Viruses that prove common descent

[xianghua]

This is about common ERVs. Which are there. We are not interested in claims that have no evidence in their favour. Here, again, is my page outlining why virologists and geneticists conclude that ERVs are of retroviral origin. This is how you back up a claim. Veritas: ERV FAQ: Why do virologists and geneticists think that ERVs come from retroviruses? Isn't that just supposition on their part?
Kindly address this evidence.

again: do you think that a spinning motor is evidence for design or not? if ts evidence for d esign- then the whole ervs a rgument is meaningless

 

[xianghua]

I can't answer that without additional intel.
How does a robot made from organic components differ from a natural system made from organic components?

so such a robot can evolve naturally and therefore a robot isnt evidence for design according to this logic.

 

[dad]

Oh he has done more then blogs, he had some crazy facebook think on ERVs I participated in for a while. The hard part was turning their spam off, why he persists is something only he understands.

Sounds like a lot of potential for bias.

 

[dad]

so such a robot can evolve naturally and therefore a robot isnt evidence for design according to this logic.

Good point. The amazing creation and creatures and man's bodies speak loudly that it could have been no accident. In fact they speak so loud they say the fool is the only one that thinks otherwise.

 

[mark kennedy]

Sounds like a lot of potential for bias.

As long as he has been doing this it's disappointing that he didn't take more of an interest in the Life Sciences. It's really the whole point for me, ERVs as viruses seems like a lot of highly complex research yielding nothing conclusive or particularly informative. Bias is the least of my concerns, getting someone interested in these discussions to take an interest in actual genetics, now that would be doing something.

 

[dad]

As long as he has been doing this it's disappointing that he didn't take more of an interest in the Life Sciences. It's really the whole point for me, ERVs as viruses seems like a lot of highly complex research yielding nothing conclusive or particularly informative. Bias is the least of my concerns, getting someone interested in these discussions to take an interest in actual genetics, now that would be doing something.

The problem may partially lie in some people having a keen interest in fighting God, and dissing creation. It is easy to hide in confusing babble and scientific sounding nonsense. All smoke no fire.
No matter how ervs get around now, it basically has NOTHING to do with creation, or how they used to transfer etc.

 

[mark kennedy]

The problem may partially lie in some people having a keen interest in fighting God, and dissing creation. It is easy to hide in confusing babble and scientific sounding nonsense. All smoke no fire.
No matter how ervs get around now, it basically has NOTHING to do with creation, or how they used to transfer etc.

What I'm getting is ERVs actually have a purpose but occasionally they get loose and into things they shouldn't. Sometimes they can get into the germline but they are associated with things like cancer and may be a contributing factor to Multiple Sclerosis. One brief discussion I seen says they found them in the placenta of a mammal, can't recall the species. My thing has been that ERVs in the human genome making up 8% of the genome is just ridiculous. The largest family of ERVs in the Chimpanzee genome, about a hundred members, would have came about right at the time of the split. Mind you this wouldn't be a couple here and there, they would have been inundated with them. There is no more vulnerable time for a fetus then the germline, ever heard of stem cells, that's where they come from.

Technical details aside for the moment, the sweeping assumptions associated with this homology argument fly in the face of common sense and logic. ERVs on this scale would devastate the genome. It's almost comical that Barry wants to link to an FAQ that links to a study that postulates that ERVs can prevent further invasions. The reconstruction of the 'Phoenix virus', showed a very interesting functional constraint, some mechanism prevented the ERVs from getting into the genes. The high degree of fidelity of the transcription process makes these arguments regarding germline invasions on this scale improbable to the level of ridiculous at the most basic level.

 

[dad]

What I'm getting is ERVs actually have a purpose but occasionally they get loose and into things they shouldn't. Sometimes they can get into the germline but they are associated with things like cancer and may be a contributing factor to Multiple Sclerosis. One brief discussion I seen says they found them in the placenta of a mammal, can't recall the species. My thing has been that ERVs in the human genome making up 8% of the genome is just ridiculous. The largest family of ERVs in the Chimpanzee genome, about a hundred members, would have came about right at the time of the split.

The split?

Mind you this wouldn't be a couple here and there, they would have been inundated with them. There is no more vulnerable time for a fetus then the germline, ever heard of stem cells, that's where they come from.

Technical details aside for the moment, the sweeping assumptions associated with this homology argument fly in the face of common sense and logic. ERVs on this scale would devastate the genome. It's almost comical that Barry wants to link to an FAQ that links to a study that postulates that ERVs can prevent further invasions. The reconstruction of the 'Phoenix virus', showed a very interesting functional constraint, some mechanism prevented the ERVs from getting into the genes. The high degree of fidelity of the transcription process makes these arguments regarding germline invasions on this scale improbable to the level of ridiculous at the most basic level.

We'll have to disagree that the transcription process we see today is even relative to the origins issues.

 

[mark kennedy]

The split?

The supposed split between chimpanzees and human lines. The dating of the youngest ERVs, the most abundant according to the research, occurred during that period for the chimpanzee genome.

We'll have to disagree that the transcription process we see today is even relative to the origins issues.

There is transcription, the process by which the DNA is copied. Then there is translation which is the process by which it's translated into protein products. What we do know and no one can argue is that the fidelity of the transcription of the DNA is highly conserved, there can be no question about that:

In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair…It has been estimated that in humans and other mammals, uncorrected errors (= mutations) occur at the rate of about 1 in every 50 million (5 x 10^7) nucleotides added to the chain. (Not bad — I wish that I could type so accurately.) But with 6 x 10^9 base pairs in a human cell, that means that each new cell contains some 120 new mutations. (Mutations)
​

Darwinians believe that those uncorrected errors are responsible for evolution on a universal scale. It fosters a gross ignorance of how genomics actually work. Mutations in the germline would be the most devastating of mutations since they happen so early in development. They have not even made the effort to demonstrate how these germline invasion are even possible, let alone feasible.

Among the mutations that affect a typical gene, different kinds produce different impacts. A very few are at least momentarily adaptive on an evolutionary scale. Many are deleterious. (Rates of Spontaneous Mutations)
​

Mutations and germline invasions are not an explanation for evolution, they are an affront to science and reason when they are purported to be evidence of universal common descent. They are the main reason such a metamorphosis is sensible, even as idle speculation.

Grace and peace,
Mark

 

[JDD_III]

ERVs are a type of "The chicken or the egg" scenario.

Which you subscribe to depends on your base assumption.

If you do not assume viruses arose before mammalian life then you could propose the origin of retroviruses came from existing genomic sequences.

 

[dad]

The supposed split between chimpanzees and human lines. The dating of the youngest ERVs, the most abundant according to the research, occurred during that period for the chimpanzee genome.

Oh. Ha. I guess there are people that actually believe that.

There is transcription, the process by which the DNA is copied. Then there is translation which is the process by which it's translated into protein products. What we do know and no one can argue is that the fidelity of the transcription of the DNA is highly conserved, there can be no question about that:

OK, so in other words things NOW work a certain way in this present time and nature. They translate, transcribe and such a certain way and for certain reasons. Noah had cells, and things got transferred and such also in his day. If the laws and nature were not the same then the way things did all that was not the same either. Since we don't know how nature was, we cannot look at how things transcribe and transfer now as any indication of how they did then. In other words, how ervs ended up where they are now need not have anything to do with how ervs NOW transfer or get around.

In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair…It has been estimated that in humans and other mammals, uncorrected errors (= mutations) occur at the rate of about 1 in every 50 million (5 x 10^7) nucleotides added to the chain. (Not bad — I wish that I could type so accurately.) But with 6 x 10^9 base pairs in a human cell, that means that each new cell contains some 120 new mutations. (Mutations)​

Yes, NOW. Not then, that we know. Chimps could have gotten viri from man other ways then, or visa verso.

​

Darwinians believe that those uncorrected errors are responsible for evolution on a universal scale

Believe being the key word. They have no idea, and rely totally on looking at how things now get around.

. It fosters a gross ignorance of how genomics actually work. Mutations in the germline would be the most devastating of mutations since they happen so early in development. They have not even made the effort to demonstrate how these germline invasion are even possible, let alone feasible.

You could be right. But even the germ line now could not indicate to us how it worked then!

Among the mutations that affect a typical gene, different kinds produce different impacts. A very few are at least momentarily adaptive on an evolutionary scale. Many are deleterious. (Rates of Spontaneous Mutations)​

Mutating is how things now work. Who says there even was any mutation in Adam's day? We don't know.

​

Mutations and germline invasions are not an explanation for evolution, they are an affront to science and reason when they are purported to be evidence of universal common descent. They are the main reason such a metamorphosis is sensible, even as idle speculation.

Grace and peace,
Mark

I agree..albeit for different reasons. Their diabolical anti creation fibs and stories are a crime against humanity.

 

[dad]

ERVs are a type of "The chicken or the egg" scenario.

Which you subscribe to depends on your base assumption.

If you do not assume viruses arose before mammalian life then you could propose the origin of retroviruses came from existing genomic sequences.

I suppose one could propose the universe sailed out of a pepper sized speck if one wanted. Science should involve some degree of knowledge though.

 

[mark kennedy]

Oh. Ha. I guess there are people that actually believe that.

It's all supposition, trust me.

OK, so in other words things NOW work a certain way in this present time and nature. They translate, transcribe and such a certain way and for certain reasons. Noah had cells, and things got transferred and such also in his day. If the laws and nature were not the same then the way things did all that was not the same either. Since we don't know how nature was, we cannot look at how things transcribe and transfer now as any indication of how they did then. In other words, how ervs ended up where they are now need not have anything to do with how ervs NOW transfer or get around.

Hang on, you almost have the right idea here. In the time of Noah the mutations had not had time to accumulate so it meant bigger gene pools. Now once things have speciated there are bottlenecks, adaptive evolution isn't going to happen on that scale. Now as far as the ERVs, infection in the germline is pretty rare and certainly nothing heritable has been documented. Once again, that kind of transfer still happens but on the scale they are talking about, forget it.

Yes, NOW. Not then, that we know. Chimps could have gotten viri from man other ways then, or visa verso. Believe being the key word. They have no idea, and rely totally on looking at how things now get around.
You could be right. But even the germ line now could not indicate to us how it worked then!

There is every indication that this isn't something subject to change over time. God provided for the passing of heritable traits, known in science as the laws of inheritance. It's as simple as this, they take an occasional mutation with a beneficial effect or a mutation in roughly the same place in two genomes and that's supposed to be proof. The far weightier matter regarding the three fold expansion of the human brain from that of apes they ignore.

Mutating is how things now work. Who says there even was any mutation in Adam's day? We don't know.

Probably weren't, the living systems of the time probably had pristine genomes that accumulated mutations over time.

I agree..albeit for different reasons. Their diabolical anti creation fibs and stories are a crime against humanity.

Look at it realistically, what do you expect from people who have never really known anything but the natural order. If you remember right, the gospel was made clear to you not by your own powers of perception but because God made himself known to you by some means. That's how I remember my conversion, so I understand people who do not deviate from naturalistic reasoning, it's all they have ever known.

Grace and peace,
Mark

 

[Barry Desborough]

Participants, please don't think that because I don't always reply promptly, that I don't have anything to say in response. I guess most of you are in the U.S. I'm on Central European Time. An added problem is that the site's notification system is rather hit-and-miss. I don't always get notification of posts. I have to poll the discussion.

I will respond to the above posts (at least the comments that are coherent and on-topic) as soon as I can spare the time.

 

[mark kennedy]

Participants, please don't think that because I don't always reply promptly, that I don't have anything to say in response. I guess most of you are in the U.S. I'm on Central European Time. An added problem is that the site's notification system is rather hit-and-miss. I don't always get notification of posts. I have to poll the discussion.

I will respond to the above posts (at least the comments that are coherent and on-topic) as soon as I can spare the time.

Take your time Barry, looking forward to it.

 

[Barry Desborough]

again: do you think that a spinning motor is evidence for design or not? if ts evidence for d esign- then the whole ervs a rgument is meaningless

If you wish to argue for design, please start your own discussion. The subject of this one is ERVs, and their significance in the case for common descent. Even if life was designed by some undesigned designer, the evidence from ERVs still stands. The undesigned designer must have created ancestral forms that subsequently speciated.

I asked you to address the evidence that ERVs are of retroviral origin. You ignored the request. You ignored the evidence. You are not the only one to studiously ignore it. But here's another chance. What follows is a copy and paste of a page from my FAQ. Let's see if you or anyone else has what it takes to address this evidence. I very much doubt it, but here's your chance to put your money where your mouth is.

-----------------------------------------------------

Much material in this page has been lifted from Abbie Smith.Hope you don't mind Abbie,

Every detail of every full ERV is replete with complex and subtle details attesting to its origin in retroviruses. ERVs have the same structure as retroviral integrations. This is some -10 kilobases of genes specific to the retroviral replication cycle. All retroviruses and complete ERVs include genes we call gag, pol and env. The function of these genes will be gone into in detail in the following notes. In addition, several other features common to retroviral integrations and ERVs only make sense in terms of the requirements of the retroviral replication cycle.

"The gag gene encodes for ‘Gag’ the giant protein, which gets chopped into several smaller proteins, Matrix, Capsid, and Nucleocapsid (and sometimes a few more tiny ones, depending on the retrovirus)."

"Matrix is the structural protein just inside the envelope (the membrane the virus stole from its host cell). It has ‘outside’ functions (targeting the virus assembly to the right kind of cell membrane, keeping the outside protein env, in order) and ‘inside’ functions (targeting the reverse transcribed DNA to the new host cell nucleus). Jack of all trades protein, like lots of retroviral proteins. They run a tight ship."

"Capsid forms the viral ‘core’. Normally when you think of a ‘virus’, you think of this shape, an icosahedron. Retroviral ‘cores’ really look more like a cylinder-cone-thingie, like the bottom pic here. That particular pic is also worth a second look– More protein cuts to Capsid need to take place after a baby virus buds off from its host cell to make an immature virus mature. Blocking this maturation step is what the next family of anti-HIV-1 retrovirals do. *thumbs up*"

"Nucleocapsid is a structural protein that wraps up the retroviral genome to make sure its packaged properly into the Capsid."

Pol codes for all the enzymes a retrovirus needs:"

"Protease– Chomps big proteins into all the little functional proteins, like we saw with Gag getting chomped into Matrix/Capsid/Nucleocapsid. The name ‘protease’ can be a little confusing because all organisms have ‘proteases‘, but only the protease that the retrovirus carries with it is the ‘right‘ protease to cleave in all the ‘right’ spots to get all the ‘right’ proteins in the end. Instead of giving retroviral proteases a special name, they just named it ‘Protease’. heh. Protease inhibitors are a great target for anti-retrovirals."

"Reverse Transcriptase– Another target for anti-retrovirals. Though the process of reverse transcription can be found in you and I (coooool), retroviruses need to carry an enzyme with them to convert viral RNA into DNA on demand. This process not only requires converting an RNA genome into a DNA genome, but also:"

"RNase H– The RT enzyme has (at least) two active sites. One performs the process of reverse transcription. Another active site has RNase activity (chops up RNA, specifically, RNA Hybridized with DNA haha!). RNase H chews up the old RNA template after a single strand of DNA has been made, so the single strand of DNA can be made into double stranded DNA, and subsequently inserted into the host cells genome. This might make more sense if you see this animation. *might* The process of reverse transcription is rather absurd."

"Integrase– Host cells don't come packed with the necessary biochemical machinery to move DNA out of the cytoplasm into the nucleus, to be inserted into the host DNA. So once again, retroviruses need to bring an enzyme capable of performing those activities. Integrase should be a perfect target for antiretrovirals… But we havent figured any out yet…"

Env. See http://scienceblogs.com/erv/2008/07/17/intro-to-ervs-envy-my-env/

LTRs. See this page. RNA polymerase's normal function is to convert nuclear DNA into messenger RNA that makes for proteins. It does not normally make RNA that 'codes" for promoters. Our bodies have no need for them. But retroviruses need their promoters to be converted back to RNA for when the replication cycle begins again. Long terminal repeats (LTRs) cause the RNA polymerase to produce them by a complicated "hack". The point is, that LTRs basic and original function is a part of the replication process of retroviruses. They cannot be part of any supposed original "design" of our genomes. That would not make any sense.

See Veritas: ERV FAQ: ERVs promote the transcription of host DNA. Doesn't this prove they are designed? and http://scienceblogs.com/erv/2009/07/16/intro-to-ervs-ltr-gator

Retroviruses exhibit the distinctive viral codon bias.

The Phoenix virus was resurrected from the multiple instances of an ERV which is to be found in each human cell. Each instance is a 'failed' retrovirus, but when a 'majority vote' for each base was taken, the resulting DNA produced, "viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny." See also The "Phoenix Virus": an explanation of an experiment.

A retrovirus has been caught in the act of becoming endogenized: See The koala retrovirus KoRV and The Koala's Tale.

Retroviruses leave a telltale trace of integration in the form of a repeated host sequence either side of the integrated provirus. This is also evident in ERVs. From Virology Blog: Retroviral Integration and the XMRV Provirus, "The image below shows some of the characteristic features of retroviral integration. A the top is the unintegrated linear DNA of avian sarcoma/leukosis virus produced by reverse transcription. Upon completion of integration, two base pairs (AA•TT) are lost from both termini, and a 6-bp target site in host DNA (pink) is duplicated on either side of the proviral DNA. This target site varies in length from 4 to 6 bp among different retroviruses. The proviral DNA (middle) ends with the conserved 5′-T G…C A-3′ sequence. The provirus serves as a template for the production of the viral RNA genome (bottom)."

 

[mark kennedy]

If you wish to argue for design, please start your own discussion. The subject of this one is ERVs, and their significance in the case for common descent. Even if life was designed by some undesigned designer, the evidence from ERVs still stands. The undesigned designer must have created ancestral forms that subsequently speciated.

I asked you to address the evidence that ERVs are of retroviral origin. You ignored the request. You ignored the evidence. You are not the only one to studiously ignore it. But here's another chance. What follows is a copy and paste of a page from my FAQ. Let's see if you or anyone else has what it takes to address this evidence. I very much doubt it, but here's your chance to put your money where your mouth is.

I did, you never addressed it in our formal debate and your debate tactics haven't improved in all the time since.

(Initial sequence of the chimpanzee genome and comparison with the human genome. Nature 2005)​

Seems like we did this before, you want everyone to believe that almost 8% of the human genome is the result of dangerous germline invasions.

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...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)
​

This indicates the Chimpanzee is being inundated by ERVs with over a million base pairs becoming permanently fixed right at the time of the split. ERV germline invasions are rare at best and to have so many, many with open reading frames is a formula for extinction. Which means you ignore the differences and overstate things in common. What you are attempting to do is evade in the inverse logic.

Much material in this page has been lifted from Abbie Smith.Hope you don't mind Abbie,

Really don't see the point, let's move on.

Every detail of every full ERV is replete with complex and subtle details attesting to its origin in retroviruses. ERVs have the same structure as retroviral integrations. This is some -10 kilobases of genes specific to the retroviral replication cycle. All retroviruses and complete ERVs include genes we call gag, pol and env. The function of these genes will be gone into in detail in the following notes. In addition, several other features common to retroviral integrations and ERVs only make sense in terms of the requirements of the retroviral replication cycle.

Well you almost characterized them and little else. It's odd that your saying they are all complete when the ones in the human genome are so riddled in mutations that they are no longer functional.

"The gag gene encodes for ‘Gag’ the giant protein, which gets chopped into several smaller proteins, Matrix, Capsid, and Nucleocapsid (and sometimes a few more tiny ones, depending on the retrovirus)."

Starting to see quotes without source material, not a good sign.

"Matrix is the structural protein just inside the envelope (the membrane the virus stole from its host cell). It has ‘outside’ functions (targeting the virus assembly to the right kind of cell membrane, keeping the outside protein env, in order) and ‘inside’ functions (targeting the reverse transcribed DNA to the new host cell nucleus). Jack of all trades protein, like lots of retroviral proteins. They run a tight ship."

"Capsid forms the viral ‘core’. Normally when you think of a ‘virus’, you think of this shape, an icosahedron. Retroviral ‘cores’ really look more like a cylinder-cone-thingie, like the bottom pic here. That particular pic is also worth a second look– More protein cuts to Capsid need to take place after a baby virus buds off from its host cell to make an immature virus mature. Blocking this maturation step is what the next family of anti-HIV-1 retrovirals do. *thumbs up*"

"Nucleocapsid is a structural protein that wraps up the retroviral genome to make sure its packaged properly into the Capsid."

Pol codes for all the enzymes a retrovirus needs:"

"Protease– Chomps big proteins into all the little functional proteins, like we saw with Gag getting chomped into Matrix/Capsid/Nucleocapsid. The name ‘protease’ can be a little confusing because all organisms have ‘proteases‘, but only the protease that the retrovirus carries with it is the ‘right‘ protease to cleave in all the ‘right’ spots to get all the ‘right’ proteins in the end. Instead of giving retroviral proteases a special name, they just named it ‘Protease’. heh. Protease inhibitors are a great target for anti-retrovirals."

"Reverse Transcriptase– Another target for anti-retrovirals. Though the process of reverse transcription can be found in you and I (coooool), retroviruses need to carry an enzyme with them to convert viral RNA into DNA on demand. This process not only requires converting an RNA genome into a DNA genome, but also:"

"RNase H– The RT enzyme has (at least) two active sites. One performs the process of reverse transcription. Another active site has RNase activity (chops up RNA, specifically, RNA Hybridized with DNA haha!). RNase H chews up the old RNA template after a single strand of DNA has been made, so the single strand of DNA can be made into double stranded DNA, and subsequently inserted into the host cells genome. This might make more sense if you see this animation. *might* The process of reverse transcription is rather absurd."

"Integrase– Host cells don't come packed with the necessary biochemical machinery to move DNA out of the cytoplasm into the nucleus, to be inserted into the host DNA. So once again, retroviruses need to bring an enzyme capable of performing those activities. Integrase should be a perfect target for antiretrovirals… But we havent figured any out yet…"

Env. See http://scienceblogs.com/erv/2008/07/17/intro-to-ervs-envy-my-env/

Does your blog link come with a bibliography?

LTRs. See this page. RNA polymerase's normal function is to convert nuclear DNA into messenger RNA that makes for proteins. It does not normally make RNA that 'codes" for promoters. Our bodies have no need for them. But retroviruses need their promoters to be converted back to RNA for when the replication cycle begins again. Long terminal repeats (LTRs) cause the RNA polymerase to produce them by a complicated "hack". The point is, that LTRs basic and original function is a part of the replication process of retroviruses. They cannot be part of any supposed original "design" of our genomes. That would not make any sense.

See Veritas: ERV FAQ: ERVs promote the transcription of host DNA. Doesn't this prove they are designed? and http://scienceblogs.com/erv/2009/07/16/intro-to-ervs-ltr-gator

Retroviruses exhibit the distinctive viral codon bias.

The Phoenix virus was resurrected from the multiple instances of an ERV which is to be found in each human cell. Each instance is a 'failed' retrovirus, but when a 'majority vote' for each base was taken, the resulting DNA produced, "viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny." See also The "Phoenix Virus": an explanation of an experiment.

A retrovirus has been caught in the act of becoming endogenized: See The koala retrovirus KoRV and The Koala's Tale.

Retroviruses leave a telltale trace of integration in the form of a repeated host sequence either side of the integrated provirus. This is also evident in ERVs. From Virology Blog: Retroviral Integration and the XMRV Provirus, "The image below shows some of the characteristic features of retroviral integration. A the top is the unintegrated linear DNA of avian sarcoma/leukosis virus produced by reverse transcription. Upon completion of integration, two base pairs (AA•TT) are lost from both termini, and a 6-bp target site in host DNA (pink) is duplicated on either side of the proviral DNA. This target site varies in length from 4 to 6 bp among different retroviruses. The proviral DNA (middle) ends with the conserved 5′-T G…C A-3′ sequence. The provirus serves as a template for the production of the viral RNA genome (bottom)."

What they found in the Initial Sequence of the Human Genome. Their estimates apply only to the human genome, comparisons wouldn't come for several years:

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. This comparison put's the amount of DNA from retroviruses at 5.44%. In the Chimpanzee genome it's almost 8%, 'With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome.' (Nature 2005).

Against this background, it was surprising to find 234 ERV class 1 > then a million base pairs in the Chimpanzee genome but absent in human DNA:

Notice the ERV class 1 and this discussion from the Chimpanzee Genome paper:

Against this background, it was surprising to find that the chimpanzee genome has two active retroviral elements (PtERV1 and PtERV2) that are unlike any older elements in either genome; these must have been introduced by infection of the chimpanzee germ line. The smaller family (PtERV2) has only a few dozen copies, which nonetheless represent multiple (~5–8) invasions, because the sequence differences among reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human.

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)

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've done this, long technical discussions of ERVs doesn't help your case, it buries it. When your actaully interested in doing the reading and coming to an informed conclusion I'll be waiting, but not holding my breath.

Have a nice day
Mark

 

[Barry Desborough]

Replies in red.

I did, you never addressed it in our formal debate and your debate tactics haven't improved in all the time since.

Snide rhetorical jabs do not help your "case".

(Initial sequence of the chimpanzee genome and comparison with the human genome. Nature 2005)​

Seems like we did this before, you want everyone to believe that almost 8% of the human genome is the result of dangerous germline invasions.

It's what the researchers conclude from the full genome surveys.

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...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)
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This indicates the Chimpanzee is being inundated by ERVs with over a million base pairs becoming permanently fixed right at the time of the split. ERV germline invasions are rare at best (evidence?) and to have so many, many with open reading frames is a formula for extinction. Which means you ignore the differences and overstate things in common. What you are attempting to do is evade in the inverse logic.





Really don't see the point, let's move on. If you don't see the point, don't move on. Ask for clarification of whatever you don't understand.



Well you almost characterized them and little else. It's odd that your saying they are all complete (this is a blatant lie) when the ones in the human genome are so riddled in mutations that they are no longer functional. I told you that ERVs are largely nonfunctional due to mutations. Try to keep up.



Starting to see quotes without source material, not a good sign. (A link is provided.)



Does your blog link come with a bibliography? All relevant sources are provided. Sometimes they are a couple of links away. The blog is only an educational piece. You need to study it carefully if you doubt its accuracy.


What they found in the Initial Sequence of the Human Genome. Their estimates apply only to the human genome, comparisons wouldn't come for several years:

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. This comparison put's the amount of DNA from retroviruses at 5.44%. In the Chimpanzee genome it's almost 8%, 'With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome.' (Nature 2005).

Against this background, it was surprising to find 234 ERV class 1 > then a million base pairs in the Chimpanzee genome but absent in human DNA:

Notice the ERV class 1 and this discussion from the Chimpanzee Genome paper:

Against this background, it was surprising to find that the chimpanzee genome has two active retroviral elements (PtERV1 and PtERV2) that are unlike any older elements in either genome; these must have been introduced by infection of the chimpanzee germ line. The smaller family (PtERV2) has only a few dozen copies, which nonetheless represent multiple (~5–8) invasions, because the sequence differences among reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human.

Figure 4.4.1. Human endogenous retrovirus K (HERV-K) insertions in identical chromosomal locations in various primates
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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)

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. (Evidence?) The very statistical argument my opponent is trying to make is the reason the first assumption is patently false.

We've done this, long technical discussions of ERVs doesn't help your case, it buries it. When your actaully interested in doing the reading and coming to an informed conclusion I'll be waiting, but not holding my breath.

Have a nice day
Mark

So you point out the lineage-specific insertions (83 in humans and 273 in chimps) and ignore the 202,917 commonly located insertions! Classic case of confirmation bias! You also ignore several items of evidence I asked you not to. Here they are yet again.Veritas: ERV FAQ: Why do virologists and geneticists think that ERVs come from retroviruses? Isn't that just supposition on their part?

Remember, if there is anything you don't understand, ask for further explanation. But once you do, address this evidence.

One more note: this is not a simple argument from homology. So many commonly located ERVs require explanation. You have failed to offer any alternative to the blindingly obvious one.

 

[dad]

It's all supposition, trust me.



Hang on, you almost have the right idea here. In the time of Noah the mutations had not had time to accumulate so it meant bigger gene pools. Now once things have speciated there are bottlenecks, adaptive evolution isn't going to happen on that scale. Now as far as the ERVs, infection in the germline is pretty rare and certainly nothing heritable has been documented. Once again, that kind of transfer still happens but on the scale they are talking about, forget it.



There is every indication that this isn't something subject to change over time.

Specifically .. what indications? Over how much tested Time?

I think nature and laws changed, so if you had indication it didn't, that would be important.

God provided for the passing of heritable traits, known in science as the laws of inheritance. It's as simple as this, they take an occasional mutation with a beneficial effect or a mutation in roughly the same place in two genomes and that's supposed to be proof. The far weightier matter regarding the three fold expansion of the human brain from that of apes they ignore.

But the question is did He provide Adam and Noah the same way of passing traits as He did modern man, and how would we Know?

Probably weren't, the living systems of the time probably had pristine genomes that accumulated mutations over time.

But we're the genomes even like ours now? Was it different DNA or just clean DNA?

Look at it realistically, what do you expect from people who have never really known anything but the natural order. If you remember right, the gospel was made clear to you not by your own powers of perception but because God made himself known to you by some means. That's how I remember my conversion, so I understand people who do not deviate from naturalistic reasoning, it's all they have ever known.

Grace and peace,
Mark

Remember also Jesus walked and talked with Adam and Noah. I suspect we cannot hold them to our current nature rules.

 

[Barry Desborough]

Specifically .. what indications? Over how much tested Time?

I think nature and laws changed, so if you had indication it didn't, that would be important.


But the question is did He provide Adam and Noah the same way of passing traits as He did modern man, and how would we Know?



But we're the genomes even like ours now? Was it different DNA or just clean DNA?

Remember also Jesus walked and talked with Adam and Noah. I suspect we cannot hold them to our current nature rules.

I have a tree in my garden. I think that it wasn't there yesterday. Can you prove that I'm mistaken?

Dad, there s a thread where you can spout the same old nonsense you have been pushing for years. https://www.christianforums.com/threads/proof-of-same-state-past.8008486/