Viruses that prove common descent

[Barry Desborough]

Thanks...I thought you had more of a purpose in asking. The presupposition I was mostly concerned with was one which many scientists (and others) make regarding the Common Ancestor, allegedly confirmed by these genetic curiosities (like the title implies but no one can show).

Whether or not you agree with what I assess for how it needs to be confirmed, do you at least see the need for this before it is declared emphatically to be so? Don't we at least need to see that they were inserted or deleted to be able to SAY they were inserted or deleted? Otherwise why should we assume they were?

Do you have an alternative explanation? One that accounts for all the data? Here is a reminder of what an alternative explanation has to answer, either in terms of design, or just in terms of function.

a) What is reverse transcriptase designed to do?
b) What is integrase designed to do?
c) Why were ERVs designed with a viral codon bias?
d) What is the design purpose of re-transcribable promoters?
e) What were the HERVs that generated the consensus sequence that generated Phoenix designed for?
f) What is the design purpose of both exogenous and endogenous KoRV?
g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?
h) What is the design purpose of giving some people HERVs and not others?
i) What is the design purpose of creating different syncytins in different placental lineages?

 

[pshun2404]

No it does not have to answer those questions!?! That response is an attempt to divert and avoid having to address the very reasonable logical question proposed to you.

I am still waiting to see an example where what is, once was not (hence inserted) in the human or chimp genome, or what is not, once was (hence deleted)...or a creature this allegedly happened in that we are descended from, so we can compare.

You have repeatedly failed to be able to produce "confirmation" that the alleged insertions were ever inserted or the deletions were ever deleted. Imagining this, OR interpreting through the rose colored glasses of the hypothesis (already accepted), OR claiming inference FROM what one MAY induce, FAILS to demonstrate the claim of CONFIRMATION of these things, as well as common descent.

It is equally possible that the human genome is and always has been the human genome. The chimp genome has and always was the chimp genome. And the common ancestor theory (oops! Hypothesis!) has NEVER yet been demonstrated (just assumed). Deduction has been applied to the induction and as a result, your claim has been weighed in the balance, and the claim has been found wanting.

So it MIGHT BE, or COULD BE, but might be and could be do not equal IS...

 

[Barry Desborough]

No it does not have to answer those questions! That is an attempt to divert and avoid having to address the very reasonable logical question proposed to you.

I am still waiting to see an example where what is, once was not (hence inserted) in the human or chimp genome, or what is not, once was (hence deleted)...or a creature this allegedly happened in that we are descended from, so we can compare.

You have repeatedly failed to be able to produce "confirmation" that the alleged insertions were ever inserted or the deletions were ever deleted. Imagining this, OR interpreting through the rose colored glasses of the hypothesis (already accepted), or claiming inference FROM what you induce FAILS to demonstrate the claim of CONFIRMATION of these things and of common descent.

The human genome is and always has been the human genome. The chimp genome has and always was the chimp genome. And the common ancestor theory (oops! Hypothesis!) has NEVER yet been demonstrated (just assumed).

So. No alternative explanation. I thought you said that you had one. I'm just pointing out what any alternative explanation would have to - er - explain.

And I did provide confirmation. You just failed to recognise it. I repeat: the hypothesis that both genomes are related and have been subject to insertions and deletions is in the fact that when we hypothesise that these things are true, we get an extraordinary alignment of ERVs, in terms of corresponding neighbouring genetic material, sequence, contents and age estimates. Something that, as you have helped to demonstrate, cannot be adequately explained any other way.

 

[pshun2404]

So. No alternative explanation. You claimed that you had one. I'm just pointing out what any alternative explanation would have to - er - explain.

And I did provide confirmation. You just failed to recognise it. I repeat: the hypothesis that both genomes are related and have been subject to insertions and deletions is in the fact that when we hypothesise that these things are true, we get an extraordinary alignment of ERVs, in terms of corresponding neighbouring genetic material, sequence, contents and age estimates. Something that, as you have helped to demonstrate, cannot be adequately explained any other way.

You failed Barry! It is okay to admit it. It does not even mean you are incorrect. No one here will fault you for it. One can say I am no longer persuaded by what I had previously believed and fought to defend but one cannot say I do not understand the information you have insisted proves your claim, it simply does not. And I did offer an alternative explanation, they are what they always were and this is what makes US humans and chimps chimps. Yes there are similarities and also many differences because we are different creatures, that's all.

To prove an insertion one must demonstrate that it was indeed INSERTED and that can only happen when one shows it previously was not there and now is (you have failed to do this and the onus of proof was on you). Now we have had some recent examples where it has happened (like in HIV) so we know it CAN but as far as that "confirming" Common Descent" it simply does not and likewise it does not demonstrate this process (insertion or deletion) occurred in some creature 3, 5, 8, or 14 mya that we are ALLEGED to be descended from.

Same with "deletion" which implies something was there that is now missing. SHOW ME it was there in either genome or in this assumed ancestor...that's all...simple...

You cannot, correct? Yes or no will suffice...

 

[Barry Desborough]

You failed Barry! It is okay to admit it. It does not even mean you are incorrect. No one here will fault you for it. One can say I am no longer persuaded by what I had previously believed and fought to defend but one cannot say I do not understand the information you have insisted proves your claim, it simply does not. And I did offer an alternative explanation, they are what they always were and this is what makes US humans and chimps chimps. Yes there are similarities and also many differences because we are different creatures, that's all.

To prove an insertion one must demonstrate that it was indeed INSERTED and that can only happen when one shows it previously was not there and now is (you have failed to do this and the onus of proof was on you). Now we have had some recent examples where it has happened (like in HIV) so we know it CAN but as far as that "confirming" Common Descent" it simply does not and likewise it does not demonstrate this process (insertion or deletion) occurred in some creature 3, 5, 8, or 14 mya that we are ALLEGED to be descended from.

Same with "deletion" which implies something was there that is now missing. SHOW ME it was there in either genome or in this assumed ancestor...that's all...simple...

You cannot, correct? Yes or no will suffice...

I see you are reduced to arm waving, metaphorically stamping your foot, caps and italics. Go back and read my previous comment more carefully.

 

[pshun2404]

I see you are reduced to arm waving, metaphorically stamping your foot, caps and italics. Go back and read my previous comment more carefully.

I only italics or cap for emphasis...and I read all your comments and referenced blogs...very little there I did not already know.

It is so sad that an intelligent man like yourself cannot just admit they cannot provide what is logically required. I have found myself in such a place on occasion and finally just say...I stand corrected or yes I must admit I have no proof...its called intellectual integrity or being truly objective if that is less offensive. You appear to lack this humility.

So I am going to let you have the last say in our exchange, but all who viewed our exchange KNOW you failed to prove your case...I certainly welcome anyone else to show these things rationality requires...in fact please do...

 

[Barry Desborough]

I only italics or cap for emphasis...and I read all your comments and referenced blogs...very little there I did not already know.

It is so sad that an intelligent man like yourself cannot just admit they cannot provide what is logically required. I have found myself in such a place on occasion and finally just say...I stand corrected or yes I must admit I have no proof...its called intellectual integrity or being truly objective if that is less offensive. You appear to lack this humility.

So I am going to let you have the last say in our exchange, but all who viewed our exchange KNOW you failed to prove your case...I certainly welcome anyone else to show these things rationality requires...in fact please do...

Pfft.

 

[xianghua]

Virtually all ERVs non-functional. (Some components of some ERVs are beneficial. Some are implicated in late onset diseases - invisible to selection). But the vast majority of this genetic material is adaptively neutral.

true. but when a retrovirus insert into the genome its add to the genome several genes. so if only the promoter are the functioanl part (and we found that more then 50,000 of them have a conection to an erv)the rest of the viral genes also will be fixed in the genome. another possibility is that they was functional in the past and becomed non-functional by mutations.

But if you want to provide evidence that the entire genome is functional and that only a limited number of integration sites will fail to disrupt it, give it your best shot. Oh, and don't forget to explain why the ERVs themselves correspond, between species, in their content - gene variants, size, LTR-LTR discontinuity etc.

i already showed that there is a great correlation between complexity and the amount of junk in the genome. so we have a good evidence that most of the genome isnt junk at all.

 

[xianghua]

Which would not and could not explain the thousands of shared ERV's between humans and chimps.

they explain it by a design. they was in the genome since the beginning.

The actual ERV's in our collective genomes, are the result of ancient insertions in common ancestors.

again: just a belief. you cant change this fact.

What you are refering to DOES NOT EXPLAIN, in ANY way, that humans and chimps share thousands of ERV's in the exact same locations in the DNA.

again: if they are the product of design,we can explain it by a common similarity becuase of a common designer. since you cant prove they arent the product of design, you can only believe they arent. you also forgot that even if they are indeed a product of viral insertion- we can explain it by the claim that most of the genome is functional.

 

[Barry Desborough]

true. but when a retrovirus insert into the genome its add to the genome several genes. so if only the promoter are the functioanl part (and we found that more then 50,000 of them have a conection to an erv)the rest of the viral genes also will be fixed in the genome. another possibility is that they was functional in the past and becomed non-functional by mutations.




i already showed that there is a great correlation between complexity and the amount of junk in the genome. so we have a good evidence that most of the genome isnt junk at all.

Most ERVs are non-functional as proviruses. They cannot produce viable virions. If they weren't non-functional, we'd all go extinct in short order. It is possible to reconstruct some of them though. Guess what we get? Replication-competent proviruses! Veritas: ERV FAQ: What's all this about the Phoenix Virus? Sounds like a Michael Crichton science fiction story!

If complex genomes contain junk, then they contain junk.

I did ask you not to forget to explain ERV correspondences between different species, but you forgot.

 

[Barry Desborough]

they explain it by a design. they was in the genome since the beginning.




again: just a belief. you cant change this fact.




again: if they are the product of design,we can explain it by a common similarity becuase of a common designer. since you cant prove they arent the product of design, you can only believe they arent. you also forgot that even if they are indeed a product of viral insertion- we can explain it by the claim that most of the genome is functional.

Here's what you need to have answers for if you think ERVs were original, designed parts of our genomes.

a) What is reverse transcriptase designed to do?
b) What is integrase designed to do?
c) Why were ERVs designed with a viral codon bias?
d) What is the design purpose of re-transcribable promoters?
e) What were the HERVs that generated the consensus sequence that generated Phoenix designed for?
f) What is the design purpose of both exogenous and endogenous KoRV?
g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?
h) What is the design purpose of giving some people HERVs and not others?
i) What is the design purpose of creating different syncytins in different placental lineages?

 

[xianghua]

Most ERVs are non-functional as proviruses. They cannot produce viable virions. If they weren't non-functional, we'd all go extinct in short order. It is possible to reconstruct some of them though. Guess what we get? Replication-competent proviruses! Veritas: ERV FAQ: What's all this about the Phoenix Virus? Sounds like a Michael Crichton science fiction story!

http://barryhisblog.blogspot.com/p/whats-all-this-about-phoenix-virus.html

are you kidding barry? i already explained that the ervs are like a retrotransposon. so they need all those genes to insert themself into the genome.

If complex genomes contain junk, then they contain junk.

so why the correlation between complexity and this suppose "junk"? do you have any explanation for that? the design model explain it easily.

I did ask you not to forget to explain ERV correspondences between different species, but you forgot.

and i explained that if those ervs are the product of design they can be explain by a common similarity. and if they arent- its can explain by the claim that most of the genome is functional.

now, the real thing here is the question of design vs natural process. do you think that a motor like the flagellum is evidence for design or not? if we can prove that nature was designed- then we can falsified the erv argument too.

 

[Barry Desborough]

are you kidding barry? i already explained that the ervs are like a retrotransposon. so they need all those genes to insert themself into the genome.




so why the correlation between complexity and this suppose "junk"? do you have any explanation for that? the design model explain it easily.





and i explained that if those ervs are the product of design they can be explain by a common similarity. and if they arent- its can explain by the claim that most of the genome is functional.

now, the real thing here is the question of design vs natural process. do you think that a motor like the flagellum is evidence for design or not? if we can prove that nature was designed- then we can falsified the erv argument too.

You are confusing replication-competent proviruses and ERVs.

Any correlation is irrelevant. As long as a retrovirus can endogenise in an area where it does not disrupt the gamete, it will become heritable.

Endogenisation can explain all these things. How do you explain them? Full details, please.

a) What is reverse transcriptase designed to do?
b) What is integrase designed to do?
c) Why were ERVs designed with a viral codon bias?
d) What is the design purpose of re-transcribable promoters?
e) What were the HERVs that generated the consensus sequence that generated Phoenix designed for?
f) What is the design purpose of both exogenous and endogenous KoRV?
g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?
h) What is the design purpose of giving some people HERVs and not others?
i) What is the design purpose of creating different syncytins in different placental lineages?

 

[xianghua]

You are confusing replication-competent proviruses and ERVs.

how? those genes help the virus get into the genome. so its a kind of a retrotransposon. if its a kind of a retrotrannsposon, then it can explain by a method that add variations into the population.

Any correlation is irrelevant. As long as a retrovirus can endogenise in an area where it does not disrupt the gamete, it will become heritable

its very relevant. if there is only few places in the genome that we can add a new erv- then we can expect to find a lots of ervs in a shared places without a common descent.

 

[mark kennedy]

Hi guys,

Here's my FAQ on endogenous retroviruses (ERVs). They provide some of the best evidence for common descent. They show that you, me, and Charlie the chimp are cousins.

Now I'm a lifelong atheist (67 years), and I don't care whether you believe in God or not. What I do care about is the fact that evolution-denial is an impediment to our understanding of human nature. See the second link regarding this.

Questions/comments welcome.

Veritas: Endogenous Retroviruses - Frequently Asked Questions

Veritas: ERV FAQ: Aren't you just a plagiarist? Why don't you attribute your sources? And who are you anyway?

Hi again Barry, your still kicking that dead horse:

(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)
​

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.

That's right, they found in the Initial Sequence of the Human Genome. Their estimates :

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:

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.
​

Then EVRs were discovered/studied and became the best. Sort of like Tom Brady winning his 5th super bowl.

This is the worst homology argument I've ever seen. 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)

This isn't the first time I've refuted this argument back into the stone age, guess it won't be the last:

ERVs put chimp/human common ancestry beyond any reasonable doubt.

Have a nice day
Mark

 

[mark kennedy]

You are confusing replication-competent proviruses and ERVs.

Any correlation is irrelevant. As long as a retrovirus can endogenise in an area where it does not disrupt the gamete, it will become heritable.

That's a big 'if', the deleterious effects would be epic. Your assuming no ill effects, that's not how retroviral invasions work. The ones we know the most about are not germline invasions, those are actually very rare. HIV is a retrovirus and one that is very dangerous for T Cells.

Endogenisation can explain all these things. How do you explain them? Full details, please.

a) What is reverse transcriptase designed to do?
b) What is integrase designed to do?
c) Why were ERVs designed with a viral codon bias?
d) What is the design purpose of re-transcribable promoters?
e) What were the HERVs that generated the consensus sequence that generated Phoenix designed for?
f) What is the design purpose of both exogenous and endogenous KoRV?
g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?
h) What is the design purpose of giving some people HERVs and not others?
i) What is the design purpose of creating different syncytins in different placental lineages?

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. One HERV 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.

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?

So what do ERVs actually do:

We have ERVs to thank for our ability to make placentas. Go figure :-/

We suggest that species-specific ERVs contribute to the rapid divergence of the placental gene regulatory network. (ERVs and Placentas, Science Blogs)
​

Have a nice day
Mark

 

[Barry Desborough]

Oh dear.

That's a big 'if', the deleterious effects would be epic. Your assuming no ill effects, that's not how retroviral invasions work. The ones we know the most about are not germline invasions, those are actually very rare. HIV is a retrovirus and one that is very dangerous for T Cells.



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. One HERV 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.

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?

So what do ERVs actually do:

We have ERVs to thank for our ability to make placentas. Go figure :-/

We suggest that species-specific ERVs contribute to the rapid divergence of the placental gene regulatory network. (ERVs and Placentas, Science Blogs)
​

Have a nice day
Mark

Oh dear. Why didn't you bother to read Veritas: ERV FAQ: ERVs do stuff. Doesn't that prove that they didn't originate from retroviruses, but were designed? ?

 

[mark kennedy]

Oh dear.

Oh dear. Why didn't you bother to read Veritas: ERV FAQ: ERVs do stuff. Doesn't that prove that they didn't originate from retroviruses, but were designed? ?

Some things you never bothered reading:

(Retroelements and the human genome: New perspectives on an old relation)
(Endogenous retrovirus)
(Initial sequence of the chimpanzee genome)
​

Do note these are real comparative genomics, not some cut and paste link to FAQs.

 

[Barry Desborough]

Some things you never bothered reading:

(Retroelements and the human genome: New perspectives on an old relation)
(Endogenous retrovirus)
(Initial sequence of the chimpanzee genome)
​

Do note these are real comparative genomics, not some cut and paste link to FAQs.

Do you have a point to make? What is it?

 

[Barry Desborough]

how? those genes help the virus get into the genome. so its a kind of a retrotransposon. if its a kind of a retrotrannsposon, then it can explain by a method that add variations into the population.




its very relevant. if there is only few places in the genome that we can add a new erv- then we can expect to find a lots of ervs in a shared places without a common descent.

Why the same ERVs with the same LTR-LTR discontinuities and other mutations?