Viruses that prove common descent

[Barry Desborough]

it can be for several reasons. maybe it for making more variations(like transposons)in the population. myabe its just a genetic mystake that this gene was taken from the host by the virus. maybe this gene even for fighting against other viruses like in this case:

http://www.sciencemag.org/news/2016/03/viral-fossils-our-dna-may-help-us-fight-infection




its coming back to you: if its so dangerous how it becomed fixed so many times? (about 100,000). if a functional ervs is so dangerous how any insertion can become fixed and be a part of the genome?



first: can you give a reference? second: are you aware about the fact that even a
synonymous codon can result in a different function in the cell?




true. this is my other point: even if all those ervs are indeed a product of viral insertions, they cant prove a commondescent. the main reason is because the whole genome may be functional. and if it functional there are very few places (if any) in the genome that a virus can insert itself.

Busy now, but on the last point, you can't have your cake and eat it. If ERVs are designed to retrotranspose, and the whole genome is functional, then there are no places in which they can retrotranspose. Viral integration and retrotransposition involve identical processes at the DNA level, BTW. And viruses can and do integrate in a huge variety of loci. See Veritas: ERV FAQ: Don't retroviruses target particular locations in the DNA? Doesn't this explain corresponding ERVs?

 

[Barry Desborough]

1)it can be for several reasons. maybe it for making more variations(like transposons)in the population. myabe its just a genetic mystake that this gene was taken from the host by the virus. maybe this gene even for fighting against other viruses like in this case:

http://www.sciencemag.org/news/2016/03/viral-fossils-our-dna-may-help-us-fight-infection




2)its coming back to you: if its so dangerous how it becomed fixed so many times? (about 100,000). if a functional ervs is so dangerous how any insertion can become fixed and be a part of the genome?



3)first: can you give a reference? second: are you aware about the fact that even a
synonymous codon can result in a different function in the cell?




4)true. this is my other point: even if all those ervs are indeed a product of viral insertions, they cant prove a commondescent. the main reason is because the whole genome may be functional. and if it functional there are very few places (if any) in the genome that a virus can insert itself.

I've numbered your paragraphs so I can answer each point.

1) "Maybe" doesn't cut it in science. You need evidence. And your speculations make no sense in the context of a designer who can design whole genomes. Why use such messy hit-and-miss methods of integrating virtually at random? Why not just directly design in the features you want, variation and disease resistance included?

2)We are talking about the lucky descendants of lucky ancestors. All the others are dead.

3)
Causes and Implications of Codon Usage Bias in RNA Viruses
Yes, I am aware. So what?

4) Answered above.

 

[xianghua]

Busy now, but on the last point, you can't have your cake and eat it. If ERVs are designed to retrotranspose, and the whole genome is functional, then there are no places in which they can retrotranspose.

true. this is my argument in a case when those are a real viral insertions. in this case i will argue that those viruses have a very small place to insert the genome and also become fixed. this is also the problem with your papers: they check only the viral preference, but if we will combine it with a natural selection - then a viral fixation will be in a very specific luci.

1) "Maybe" doesn't cut it in science. You need evidence. And your speculations make no sense in the context of a designer who can design whole genomes. Why use such messy hit-and-miss methods of integrating virtually at random?

see above: its not random at all.

2)We are talking about the lucky survivors of lucky ancestors. All the others are dead.

how actually? if a viral insertion is so dangerous how its possible to insert the genome without making any harm?

Causes and Implications of Codon Usage Bias in RNA Viruses

are you saying that ervs have a different codon bias in the genome compare to the rest of the genome?


and of course, one big problem remain: how retrovirus survive in the first place without an host? how some hosts survive without those ervs?

 

[dad]

Ha ha ha. You've had the same old schtick for years and years, dad. Where has it gotten you? Have you ever convinced anyone with your totally evidence-free wild speculations?

Unless you can address your problem of using an unsubstansiated set of laws in the past to justify your animalistic claims trying to associate animal leftover viri with common ancestor claims...gongaroni.

 

[Barry Desborough]

Unless you can address your problem of using an unsubstansiated set of laws in the past to justify your animalistic claims trying to associate animal leftover viri with common ancestor claims...gongaroni.

"Laws in the past" are not unsubstantiated, but that is a topic too wide for this thread. Please stick yo ERVs here. I f you do want to discuss the wider topic, post your own OP and notify me when you have done so.

 

[Barry Desborough]

I reply to

Your last post.

You keep ignoring the substantial and varied evidence that ERVs are of retroviral origin. See Veritas: ERV FAQ: Why do virologists and geneticists think that ERVs come from retroviruses? Isn't that just supposition on their part?

I have shown you, multiple times, that retroviruses are incapable of integrating into specific loci. See Veritas: ERV FAQ: Don't retroviruses target particular locations in the DNA? Doesn't this explain corresponding ERVs?

However, the idea that there are specific "slots" that retroviruses, and therefore endogenized proviruses and retrotranspositions of such use, doesn't help explain why, say, chimps and humans share the same ERVs in the same locations, (integrase doesn't 'know' what its 'payload' is), nor why they exhibit evidence that they are of the same age, comparing an ERV in one species with a corresponding ERV in another.

Viral insertions may be dangerous. This is why human gene therapists hesitate to use them in all but the direst of cases. It's difficult to understand why an all-powerful designer would use them. Also, bear in mind that reverse transcription is error prone, and there is no error correction. The ERVs that have survived in our genomes are mostly there because they are failures as retroviruses, due to disabling mutations. (Frequently the same mutations in different species.)

Re. different codon biases, yes.

How do retroviruses survive without a host, and vice-versa? Co-evolution resulted in them becoming interdependent. It's a very common phenomenon in biology.

Now, xianghua, I think you have thrashed around enough. Ingenious as your speculations are, they have become wilder and wilder, and have become more and more at odds with the actual evidence, without being supported by any evidence of your own. Time for you to reflect. If you wish, develop your own hypothesis, describe it, and describe how it explains the evidence. All of it. Then post a new OP so we can discuss it more fully. Good luck.

 

[xianghua]

I reply to

You keep ignoring the substantial and varied evidence that ERVs are of retroviral origin.

again: what is your best evidence from that list? so far we have discussed about 3 of them.

I have shown you, multiple times, that retroviruses are incapable of integrating into specific loci.

not according to this paper:

http://www.sciencedirect.com/science/article/pii/S0014579398004785

"practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified `hot spots' containing integration sites used up to 280 times more frequently than predicted mathematically 41 ; 43. A recent study of the de novo retroviral integration demonstrated also preference for scaffold- or matrix-attachment regions (S/MARs) flanked by DNA with high bending potential"

far from random.

nor why they exhibit evidence that they are of the same age, comparing an ERV in one species with a corresponding ERV in another.

the same age? even according to evolution they cant be in the same age. because the spliting time between species is different (so even comparing a chimp erv with human one cant get the same result).

The ERVs that have survived in our genomes are mostly there because they are failures as retroviruses, due to disabling mutations.

how its possible? its need not only the insertion event (very rare)but also mutations on the same viral genes in the same time in a 3 bilion bp genome. so you can only claim its was useful or neutral.

Re. different codon biases, yes.

how its possible if we are talking about the same genome? and even if its was true it may be explain by a functional meaning.

How do retroviruses survive without a host, and vice-versa? Co-evolution resulted in them becoming interdependent. It's a very common phenomenon in biology.

its only a theory. you dont have any evidence that its possible. so far all experiments support that a virus cant survive without a host (and vice versa in some cases). so why we should believe against all the scientific experiments so far?

. Time for you to reflect. If you wish, develop your own hypothesis, describe it, and describe how it explains the evidence. All of it. Then post a new OP so we can discuss it more fully.

we can continue here

 

[Barry Desborough]

again: what is your best evidence from that list? so far we have discussed about 3 of them.





not according to this paper:

http://www.sciencedirect.com/science/article/pii/S0014579398004785

"practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified `hot spots' containing integration sites used up to 280 times more frequently than predicted mathematically 41 ; 43. A recent study of the de novo retroviral integration demonstrated also preference for scaffold- or matrix-attachment regions (S/MARs) flanked by DNA with high bending potential"

far from random.




the same age? even according to evolution they cant be in the same age. because the spliting time between species is different (so even comparing a chimp erv with human one cant get the same result).




how its possible? its need not only the insertion event (very rare)but also mutations on the same viral genes in the same time in a 3 bilion bp genome. so you can only claim its was useful or neutral.




how its possible if we are talking about the same genome? and even if its was true it may be explain by a functional meaning.





its only a theory. you dont have any evidence that its possible. so far all experiments support that a virus cant survive without a host (and vice versa in some cases). so why we should believe against all the scientific experiments so far?




we can continue here

Repeating questions already answered.

Demonstrating an inability to read the FAQ and understand basic points.

You've used up enough of my time.

If you cannot make a coherent alternative case of your own, we're done.

 

[dad]

"Laws in the past" are not unsubstantiated,

Thanks for admitting that. So remember never ever ever to use the present laws for the past.

Please stick yo ERVs here.

You stick to the present way viri are transferred. Remember to clearly state that it has NOTHING to do with ancient evolution, common ancestors, or origins. Whenever a claim is made that tries to connect these things, it must be exposed as a fraud.

 

[Barry Desborough]

Thanks for admitting that. So remember never ever ever to use the present laws for the past.
You stick to the present way viri are transferred. Remember to clearly state that it has NOTHING to do with ancient evolution, common ancestors, or origins. Whenever a claim is made that tries to connect these things, it must be exposed as a fraud.

And one who cannot even understand simple English. I think we're all done here.

 

[dad]

And one who cannot even understand simple English. I think we're all done here.

Understand that ervs have no meaning towards evolution of man. Understand you may not enforce present nature in the far past...evermore. Period. Really.

 

[Barry Desborough]

Understand that ervs have no meaning towards evolution of man. Understand you may not enforce present nature in the far past...evermore. Period. Really.

Failure to take up my challenge to make your case noted.

 

[dad]

Failure to take up my challenge to make your case noted.

I don't care what you say at all actually, in regards to your religion and promotion of evolution, and attempts to claim a monkey like ancestor or whatever sort of strange creature is in your head when you imagine a common ancestor.

 

[Barry Desborough]

I don't care what you say at all actually, in regards to your religion and promotion of evolution, and attempts to claim a monkey like ancestor or whatever sort of strange creature is in your head when you imagine a common ancestor.

Yes, dad. We know you are impervious to facts and reason. This is not a new revelation.

 

[dad]

Yes, dad. We know you are impervious to facts and reason. This is not a new revelation.

Blind faith doesn't cut it here, sorry. Your erv connection to evolution is roasted.

 

[pshun2404]

Brouoillette, in Science, “Viral ‘fossils’ in our DNA may help us fight infection”, March 13, 2016, says “ERVs—perhaps inherited millions of years ago—may affect genes important to placenta function and thus may improve our ability to carry a pregnancy. What’s more, there is evidence that they play a role in the early human embryo, where they may help fight off infectious viruses.”

Did you know that we have discovered an essential role some of these alleged ERVs play in moving the organism from the zygotic stage to the embryonic stage as both primary promoters, and in many cases as transcription repressors? Do you really think a viral infection produced this function so vital to the rest of our development? Time will tell, but a lot more research has to be done before we can conclude much about them. The good news is there are many approaching this from many angles.

But before I post on this subject, and before the onslaught of accusation and misrepresentation, I want to say right here and now that I believe in ERVS, AND that some ARE (without doubt) leftovers from earlier stages of humanity when they were inserted. But I am not convinced all sequences labelled ERVs actually are, and I also believe some are essential parts of the human genome that have always been present and thus are not ERVs at all. For these I would require examples of humans that sis not have them in the remote past and now do otherwise it is impossible to say they are insertions (and just because Chimps lack some that we have does not mean in them they are deletions).

But Barry...I am going to go back and read any and all links you posted before I enter the conversation. Some look like items I have already read but most are not so I am actually excited to dig in. Thanks

 

[pshun2404]

Wow...just two links completed and I can already see you are quite a legend in your own mind. These Veritas links are all from your own blog with very few references to actual scientific studies and you do not quote others or give appropriate reference data (periodical or book name, author, publisher, etc,).

I will look a little deeper, but I already see a lot of consensus based conjecture and opinion. This should make anyone taking you seriously to go...Hmmm??? But since I gave my word, I will explore as many as I can handle in my schedule.

 

[Barry Desborough]

Brouoillette, in Science, “Viral ‘fossils’ in our DNA may help us fight infection”, March 13, 2016, says “ERVs—perhaps inherited millions of years ago—may affect genes important to placenta function and thus may improve our ability to carry a pregnancy. What’s more, there is evidence that they play a role in the early human embryo, where they may help fight off infectious viruses.”

Did you know that we have discovered an essential role some of these alleged ERVs play in moving the organism from the zygotic stage to the embryonic stage as both primary promoters, and in many cases as transcription repressors? Do you really think a viral infection produced this function so vital to the rest of our development? Time will tell, but a lot more research has to be done before we can conclude much about them. The good news is there are many approaching this from many angles.

But before I post on this subject, and before the onslaught of accusation and misrepresentation, I want to say right here and now that I believe in ERVS, AND that some ARE (without doubt) leftovers from earlier stages of humanity when they were inserted. But I am not convinced all sequences labelled ERVs actually are, and I also believe some are essential parts of the human genome that have always been present and thus are not ERVs at all. For these I would require examples of humans that sis not have them in the remote past and now do otherwise it is impossible to say they are insertions (and just because Chimps lack some that we have does not mean in them they are deletions).

But Barry...I am going to go back and read any and all links you posted before I enter the conversation. Some look like items I have already read but most are not so I am actually excited to dig in. Thanks

Yes, I know. See Veritas: ERV FAQ: ERVs are essential in reproduction (syncytin and the formation of the placenta). How can this be? and Veritas: ERV FAQ: ERVs promote the transcription of host DNA. Doesn't this prove they are designed?

It's possible that the 200,000 or so ERVs and elements include some that have been misidentified as being of viral origin, but it's equally possible that other viral elements have not been identified as such due to mutational degradation.

 

[Barry Desborough]

Wow...just two links completed and I can already see you are quite a legend in your own mind. These Veritas links are all from your own blog with very few references to actual scientific studies and you do not quote others or give appropriate reference data (periodical or book name, author, publisher, etc,).

I will look a little deeper, but I already see a lot of consensus based conjecture and opinion. This should make anyone taking you seriously to go...Hmmm??? But since I gave my word, I will explore as many as I can handle in my schedule.

The blog is intended as an educational piece, but it does link to relevant literature.
See particularly, ERVs

 

[xianghua]

Repeating questions already answered.

Demonstrating an inability to read the FAQ and understand basic points.

You've used up enough of my time.

If you cannot make a coherent alternative case of your own, we're done.

ok. so lets take your position that those are a true viral insertions (just for the sake of the argument). again: this claim dont hold water because ervs have a small space in the genome that they can actually insert themself. if those scientists from the encode projects right and about up to 100% of the genome can be functional: we can explain those shared ervs without a common descent.