiting to hear what somatic HIV infections have to do with massive germline invasions.

Short of doing the exposition of the bibliography my opponent provided I don't see much else to comment on. Let's revisit the 'I shall' list and see what kind of progress my opponent is making with it.
I shall demonstrate, beyond all reasonable doubt, that ERVs (endogenous retroviruses) are the inherited remnants of retroviral integrations with ancestral gamete DNA, or the inherited remains of retrotranspositions of the same, which also integrated with ancestral gamete DNA.
One short paragraph describing the 'Phoenix Virus' so far. A rather extensive bibliography including the Wang paper on HIV infections, which are somatic infections the last time I checked. Still waiting for this revelation that shows us how this has been conclusively demonstrated because it's never been observed.

I shall show why it is unreasonable to suppose that apparently orthologous ERVs are there by design.
Still waiting for you to tell me where these orthologous ERVs are and why I should jump to that conclusion.

I shall show, by estimating from survey data, that the probability that all the apparently orthologous ERVs common to chimps and humans beings are where they are by coincidence is so vanishingly small that it reasonably dismissable.
Well bring on the survey data, I can hardly wait. I sure hope your didn't pin you hopes of nailing this one down with a paper on HIV. Because if you did it's not only 'reasonably dismissable', it's laughable. Remember the burden of proof has to be on getting these ERVs into the germline on a massive scale with a reasonably demonstrative line of evidence.

I shall show why it is unreasonable to suppose that apparently orthologous ERVs common to chimps and humans are where they are due to deterministic necessity.
All we really know about ERVs is that their reading frames are broken. The Phoenix Virus was reconstructed giving it 20 functioning amino acids along with one frameshift. That's all we know, that is the extent of you proof. What those reading frames may or may not have done before they were broken is random conjecture.

I honestly have no idea what you meant by the last one so I'll wait to see if you make good on this verbose promise.

The Theory of Evolution has been a rising star in the scientific world for well over a hundred and fifty years now. The Mendelian Laws of Inheritance, Chromosome Theory, the DNA Double Helix model and the whole genomic sequences of genetics has been the empirical engine of it's success.

Like a viral infection Darwinism invades the host, having none of the merits of a functional use it breaks under the weight of it's uselessness. Like the multitude of Darwinian homology arguments that went before it's getting progressively dysfunctional. Fragmentary fossil evidence whether bones or genetic sequences are akin archeologists trying to reconstruct ancient civilizations from broken pottery and ruined buildings.

Evolutionary biology is about how living systems adapt and the viruses described in my opponents brief exposition does nothing to inform our understanding of it. What you have here is yet another homology argument that has long outlived it's persuasive usefulness. But who knows, my opponent has one more positive argument left, perhaps he can make good on his 'I shall' promises yet.

Next up is my first positive argument. I think it's time to deconstruct this statistical probability farce once and for all.

Have a nice day
Mark
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“Gärtner, by the results of these transformation experiments, was led to oppose the opinion of those naturalists who dispute the stability of plant species and believe in a continuous evolution of vegetation. He perceives in the complete transformation of one species into another an indubitable proof that species are fixed with limits beyond which they cannot change.” (G. Mendel)
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Old 15th June 2013, 02:41 PM
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First Positive Argument: ERVs and Common Ancestry

The debate has gone as I expected, it's an homology comparison with a statistical probability argument. Most of the targets for ERVs would be somatic cells but if it managed to find it's way into the germline through a gamete it could be passed on to the offspring. While this is conceivable it would be rare at best and the burden of proof is on the evolutionist to demonstrate that 8% of the human genome is the result of these germline invasions. The only real attempt at this was my opponents brief comment on the "Phoenix Virus". As I described in my rebuttal one of the HERVs was reconstructed.
This family, termed HERV-K (HML2), makes up less than 1% of HERV elements but is one of the most studied ((Human endogenous retroviruses))
What makes this such a lackluster argument is that the Darwinian will just keep repeating that ERVs are the result of germline invasions, something that has simply been assumed as far as I can tell. Long technical discussions about how ERVs work are tedious so most Creationists won't bother with them. The researchers got the 'Phoenix Virus' to work, it had 20 amino acids and just one frameshift. In order to understand why this is important you would need to know how protein coding works on a molecular level. The amino acids need an open reading frame. When they got it working they they wanted to see how it would interact with living cells and it was introduced to live T cells. Guess what, it really can get into the DNA but I'm still waiting for the part where it's demonstrated that massive germline invasions are possible.

Let's take a look at a little Darwinian mythology and try to picture what they believe happened here. Our supposed ancestors from about 25 million years ago would have been inundated with a massive dose of these pathological ERV viruses. As a result the ERVs would replicate at random in the genomes until random mutations disrupted the reading frame, leaving fragments like the HERV K. Getting this far into the ancestry of apes in Darwinian evolution leaves you following a lot of long 'ghost lineages' but geographically always go back to the East African Rift valley. (Nature, 30 May 2013)

This is an area that has made a number of paleontologists famous, especially the Leaky family who found so many of the Homo habilis and Homo erectus fossils in and around this area. So in case you were wondering when this supposed ERV onslaught of germline invasions would have happened it would have been right around there. What the Darwinian desperately wants to prove is a correlation between the molecular evidence and the fossil record. What they are doing is taking this highly technical ERV research, molecular clock age estimates and reconcile it with the fossil record. My positive argument here will simply be this, no matter how many ways it's reconstructed ERVs are just another homology argument.

It is tempting to go more into the fossil evidence since ERVs are generally regarded as molecular fossils. What is more important is to understand that my opponent is trying to use an old statistical argument, specifically, the odds of mutations occurring at a specific loci. It's become one of the main stays of the Talk Origins arguments and since Creationists tend to ignore it they think it means it's irrefutable. It's not, it's just so obscure Creationists are bored to death with it.


Figure 4.4.1. Human endogenous retrovirus K (HERV-K) insertions in identical chromosomal locations in various primates
There are at least seven different known instances of common retrogene insertions between chimps and humans, and this number is sure to grow as both these organism's genomes are sequenced (see Prediction 4.5: Molecular evidence - Endogenous retroviruses)
That's about it, Talk Origins wants you to accept the assumption that ERVs are the result of germline invasions then drop a probability argument in your lap. The essence of the argument is the strongest argument against germline invasions in the first place. They are rare and they are pretty much random. Once they hook you with the assumption that they must be the result of a germline invasion they use the probability argument for common ancestry. The only way it would be possible for mutations and insertions to be in the same place is a common ancestor. It's just another homology argument buried in highly technical viral research but it really comes down to a false assumption and some anecdotal comparisons.

The odds of a single germline invasion from an ERV is itself, astronomical. The very statistical argument my opponent is trying to make is the reason the first assumption is patently false. We would first have to know under what conditions these ERVs inundated the common ancestor population from 25 million years ago. Darwinians simply won't do that, they want you to accept their assumption of universal common descent without question. When it comes to ERVs they want you to swallow their assumption that they are the result of germline invasions whole.

What they are neglecting when running us in circles with this is the actual burden of proof. The molecular basis for adaptive traits emerging and becoming fixed in successive generations of offspring. Rather then facing up to this challenge they prefer to dwell on obscure comparative studies and what we have in common with apes. They got by with this for decades by using chimpanzee ancestors as a menagerie of fabricated transitional fossils. Now they are simply doing the same thing with molecular homology arguments hoping no one will catch them in the act.

What we really know about ERVs:
  • Most retroviruses infect somatic cells, but might infect of germline cells on rare occasions.
  • ERVs have been inactivated by mutation for the most part and do nothing.
  • ERVs have been proposed to be involved in multiple sclerosis (MS) and HERVs were found in greater frequency in the sera of people with schizophrenia.
  • 98,000 human ERV elements and fragments making up nearly 8% of our genome and no HERVs capable of replication had been identified.

Endogenous retrovirus

The inverse logic is intuitively obvious, if the homology argument for things in common can prove common ancestry then differences can prove independent lineage, thus creation. Failure to accept the inverse logic is tantamount to an open admission of predicating all arguments on assumptions made before the evidence is considered.

The real world evidences from evolutionary biology are compelling and pose great challenges for the Creationist. The vast array of molecular machinery capable of epigenetic alterations for improved adaptive fitness are astonishing in their scope and significance. Where the Darwinian falls short of a compelling argument is they want universal common ancestry assumed across all periods of time and space a priori (without prior). All the evidence is then organized around these junk yard fabrications known collectively as Darwinian homology arguments.

Where is the proof that massive germline invasions are a viable explanation for 8% of the human genome? If the ERVs that are at identical splice sites are valid proofs of chimpanzee common ancestry then the ERVs present in the chimpanzee genome but absent in human genomes is a valid proof to the contrary.

This is the start of the second round of arguments. My opponent will respond as he sees fit and then offer his second and final positive argument. So far it's been anecdotal at best and the long bibliography was offered with sparse commentary and virtually no attempt at an exposition. Perhaps Act 2 in this attempt at a dramatic proof in the Darwinian theater of the mind will be more exciting.

BarryDesborough you have the stage.

Have a nice day
Mark
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Old 16th June 2013, 02:07 AM
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Comments on Mark’s ‘rebuttal’ of my first positive post

Originally Posted by mark kennedy View Post
...you ignore the differences and overstate things in common. What you are attempting to do is evade in the inverse logic. Orthologs assume a common ancestor, they do not prove one. … Currently I am aware of only a handful of orthologous ERVs in the human and chimpanzee genomes. ...if it's something in common is proves common ancestry and if it's not it's called natural selection. The inverse logic is never considered because common ancestry was already assumed a priori.
Repeating nonsense does not make it make sense, Mark. Non-orthologous ERVs are not evidence of uncommon ancestry. Imagine you had a brother who fathered a daughter by way of one of his sperm that had received a retroviral integration in its DNA, and the daughter inherited it. Would you argue that the girl is not your niece? And why do you expect all germ-line integration to stop after speciation? Why do you expect an ancestral species to wait until all the ERVs or pre-integration alleles in the entire population have gone to fixation before deciding to speciate? Enough of this nonsense!

Re. orthology and assumptions, it would be a real help if you read my posts carefully, Mark.
Originally Posted by BarryDesborough View Post
When we examine ERVs in different species, we may find them in corresponding locations in the DNA of those species. These are usually called orthologous ERVs, orthologous meaning equivalent by way of being derived by common ancestry. As this is the question under discussion, I shall not use the word orthologous, so as not to beg the question. Instead, I will say “corresponding” or "shared”, and will then proceed to prove that corresponding ERVs are indeed orthologous.
Regarding corresponding ERVs in both species, perhaps a Venn diagram may help. This is based on the tables of the genome surveys you have already posted links to.



Originally Posted by mark kennedy View Post
3) That's called horizontal transfer [genetic material “making it” into one lineage and not into a related lineage] ...
No. Horizontal transfer can occur as a result of retroviral activity, but it is highly unlikely to conserve loci. What it is called is incomplete lineage sorting.
Originally Posted by mark kennedy View Post
If you could characterize their sequence, location and the loci [of shared ERVs] it would be helpful.
? You've just linked to the reports of the sequencing consortia yourself!
Originally Posted by mark kennedy View Post
I have yet to see the relevance of HIV DNA integration sites to a supposed germline invasions some 25 my ago. Isn't HIV a somatic infection? We seem to have skipped over the part where massive germline invasions are possible without resulting in the extinction of the species. I understand that they happen but we are talking about 8% of the human genome here.
The studies I cited are surveys of integration sites of human, ovine, avian and murine ERVs, not just HIV. I do wonder, Mark, if you are taking this exercise seriously! All but one of the studies of integration site preferences is freely available, and you can see what they studied just from their abstracts anyway. All retrovruses integrate with somatic DNA. They integrate using an enzyme, integrase, and leave a record of the integrase gene in the integration. One of the studies I linked to goes into this in detail. Whe know exactly what integrase does, and how it does it. ERVs still code for integrase. And we know that massive germline invasions are possible, because here we are! I do find your 'logic' rather puzzling, Mark.
Originally Posted by mark kennedy View Post
With 96% of the respective genomes being the same that comes as no big surprise [that there are many fragments of ERVs in our DNA, and in that of chimpanzees.]. Comparative sequence identity does not demonstrate that 8% of the human genome is the result of germline invasions.
? You are not surprised, or you don't think it's demonstrated? Which?
Originally Posted by mark kennedy View Post
Phoenix Virus ... All it really demonstrates is that this HERV if reconstructed can go viral, so what?
So it's an endogenized retrovirus. And what about KoRV? Couldn't even been bothered to read the abstract of that either? Here's an exogenous retrovirus caught in the act of becoming endogenous. What's the purpose of this debate, Mark? I thought we agreed that it was to determine truth of the matter. You can't do that without looking at the evidence.
Originally Posted by mark kennedy View Post

Notice the ERV class I has over 200 elements closely related to a baboon endogenous retrovirus, with 88% product identity and a feline endogenous virus, 86% product identity. PtERV1-like elements are present in the rhesus monkey, olive baboon and African great apes but not in human. (Initial Sequence of the Chimpanzee Genome, 2005)
This would be a surprise if the ERVs in question in corresponding locations, but as they are definitely not orthologous, it is not.
Originally Posted by mark kennedy View Post
So far no one has demonstrated that it's even possible for there to be a germline invasion on that scale. [200,000 ERVs and fragments]
Yes they have. You linked to the genome sequencing reports yourself, and even went to the trouble of copying tables of results from them! Please try and pay more attention, Mark.
Originally Posted by mark kennedy via visitor message
I browsed your bibliography and unless or until they are translated into an actual argument they don't interest me much. Looking forward to your posts, I don't expect I will get to a response for your second positive argument until Wednesday.
And there was me thinking you were interested in the evidence.


Rebuttal of Marks 1st positive post

Originally Posted by mark kennedy View Post
While this is conceivable it would be rare at best and the burden of proof is on the evolutionist to demonstrate that 8% of the human genome is the result of these germline invasions.
You have shown the proof yourself, but you don't seem to recognize it.
Originally Posted by mark kennedy View Post
What makes this such a lackluster argument is that the Darwinian will just keep repeating that ERVs are the result of germline invasions, something that has simply been assumed as far as I can tell.Long technical discussions about how ERVs work are tedious so most Creationists won't bother with them.
Why am I not surprised? A conclusion is not an assumption. The detailed structure of ERVs is proviral. They can be resurrected to function as retroviruses. They have been seen invading germlines. They are present in identical locations in the DNA of every single one of your cells. They could not have got there by direct infection. They had to have been inherited.
The researchers got the 'Phoenix Virus' to work, it had 20 amino acids and just one frameshift. In order to understand why this is important you would need to know how protein coding works on a molecular level. The amino acids need an open reading frame. When they got it working they they wanted to see how it would interact with living cells and it was introduced to live T cells. Guess what, it really can get into the DNA but I'm still waiting for the part where it's demonstrated that massive germline invasions are possible.
^What's this nonsense?

From (Dewannieux et al., 2006),
Originally Posted by Dewannieux et al.
To construct a consensus HERV-K(HML2) provirus, we assembled all of the complete copies of the 9.4-kb proviruses that are human specific (excluding those with the 292-nt deletion at the beginning of the env gene) and aligned their nucleotide sequence to generate the consensus in silico, taking for each position the most frequent nucleotide. The resulting provirus sequence contains, as expected, ORFs for all of the HERV-K(HML2)-encoded proteins (Gag, Pro, Pol, Env, and the accessory Rec protein), with gag, pro, and pol separated by 1 frameshifts. Noteworthily, this consensus provirus is distinct from each of the sequences used to generate it, with at least 20 amino acid changes on the overall sequences.
My emphasis.
Originally Posted by mark kennedy View Post
Our supposed ancestors from about 25 million years ago would have been inundated with a massive dose of these pathological ERV viruses.
That's very unlikely, and I have never seen any evidence for it.
Originally Posted by mark kennedy View Post
my opponent is trying to use an old statistical argument, specifically, the odds of mutations occurring at a specific loci.
No I am not. Try reading over my posts again.
Originally Posted by mark kennedy View Post
That's about it, Talk Origins wants you to accept the assumption that ERVs are the result of germline invasions then drop a probability argument in your lap.
There is no assumption here. It is a conclusion arrived at by applying reason to the evidence. The fact that you refuse to recognize that it is not assumption does not make it into an assumption!
Originally Posted by mark kennedy View Post
The odds of a single germline invasion from an ERV is itself, astronomical.
This is just an unsupported assertion.
Originally Posted by mark kennedy View Post
What they are neglecting when running us in circles with this is the actual burden of proof. The molecular basis for adaptive traits emerging and becoming fixed in successive generations of offspring.
What?
Originally Posted by mark kennedy View Post
What we really know about ERVs:
  • Most retroviruses infect somatic cells, but might infect of germline cells on rare occasions.
  • ERVs have been inactivated by mutation for the most part and do nothing.
  • ERVs have been proposed to be involved in multiple sclerosis (MS) and HERVs were found in greater frequency in the sera of people with schizophrenia.
  • 98,000 human ERV elements and fragments making up nearly 8% of our genome and no HERVs capable of replication had been identified.

Endogenous retrovirus

The inverse logic is intuitively obvious, if the homology argument for things in common can prove common ancestry then differences can prove independent lineage, thus creation. Failure to accept the inverse logic is tantamount to an open admission of predicating all arguments on assumptions made before the evidence is considered.
Around 200,000 ERV elements actually. You post stuff and don't recognize what you are posting. Extraordinary, but hardly the "reasonable doubt" in the title of the debate. And one more time, the fact that a relative of yours gets a gamete infected and passes it on to a child does not mean that child is not related to you!
Originally Posted by mark kennedy View Post
Where is the proof that massive germline invasions are a viable explanation for 8% of the human genome?
In the genome survey you have linked to, and in the evidence I have given you, but that you have either neglected to read, misunderstood or distorted.
Originally Posted by mark kennedy View Post
If the ERVs that are at identical splice sites are valid proofs of chimpanzee common ancestry then the ERVs present in the chimpanzee genome but absent in human genomes is a valid proof to the contrary.
One more time, the fact that a relative of yours gets a gamete infected and passes it on to a child does not mean that child is not related to you!

Perhaps when this debate is over, we can start a tutorial thread, such as the ones I have run for other students on other sites. I did want this debate to be an informal discussion. It is such a pity. My time is precious, and you appear to have been wasting it. I will, however, see the debate through. My second positive post will be up within a couple of days, hopefully.

Last edited by BarryDesborough; 16th June 2013 at 04:16 AM. Reason: To correct an attribution
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Old 19th June 2013, 09:35 AM
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Positive Case, Post 2

First, a recap.

Features of retroviruses.

We find, in the genomes of organisms, including ourselves, structures virtually identical to retroviral proviruses, but with certain features that differ from them. The differences and similarities are highly informative. These structures are called endogenous retroviruses, or ERVs.

Features of ERVs
  • There is usually no sign of active retroviruses that can be associated with ERVs.
  • There are many thousands or ERVs in a typical genome.
  • Each ERV is to be found in the nuclear DNA of every single nuclear cell of any given organism, in exactly the same location in the DNA. The contents of any given ERV are uniform, going from cell to cell.
  • ERVs have the same detailed structure as retroviral proviruses, but they are usually incapable of producing virions.
  • ERVs have the same distinctive codon bias as retroviral proviruses.
  • Most ERVs are to be found in every member of a given species, always in the same location in nuclear DNA of every nuclear cell.

Endogenization is the account that holds that ERVs are inherited from ancestors who acquired them via retroviral integration into germ line cells.

Here are some of the advantages of the the endogenization account for explaining the similarities and differences between somatic proviruses and ERVs.
  • It explains their presence in the absence of active retroviruses. This is to be expected if they are inherited remnants of ancient proviruses.
  • It explains their high numbers. All ancestors, going back over millions of years, are potential bequeathers of ERVs.
  • It explains why they are in every cell, in the same location, and why they are uniform. They got there by normal mitosis, which is a high fidelity duplication process.
  • It explains why they have the same structure as proviruses (they are copies of proviruses) and it explains why they are so inactive as proviruses - only proviruses not subject to adequately negative selection pressure allow their hosts to bequeath their DNA to their descendants.
  • It explains the viral codon bias. Again, they are copies of proviruses.
  • It explains their universality in the population. Genetic drift will eventually ensure that any given ERV will either become fixed in the population, or will disappear.
Additional support for endogenization.

Let's look at some of the objections to endogenization and see if they are reasonable ones.

1) An ERV does not derive from a retrovirus. There are so many uniquely retroviral features of ERVs that make this idea unworkable. Even when a fragment of an ERV does something (you would never want an ERV to function in its entirety) the rest of the ERV makes no sense. Why the reverse transcriptase? Why the integrase? Why the repetition of DNA, like bookends, either side of the up and downstream LTRs, exactly where we would expect to see the if the ERV had been integrated by integrase?

2) Different species can be directly infected by the same retrovirus. Yes they can, but retroviruses do not target specific locations in DNA. Gene therapists and genetic engineers would sell their souls in an instant if they could find a way of doing that. That's one of the main reasons they research the action of integrases and integration target preference so diligently. Common ERVs exist in corresponding locations in the DNA of all your cells, all of my cells, and all of Charlie the chimp's cells because we have all inherited them from ancestors we all share. There is no other explanation that makes any sense.

3) Only a handful of ERVs are shared between chimps and humans. This is untrue. It seems to stem from a misreading (probably due to confirmation bias) of Theobald's piece in Talk Origins which mentions the handful of commonly located ERVs unique to humans and chimps that were known at the time. This is no help anyway. I'm going to be ridiculously generous and use a probability of common location by coincidence of 1/100. Using this figure, the probability of seven such common ERVs by coincidence is 1/1007 = 1/100,000,000,000,000. One in a hundred billion. IOW, you would have to search a hundred billion earths, each with their own unrelated chips and humans, in order to find the one earth where it misleadingly appears that the two species are related.

The real figure for shared ERVs and ERV fragments is not seven. It's more like 200,000. With a probability as much as 1/100 for a single coincidence, that's a likelihood of one in ten followed by 399,999 zeros!

4) ERVs are not junk. Not entirely. They are the remnants of fully working sets of genes - for making retroviruses.

5) ERVs could have been designed - particularly to aid evolution by increasing variation and gene sharing. Doesn't make much sense in the light of the facts that retroviruses are "designed" to make retroviruses, that only components of some ERVs have an exaptated function, while other components do nothing, or even cause diseases. And even if a Mischievous Designer did make retroviruses and let them loose, endogenization in common ancestors is still the only explanation for multiple commonly located ERVs.

6) There are common ERVs that do not conform to the generally accepted phylogeny. That is true, but rare. I only know of one confirmed case, and one suspected, possible case. This is trotted out as if it is a show stopper, but the only viable explanation is incomplete lineage sorting, and it doesn't falsify common descent. You are still left with the task of explaining the ERVs that are commonly located in different species.There will be other differences that will have happened after speciation, of course. These are independent endogenizations. In closely related, recently separated species, we would expect them to share the majority of their ERVs, and then have some different new ones acquired after speciation, which we would expect to appear more recent (less mutated and recombined). This is exactly what we see with chimps and humans.

7) 200,000 ERVs in 25 million years would drive a species to extinction. Well, make up your mind whether there are just a handful or 200,000 ERVs! Reverse transcription is error prone. It doesn't need to be accurate if enough cells get to reproduce the virus. Most ERVs are inactive - either because of mutation and cutting up by recombination, but also because, probably, many of them were never viable viruses in the first place. Let's take Marks 25 million years. Don't know where he gets it from, but let's take it. 200,000 ERVs. That's 1 successful endogenization every 125 years. (Successful, meaning it doesn't kill the host and then proceeds to become fixed in the population. Doesn't seem unreasonable to me.

8) A few components of a few ERVs are known to do something useful and even vital. In the case of syncytins - they look like mutated retroviral env genes, and are found in ERVs where you expect to find env genes - we have genes that allow placental attachment. Env genes help the virion to attach to the host cell. Syncytins are vital to some species (not to all species, but to the species they are vital to). But there are different syncytins, in different ERVs, in different places in the DNA of several different mammalian lineages. What for? Common designer? Hardly. And several ERV components are implicated in late onset diseases, particularly cancers. And what are all those other non-beneficial, non-deadly retroviral components for? It's clear that they were for getting retroviruses reproduced. Why the heck would an intelligent designer put useful, deadly and unnecessary retroviral genes in a structure that falsely mimics an ERV, mimics an evolutionary phylogeny, and puts fake watermarks of the non-existent action of a non-existent integrase enzyme in there too? And by the way, the position of an item of genetic material is largely irrelevant. Not always, but as a general rule. Otherwise, GM would not work.

9) ERVs promote transcription of native DNA. Yes, many of them do. Retroviruses come with their own promoters. They are needed to get their own genes transcribed. But mutate the provirus and chop it up, littering the genome with odd promoters in odd places there is a good chance they will promote something. This is not design.

OK. I'm nearing my character/word limit. There are a couple of extra points that will have to wait for when I respond to Mark's next positive post. I have not provided proper citations, as Mark had requested me to do, but did not do so himself. I'm pretty sure all the links work OK, though.

To Mark

Over to you to try and rebut this, and then you have a last chance to put your case and come up with reasonable doubts. I shall respond, and then sum up. I remind you of your commitment to give notice of source material while I still have the chance to comment on it. That means it must appear in your next two posts, and not for the first time in your summing up.

Originally Posted by mark kennedy View Post
New source material can be introduced in a timely fashion but there should be no surprises. You opponent deserves to be forewarned and allowed ample time to review the material especially if it's highly technical in nature.

Last edited by BarryDesborough; 19th June 2013 at 09:57 AM. Reason: Added link to Theobald
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Old 19th June 2013, 12:59 PM
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Classic Darwinian homology argument. I will dispense with the discussion of how ERVs work as viruses. I can concede every point made about the functionality of Endogenous retroviruses and Reverse transcriptase, in fact, my primary argument is based on it. Most retroviruses:
...infect somatic cells, but occasional infection of germline cells (cells that produce eggs and sperm) can also occur. Rarely, retroviral integration may occur in a germline cell that goes on to develop into a viable organism. (Endogenous retrovirus, Wikipedia)
There are two papers cited in the positive argument indicating how HIV works including lab procedures and known integration sites.
Retroviral copies of greater than or equal to 2 kb were found (i) exclusively in a discrete set of later replicating domains, most of which have the staining characteristics of constitutive heterochromatin, (ii) widely represented in disparate types of chromosome domains, or (iii) almost completely confined to CpG Alu-rich regions that are known to be early replicating. (Integration site preferences of endogenous retroviruses. Chromosoma. 1991 Dec;101)
This tells us where copies greater then 2kb were found and their characteristics, nothing more.
The integrase proteins from HIV-1, visna virus, and RSV were purified from a standard bacterial expression system..Knowledge of the biochemistry of how integrase functions is critical for obtaining a more complete view of the virus life cycle and for new treatments for the acquired immunodeficiency syndrome and other retrovirus-related diseases. (The Journal of Biological Chemistry Oct 6 2000)
Again we have a study of HIV, which is a somatic cell invasion. The reason they are looking at this one is because it's a devastating disease resulting from an ERV invasion. It destroys the immune system because it targets T Cells, if it's that devastating for the immune system what makes us think it's going to be benign in the germcells? Barry wants to claim the Phoenix Virus somehow confirms that 8% of the human genome is the result of germline invasions, so I looked at the research and found this:
They take all of the complete copies of the 9.4-kb HERV-K(HML2) provirus. Reconstruct 20 amino acid sequences with only one frameshift in the original reading frame. 'Phoenix Virus', the first infectious HERV available at the date of the publication Oct. 31, 2006. 293T cells were infected.
He just comes back and begs the question of proof without so much as an attempt at an exposition of the research. Obviously he is not reading his own source material and working hard just to understand the fundamentals. While it's commendable that he is willing to learn more he is oblivious that the research is virtually useless for an effective homology argument. For the sake of argument and because it does nothing but support mine I'll continue my exposition of the Phoenix Virus research:
the characterization of the insertion sites of 11 (nearly) full-length HERV-K(HML2) endogenous elements gave a rather different result, with five of them found far from known human genes (>100 kb on each side), four being in the vicinity (<20 kb) of genes, and only two inserted within genes (M. Dewannieux, unpubl.). This discrepancy is probably due to the strong counter-selection that should operate in vivo against insertions within genes, which are most probably deleterious for the proper expression of the targeted genes. (Identification of an infectious progenitor for the multiple-copy HERV-K human endogenous retroelements (Genome Research, Oct. 31,2006)
The HERV-K (HML2) is less then 1% of the human genome and yet it is the most studied. When they revive this sequence they actually manage to reconstruct it but with one frameshift. What is interesting about the results is that only two are within genes. The explanation being that they are probably deleterious so their are defenses that prevent this. Doesn't it make sense that the germline cells would be protected as well?

This is begging the question of proof on your hands and knees and it's typical of Darwinian logic. Take one anecdotal fragment of a phenomenon and project it over millions of years and countless taxon. Here is the main emphasis of the argument. Notice it assumes an advantage from an event without making the slightest attempt to qualify the cause. It's anecdotal at best:

Here are some of the advantages of the the endogenization account for explaining the similarities and differences between somatic proviruses and ERVs.

It explains their presence in the absence of active retroviruses. This is to be expected if they are inherited remnants of ancient proviruses.
There is no prediction, certainly no null hypothesis. From acute and largely irrelevant data it makes a blatantly false assumption that they are ancient germline invasions. These invasions are known to be rare and either neutral or deleterious and only in the rarest cases effect the germline. In the germline cells a virus that serves only to replicate itself would be devastating.

It explains their high numbers. All ancestors, going back over millions of years, are potential bequeathers of ERVs.
What explains it? There isn't a shred of proof that ERVs can invade the germline on this scale since they are rare at best at this highly vulnerable stage. The stages of cleavage and gastrulation are the foundational developmental points of living systems. Yet it is exactly here that Barry would have us believe that 8% of the human genome was formed. It must begin in early development. Yet it is precisely here, in early development, that organisms are least tolerant of mutations.

It explains why they are in every cell, in the same location, and why they are uniform. They got there by normal mitosis, which is a high fidelity duplication process.
We haven't even discussed the cells and more importantly, the high fidelity of the duplication process is the most serious flaw in your argument. All you want to talk about is how ERVs work, not once have you attempted to qualify or quantify how they can be integrated into the germline.

It explains why they have the same structure as proviruses (they are copies of proviruses) and it explains why they are so inactive as proviruses - only proviruses not subject to adequately negative selection pressure allow their hosts to bequeath their DNA to their descendants.
And pesto! There they are passing them on to their descendants. I knew there would be drama but this clumsy attempt at slight of hand was ill advised.

It explains the viral codon bias. Again, they are copies of proviruses.
What can I say no it doesn't and so what?

It explains their universality in the population. Genetic drift will eventually ensure that any given ERV will either become fixed in the population, or will disappear.
Now through genetic drift it's a virus induced mutation, becoming permanently fixed in populations. No explanation how it got by the DNA repair mechanisms or wasn't purged through recombination. It's just there as the result of highly improbable germline invasions on a massive scale. That, during a time when our ancestors would have been diversifying into all the main categories of monkeys and apes and highly conserved genes would have been moving at an unprecedented rate toward fixation as well. Neither the major morphological traits have a viable cause nor does the ERV elements have a reasonable cause but we are supposed to assume they happened on an impossible scale simultaneously.

2) Different species can be directly infected by the same retrovirus. Yes they can, but retroviruses do not target specific locations in DNA. Gene therapists and genetic engineers would sell their souls in an instant if they could find a way of doing that. That's one of the main reasons they research the action of integrases and integration target preference so diligently. Common ERVs exist in corresponding locations in the DNA of all your cells, all of my cells, and all of Charlie the chimp's cells because we have all inherited them from ancestors we all share. There is no other explanation that makes any sense.
You have yet to show a single orthologous site but you want us to assume they are all orthologous. Stereotypical homology argument, pedantic flights of conjecture and speculation made on biased foundational propositional facts supported by pure, undiluted presupposition.

3) Only a handful of ERVs are shared between chimps and humans. This is untrue. It seems to stem from a misreading (probably due to confirmation bias) of Theobald's piece in Talk.Origins which mentions the handful of commonly located ERVs unique to humans and chimps. This is no help anyway. I'm going to be ridiculously generous and use a probability of common location by coincidence of 1/100. Using this figure, the probability of seven such common ERVs by coincidence is 1/1007 = 1/100,000,000,000,000. One in a hundred billion. IOW, you would have to search a hundred billion earths, each with their own unrelated chips and humans, in order to find the one earth where it misleadingly appears that the two species are related.
The Talk Origins argument is based on ERVs being only 1% of the human genome overall, I doubt seriously you even read it. You never made the slightest attempt to qualify the statistics and when these probability arguments are inverted evolutionists invariably become silent. What are the odds of a single ERV infecting a germline cells during germline development? I predict your response will be fallacious, dismissive or silent. Your statistics are based on nothing tangible, not a single ERV is characterized in your discussion, none of the locations are indicated and the homology is blatantly assumed. Science is about directly observed or demonstrated phenomenon not assuming a phenomenon occurred millions of years ago on a massive scale when it is rarely seen in our day, if ever.

The real figure for shared ERVs and ERV fragments is not seven. It's more like 200,000. With a probability as much as 1/100 for a single coincidence, that's a likelihood of one in ten followed by 399,999 zeros!
The number of ERVs in the human genome at the publication of the Human Genome paper in 2001 was right around 200,000. You want us to assume that all of them are identical. Then in 2005 when they were actually compared to the Chimpanzee genome it was found that the largest and most abundant family of ERVs in the Chimpanzee genome was absent in the human genome. Then you want to dismiss Pterv because it's not an orthologous and have me assume that all the others are identical.

When they compared the protein coding genes they found that only 29% were identical, on average having one different codon in each lineage. Given the devastating effects of frameshifts on protein coding genes, the odds of a single mutation in a protein coding gene are themselves astronomical. When you have it happen in over 70% of the protein coding genes the odds would be far more zeros then an evolutionist would bother trying to calculate and these are key to the adaptive evolution of our supposed lineage.

You have done none of the requisite reading, not even bothering to attempt an exposition of your own source material. Homology arguments never stand up to close scrutiny and yet demand that you make sweeping, impossible assumptions regarding fantastic, even mythic changes and transitions on the slightest of proofs and evidences. When the creationist refuses to make the a priori assumption of universal common descent they are assumed to be ignorant of science. Then when they we refuse to make the equally unfathomable assumptions regarding massive ERV invasions of the germline we are given anecdotal evidence and asked to make further assumptions from unqualified and inconclusive empirical data. It's not only unreasonable to make these demands, it's fallacious and altogether unscientific in it's orientation.

The inverse logic is intuitively obvious. If the things in common are viable proof of common ancestry then differences are evidence of independent lineage and thus, creation. I do not need your permission to make this obvious choice between the flights of Darwinian fantasy and the confirmed history of creation as told by the Creator Himself.

Having demonstrated that you are incapable of a serious exposition of the requisite scientific literature I can only conclude you are repeating this defunct homology argument without qualification. The Phoenix Virus was actually quite informative but there was no attempt on your part do make even the most basic insights into the findings. Because of that my final positive argument will be about the deleterious effects of mutations on genomic machinery.

Mutations, whether they are the result of copy errors or viral infections are the worst explanation possible for adaptive evolution. They are the nemesis of living systems while other far more worthy candidates epigenesis are available, quantified and qualified for any motivated and serious student of evolutionary biology. The only reason that Darwinians will not touch them with a ten foot pole is because they have limits beyond which they cannot evolve. See my signature.

With that I will be taking a couple of days to prepare my final argument. Then I will wait patiently for Barry to respond and we will be writing our conclusions. As far as formal debates go this one has been the weakest I have seen on here and it is beyond disappointing to see someone just beginning to take an interest in the Life Sciences to be derailed by this miserable excuse for a homology argument.

Have a nice day
Mark
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Old 22nd June 2013, 10:46 AM
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The Inverse Logic is Intuitively Obvious

Evolution is defined scientifically as the change of alleles in populations over time. Darwinism is the a priori assumption of universal common descent by exclusively naturalistic means. The most common and persuasive argument for common descent the Darwinian has is homology or things the two lineages have in common, especially things that are identical. Homology arguments have been the cornerstone of Darwinian logic since Huxley (Darwin's bulldog) first started attacking the concept of creation. For a long time I found these arguments highly persuasive and regarded them as profoundly empirical until I discovered that the Achilles' heel of Darwinian logic was the role of mutations in their scenario of natural history.

When the comparison of Chimpanzee and Human genomes was published back in the fall of 2005 there were 2 primary differences identified. Single base substitutions where a single base pair (GT-guanine-cytosine and AT adenine-thymine) are switched and indels (insertions/deletions) which is any section that is present in one genome but absent in the other. We have been told since the advent of the DNA double helix model that after meticulous and determined searches scientists could find no more then 1% of the DNA in Humans and Chimpanzees were different. When it comes to single base substitutions that's true but with the inclusion of indels (aka gaps) the divergence jumps to 4%. After this was determined beyond all skepticism Darwinians, even reputable scientists, continued to tell us that we were 98% the same as Chimpanzees in our DNA. The reason for this is mutations.

Most of the time when a mutation occurs in the DNA it's neutral (does nothing), the vast majority of the time when it has an effect it's deleterious (harmful). The main cause of mutations is copy errors and there are quality control checks and DNA repair mechanisms throughout the life cycle of the cell that prevent the vast majority of them from getting though. When they do manage to get by the quality control checks natural selection eliminates them through the death of the carrier. In order for a mutation to be permanently fixed and passed on from one generation to another it has to be present in the germline cells. This is the last place you would want to have a mutation, it is no where more dangerous to the offspring.

Mutations are rare enough given the high degree of fidelity in the reproduction of DNA during the cell cycle reproduction. Those effecting fitness would be even more rare, since they are profoundly dangerous to the health of the genome and host organism. The rarest of all would be those that have a beneficial effect and even those, come with a high cost to establish them as permanent part of the genome. These facts of evolutionary biology and genetics make Darwinian logic untenable, unreasonable and absolutely impossible. The tragic fact is that despite this obvious and glaring flaw in Darwinian logic, universal common descent can never be and is never questioned.

The inverse logic of Darwinism is intuitively obvious. The only alternative to universal common descent by exclusively naturalistic means is God creating life by divine fiat. The ability of living systems to adapt and develop over time must be the result either of mutations (Darwinian logic) or created by God (Divine Providence), there is no third alternative.

What we have here in this debate is a Darwinian assumption that ERVs, which make up 8% of the human genome are the result of viral infections. Not once has my opponent managed a substantive proof that this is a reliable fact. He certainly never felt compelled to offer any kind of empirical evidence. His entire argument comes down to a couple of sentences commenting on the Phoenix virus, a potentially dangerous experiment that proves absolutely nothing.

Barry has failed the burden of proof on two main points miserably. One, that germline invasions on this scale are even possible and that the vast majority of ERVs are orthologous (identical sequences and locations). I need not bother accumulating more proof, his arguments have fallen by their own weight due to the fatal flaws in the foundational assumptions. There is no rational reason, let alone empirical proof that viral infections can invade the germline on this scale. What is more, ERVs are riddled with mutations that are accumulated at random. It is impossible by any stretch of the imagination that they could be orthologous on the scale he is describing. Not one single orthologous ERV has been described in his argument, it is simply assumed.

I will not dignify this dismal excuse for a homology argument with further consideration. The glaring errors and fatal flaws are evident and obvious. Barry can respond to this argument as he sees fit. Whether he does so intelligently or foolishly there hasn't been a single substantive argument made for these two foundational proofs so far, nor do I expect one now.

The inverse logic is intuitively obvious. If things in common are a valid proof of common ancestry then differences are valid proofs of independent origins of the Chimpanzee and Human genomes, thus creation. The assumption that 8% of the human genome is the result of germline invasions is absurd and suspended by nothing but pure, undiluted presupposition. ERVs being orthologous in more then a few ERVs is also a false assumption with no rational or empirical basis.

That ends my final positive argument and I will wait for Barry to respond and we can both write our concluding remarks then.

Have a nice day ,
Mark
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Old 23rd June 2013, 12:45 PM
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First, a few observations of Mark's ‘rebuttal’ of my second post advocating the debate proposition.

A lot of it is meaningless word salad, or irrelevant, so I’ll just concentrate on the parts that are relevant and that parse (sort of).
Originally Posted by mark kennedy View Post
Classic Darwinian homology argument. [Mark commenting on my previous post]
No, Mark. That’s been explained to you several times now. It is much more than that. The orthology is concluded from specific evidence concerning retroviruses. The fact that you have not properly considered the evidence and reasoning does not mean it does not exist.
Originally Posted by mark kennedy View Post
I will dispense with the discussion of how ERVs ares work as viruses. I can concede every point made about the functionality of Endogenous retroviruses and Reverse transcriptase, in fact, my primary argument is based on it. Most retroviruses:

...infect somatic cells, but occasional infection of germline cells (cells that produce eggs and sperm) can also occur. Rarely, retroviral integration may occur in a germline cell that goes on to develop into a viable organism. (Endogenous retrovirus, Wikipedia)
That’s a bit muddled. Exogenous retroviruses work as viruses. Most endogenous retroviruses are incapable of replication. But yes, ERVs can have functions useful or even vital to their possessors, and this does not prove that they were not, ultimately, of retroviral origin. And yes, endogenization (survivable integration with the germline) is rare, but happens. Maybe we are getting somewhere at last.
Originally Posted by mark kennedy View Post
It [HIV] destroys the immune system because it targets T Cells, if it's that devastating for the immune system what makes us think it's going to be benign in the germcells?
It’s not going to be benign, most of the time. But as has been pointed out to you, reverse transcription is a very error-prone process. It would have to work without error, and integration would have to be in a disruptive location in order to have its devastating effect every time. You have just conceded that retroviruses do successfully invade the germline, however rarely. How else are we to to explain the appearance of ERVs? And if they were all always devastating, all of us (and all our retroviruses) would have been long extinct. But here we are, with all our ERVs!
Originally Posted by mark kennedy View Post
Barry wants to claim the Phoenix Virus somehow confirms that 8% of the human genome is the result of germline invasions...
{Barry strums fingers on desk. Gnaws at leg stump. Whimpers. Tears at remaining hair.} Mark, I’ve said it before. It would be helpful if you actually read my posts properly. The phoenix virus is powerful evidence that ERVs derive from retroviruses, because a fully working retrovirus was easily reconstructed from ERVs. The 8% figure, on the other hand, comes from the human and chimp sequencing work that you have already referred to and linked to several times yourself! The figure does not derive from the “phoenix experiment”!
Originally Posted by mark kennedy View Post
What is interesting about the results is that only two [HERV-K (HML2)s] are within genes. The explanation being that they are probably deleterious so their [sic] are defenses that prevent this. Doesn't it make sense that the germline cells would be protected as well?
This is mistaken. The “defences” are against certain (but not all) types of damage and mutation detected during meiosis and mitosis but not against endogenization. There is no checksumming in the genome. If a chunk of alien DNA gets spliced into the nuclear DNA, there are no cellular resources to detect it and do anything about it as long as both strands are complementary, as retroviral integrations are. Integration does not damage the host DNA in any way that the cell can detect. It’s simply that fatal endogenizations (at least ones that kill before you get a chance to reproduce) don’t get passed on - obviously. It is interesting that integrations into a protein coding gene can be survivable and not impact reproductive fitness. Either it doesn’t affect the transcripts, or there are multiple copies of the gene - which is a common occurrence, or the broken gene is survivable. The genome is less of an intricate machine, any part of which, if you modify it, it will break, but more of an “ecosystem” or “society” of genetic elements, all trying to either get along, or compete. It is resilient, and copes with a certain level of dysfunctionality. I think creationist propaganda has done you a disservice by portraying molecular biology as a delicately integrated machine, where if any part of it does not function, the whole shebang falls over on its back and croaks.
Originally Posted by mark kennedy View Post
These invasions are known to be rare and either neutral or deleterious and only in the rarest cases effect [sic] the germline. In the germline cells a virus that serves only to replicate itself would be devastating.
A “virus in the germline” is an ERV. It can function as a retrotransposon. Retrotranspositions are not always devastating. A large proportion of ERVs are retrotranspositions that do not possess env genes.
Originally Posted by mark kennedy View Post
There isn't a shred of proof that ERVs can invade the germline on this scale since they are rare at best at this highly vulnerable stage.
Once more, you yourself have linked to the whole genome studies which show this statement to be false.
Here are some studies of endogenization.

http://www.ncbi.nlm.nih.gov/pmc/arti...00358-0132.pdf
(Efficient insertion of genes into the mouse germ line via retroviral vectors.)

http://www.ncbi.nlm.nih.gov/pmc/arti...00049-0193.pdf
(Spontaneous germ line virus infection and retroviral insertional mutagenesis in eighteen transgenic Srev lines of mice.) Thank you, LoudMouth http://www.christianforums.com/t7751946-3/#post63300047 .

And you know all about KoRV, because you read the abstracts, at least, didn’t you?

Here’s another study for you to ignore, the jaagsiekte sheep retrovirus which has a very similar endogenous form. A history of ovine pulmonary aden... [Curr Top Microbiol Immunol. 2003] - PubMed - NCBI

Work the numbers. The oldest known endogenization is estimated to have occurred more than 100 million years ago. 200,000 fixed ERVs over 100 million years. Yes. Rare, but there.
Originally Posted by mark kennedy View Post
We haven't even discussed … the high fidelity of the duplication process is the most serious flaw in your argument.
The high fidelity replication process duplicates the low fidelity results of reverse transcription, with high fidelity. A high fidelity copy of a error is a high fidelity copy of an error.
Originally Posted by mark kennedy View Post
And pesto [sic]! There they are passing them [non-deleterious integrations] on to their descendants. I knew there would be drama but this clumsy attempt at slight [sic] of hand was ill advised.
Would you expect a severely deleterious integration to be passed on? What’s to prevent non-deleterious integrations being passed on?
Originally Posted by mark kennedy View Post
What can I say no it doesn't [explain viral codon bias] and so what?
This just tells me that you are so cock-sure that what you believe is correct, that you can'teven be bothered to try and verify it. Sloth is a deadly sin, Mark.
Originally Posted by mark kennedy View Post
You have yet to show a single orthologous site but you want us to assume they are all orthologous.
You’ll be asking me for proof that the grass is green next, Mark. Nobody doubts that there are pairs of ERVs in common between chimps and human in exactly corresponding locations in the DNA. You yourself have linked to the surveys of the human and chimp genomes that show us 200,000 such pairs of ERVs. I don’t want you to assume they are orthologous, I want you to read and consider the evidence and the reasoning that leads us to that conclusion. You can lead a donkey to water, as they say...
Originally Posted by mark kennedy View Post
The number of ERVs in the human genome at the publication of the Human Genome paper in 2001 was right around 200,000. You want us to assume that all of them are identical.
Give me strength. No. I want you to follow the reasoning that leads to the conclusion that the majority of them have a corresponding ERV in the chimp genome. Either identical, or with minor mutations at a level consistent with speciation a handful of millions of years ago. It is pretty easy to follow, but you have been unable to follow it. I’m sure it’s not out of stupidity, but out of a mental block.
Originally Posted by mark kennedy View Post
Then in 2005 when they were actually compared to the Chimpanzee genome it was found that the largest and most abundant family of ERVs in the Chimpanzee genome was absent in the human genome.
275 chimp-specific ERVs as compared 200,000 common ERVs. And this sort of result is exactly what we would expect to happen after speciation. You have been corrected on this point so many times, it’s too tedious to count. PtERVs are not being dismissed. They are perfectly consistent with common ancestry for two different species. Their common ancestor would have bequeathed them a number of ERVs, and then, after they speciated, they would have independently acquired different endogenizations. This is exactly what we see.
Originally Posted by mark kennedy View Post
When they compared the protein coding genes they found that only 29% were identical, on average having one different codon in each lineage. Given the devastating effects of frameshifts on protein coding genes...
Substitutions are not frameshifts. Synonymous substitutions rarely have any effect, and other substitutions, unless they affect protein folding or directly affect active sites, will have little effect on a protein enzyme. Living chemistry is far more resilient than you seem to assume.
Originally Posted by mark kennedy View Post
The inverse logic is intuitively obvious.
To your intuition, perhaps. But intuition is variable between individuals and is not a reliable guide to the truth. That’s why science was developed.

From The Origin of Species, Chapter 6, "Organs of extreme perfection and complication".
To suppose that the eye with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I freely confess, absurd in the highest degree. Yet reason tells me, that if numerous gradations from a perfect and complex eye to one very imperfect and simple, each grade being useful to its possessor, can be shown to exist; if further, the eye does vary ever so slightly, and the variations be inherited, which is certainly the case; and if any variation or modification in the organ be ever useful to an animal under changing conditions of life, then the difficulty of believing that a perfect and complex eye could be formed by natural selection, though insuperable by our imagination, can hardly be considered real.
And from What is True? in A Devil's Advocate by Richard Dawkins,
Modern physics teaches us that there is more to truth than meets the eye; or than meets the all too limited human mind, evolved as it was to cope with medium-sized objects moving at medium speeds through medium distances in Africa.
Your error has been explained to you so many times, I have to conclude that it would be a waste of time explaining the bleeding obvious to you yet one more time. Go back over my posts and find the niece analogy.
Originally Posted by mark kennedy View Post
Mutations, whether they are the result of copy errors or viral infections are the worst explanation possible for adaptive evolution.
The ERV case for common descent has little direct connection with the subject of mutations. It merely points out that if we share multiple integrations into our DNA at corresponding loci, they must have derived from germ-line integrations into the germ-line cells of our common ancestors.

OK. On to Mark's second attempt to express reasonable doubt.
Originally Posted by mark kennedy View Post
Evolution is defined scientifically as the change of alleles in populations over time. Darwinism is the a priori assumption of universal common descent by exclusively naturalistic means.
Nerp! Nerp! Nerp!
Even if mistaken, a conclusion is not an a priori assumption. Philosophy 101.
The main cause of mutations is copy errors and there are quality control checks and DNA repair mechanisms throughout the life cycle of the cell that prevent the vast majority of them from getting though.
But they cannot detect insertions with complementary strand insertions.
Mutations are rare enough given the high degree of fidelity in the reproduction of DNA during the cell cycle reproduction. Those effecting fitness would be even more rare, since they are profoundly dangerous to the health of the genome and host organism. The rarest of all would be those that have a beneficial effect and even those, come with a high cost to establish them as permanent part of the genome.
Yet because they are beneficial, they increase in copy frequency. (The very definition of "beneficial"!
The inverse logic of Darwinism is intuitively obvious.
All varieties of woo are "intuitively obvious" to those who believe in them.
What we have here in this debate is a Darwinian assumption that ERVs, which make up 8% of the human genome are the result of viral infections.
Conclusions from evidence and basic reasoning are not "assumptions".
Barry has failed the burden of proof on two main points miserably. One, that germline invasions on this scale are even possible
Yet you concede that they have happened!
and that the vast majority of ERVs are orthologous (identical sequences and locations).
Yet you have repeatedly linked to the proof that they are.
What is more, ERVs are riddled with mutations that are accumulated at random.
This is the main reason why they have not been expunged from our genomes.
The inverse logic is intuitively obvious. If things in common are a valid proof of common ancestry then differences are valid proofs of independent origins
OK. Chimps and humans share common ancestors that both existed, and did not exist. And you call that a rational position?

Last edited by BarryDesborough; 24th June 2013 at 03:01 AM.
 


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