Endogenous Retroviruses and Human Evolution v. 2

Loudmouth

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The previous thread got bogged down with the usual rabbit trails, so I thought we would start fresh with this thread.

In this thread I will be presenting evidence supporting the evolution of humans from an ancestor shared with other apes. Specifically, I will be presenting endogenous retroviruses (ERV's) as genetic markers that can be used to scientifically test the hypothesis that humans share a common ancestor with apes, and that our genomes have diverged from those other species in a manner consistent with evolutionary mechanisms.

If someone wants to challenge this argument, they must present observable evidence and a testable hypothesis.

To get this thread moving, I would first like to define what an endogenous retrovirus (ERV hereafter) is. An ERV is the left over gene sequence from a retroviral infection. Why are they called retroviruses? Because they are from the 1970's? Nope. They are called retroviruses because the go from RNA to DNA using a reverse trascriptase, the reverse of how things work usually work in the cell. Once a DNA copy of the RNA viral genome is made, then the DNA linear copy is inserted into the host genome, analogous to pasting a paragraph into a book chapter. The viral DNA becomes part of that cells genome. Once in the genome, the promoters in the viral DNA lead to expression of the viral proteins, and eventually the production of viral particles at the surface of the cell. Here is a nice diagram of the retroviral cycle:

retro2.gif


If this occurs in a germ line cell, either a sperm or egg, and the virus fails to kill that cell, then the ERV can become a permanent part of a child's genome, in every cell in their body. As it turns out, a decent chunk of our genome is made up of the remnants of retroviral insertions. The following table is from the human genome paper, and it lists just over 200,000 ERV's in the human genome across three classes.

409860at-011.gif

Initial sequencing and analysis of the human genome : Article : Nature

What is also interesting about retroviruses is that they insert randomly across many, many loci. For example, the authors of the following paper allowed three different retroviruses (MLV, ASLV, and HIV) to insert into the same genome, and then they tracked where that virus inserted. The following table from that paper shows all of the human chromosomes, and the spot in each chromosome where a retrovirus inserted.

pbio.0020234.g001.jpg

Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

As you can see, insertions occurred along all 22 chromosomes and the X chromosome. They did find that HIV insertion had "hotpsots", but those hotspots covered nearly half of the genome.

"For HIV the frequency of integration in transcription units ranged from 75% to 80%, while the frequency for MLV was 61% and for ASLV was 57%. For comparison, about 45% of the human genome is composed of transcription units (using the Acembly gene definition)."
Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

Beware creationists telling you that viruses insert into hotspots instead of inserting randomly. What the creationists will not tell you is that hotspots cover more than one base, and usually large chunks of the genome.

Before we go on, can we all agree that the best explanation for ERV's in the human genome is ancient retroviral insertions, and that retroviruses insert all over the genome? Does anyone have observations that challenge this conclusion?
 

SkyWriting

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The previous thread got bogged down with the usual rabbit trails, so I thought we would start fresh with this thread.

In this thread I will be presenting evidence supporting the evolution of humans from an ancestor shared with other apes. Specifically, I will be presenting endogenous retroviruses (ERV's) as genetic markers that can be used to scientifically test the hypothesis that humans share a common ancestor with apes, and that our genomes have diverged from those other species in a manner consistent with evolutionary mechanisms.

If someone wants to challenge this argument, they must present observable evidence and a testable hypothesis.

To get this thread moving, I would first like to define what an endogenous retrovirus (ERV hereafter) is. An ERV is the left over gene sequence from a retroviral infection. Why are they called retroviruses? Because they are from the 1970's? Nope. They are called retroviruses because the go from RNA to DNA using a reverse trascriptase, the reverse of how things work usually work in the cell. Once a DNA copy of the RNA viral genome is made, then the DNA linear copy is inserted into the host genome, analogous to pasting a paragraph into a book chapter. The viral DNA becomes part of that cells genome. Once in the genome, the promoters in the viral DNA lead to expression of the viral proteins, and eventually the production of viral particles at the surface of the cell. Here is a nice diagram of the retroviral cycle:

retro2.gif


If this occurs in a germ line cell, either a sperm or egg, and the virus fails to kill that cell, then the ERV can become a permanent part of a child's genome, in every cell in their body. As it turns out, a decent chunk of our genome is made up of the remnants of retroviral insertions. The following table is from the human genome paper, and it lists just over 200,000 ERV's in the human genome across three classes.

409860at-011.gif

Initial sequencing and analysis of the human genome : Article : Nature

What is also interesting about retroviruses is that they insert randomly across many, many loci. For example, the authors of the following paper allowed three different retroviruses (MLV, ASLV, and HIV) to insert into the same genome, and then they tracked where that virus inserted. The following table from that paper shows all of the human chromosomes, and the spot in each chromosome where a retrovirus inserted.

pbio.0020234.g001.jpg

Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

As you can see, insertions occurred along all 22 chromosomes and the X chromosome. They did find that HIV insertion had "hotpsots", but those hotspots covered nearly half of the genome.

"For HIV the frequency of integration in transcription units ranged from 75% to 80%, while the frequency for MLV was 61% and for ASLV was 57%. For comparison, about 45% of the human genome is composed of transcription units (using the Acembly gene definition)."
Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

Beware creationists telling you that viruses insert into hotspots instead of inserting randomly. What the creationists will not tell you is that hotspots cover more than one base, and usually large chunks of the genome.

Before we go on, can we all agree that the best explanation for ERV's in the human genome is ancient retroviral insertions, and that retroviruses insert all over the genome? Does anyone have observations that challenge this conclusion?


Viruses spread through the air from species to species.
DNA also transfers species to species through diet.

Horizontal transfer - an introduction
Gene transfer between organisms without reproduction


Complete Genes May Pass from Food to Human Blood

Why West Africans keep hunting and eating monkey meat despite Ebola concerns


This is the one downside to eating greasy, grimey, gopher guts.
 
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The IbanezerScrooge

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Viruses spread through the air from species to species.
DNA also transfers species to species through diet.

Horizontal transfer - an introduction
Gene transfer between organisms without reproduction


Complete Genes May Pass from Food to Human Blood

Why West Africans keep hunting and eating monkey meat despite Ebola concerns


This is the one downside to eating greasy, grimey, gopher guts.

ERV's are not target specific, meaning that the DNA insertions that result from those infections are random and could be anywhere within the host genome. The likelihood of 2 different organisms being infected by the same virus and having viral DNA inserted into the same place within their genomes is infinitesimally small. While HGT could result in 2 organisms having similar DNA sequences within their genomes the nature of observed ERV DNA insertion rules out the possibility that the ERV's we see located in the same places within the genomes of different organisms were the result of separate infections. The well understood mechanism of inheritance explains what we see very, very well.

Do you accept this? If not (firstly, why not?), there's not much sense in continuing the conversation because it is the crux of the Shared ERV -> Common ancestry conclusion.
 
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Justatruthseeker

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So you agree that the ERVs found in the human genome are there because of retroviral insertion?

I agree - along with the DNA they brought from their previous host, I see nothing wrong with that hypothesis.
 
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Justatruthseeker

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ERV's are not target specific, meaning that the DNA insertions that result from those infections are random and could be anywhere within the host genome.

Do you accept this? If not (firstly, why not?), there's not much sense in continuing the conversation because it is the crux of the Shared ERV -> Common ancestry conclusion.

Not in the least. It's one of evolutionist's arguments they share common decent because they target specific sites.

http://www.evolutionarymodel.com/ervs.htm

So just what am I to believe now??????

On the contrary - specific virus devise specific ways of getting past cell defenses - which are passed on to their offspring - are they not even in evolutionary theory? Which is why they are always found targeting specific sites in the genome. Not because of any shared ancestory. The loci is shared because they have mechanism's already in place to bypass the defenses at those specific loci. The data is correct - it is just the flawed interpretation that it means familial decent that is wrong. So flawed we are now told that there is no pattern , even if they used that very pattern to argue their case...

Contradiction after contradiction is all I see before me.
 
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Loudmouth

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Not in the least. It's one of evolutionist's arguments they share common decent because they target specific sites.

No, it isn't. You have the entire argument backwards.

"Given the size of vertebrate genomes (>1 × 10^9 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14)."
http://www.pnas.org/content/96/18/10254.full


"As previously mentioned, parallel integration is ruled out as an explanation for the many shared ERVs by the highly random target selection of integrase."

That's from the website you are citing. It clearly states that there is no target specificity.

On the contrary - specific virus devise specific ways of getting past cell defenses - which are passed on to their offspring - are they not even in evolutionary theory? Which is why they are always found targeting specific sites in the genome.

They are not found targeting specific sites to any significant extent, certainly not enough to produce the same insertion 99.9% of the time.

The loci is shared because they have mechanism's already in place to bypass the defenses at those specific loci.

That is 100% made up.
 
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Justatruthseeker

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For example: Evolutionists say that 100K (random number not meant to reflect any reality anyone believes in) years ago the lineage split. In reality it is 100K years ago that the retrovirus went from host to host upon casual contact (area). When a population must have been say 2 to 8 say, to become set in any general population today.

Does anyone disagree that in whatever theory one has - except magic - the population must be small to be passed one from one generation to the next by propagation?
 
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Loudmouth

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For example: Evolutionists say that 100K (random number not meant to reflect any reality anyone believes in) years ago the lineage split. In reality it is 100K years ago that the retrovirus went from host to host upon casual contact (area). When a population must have been say 2 to 8 say, to become set in any general population today.

That would produce ERV insertions at different positions in the genome. That is not what we see. We see ERV insertions at the same location in each genome.

You share over 200,000 ERVs with your siblings at the same location in each of your genomes, not because you were each infected 200,000 times in your lifetime, but because you inherited those 200,000 ERVs from your parents.

Does anyone disagree that in whatever theory one has - except magic - the population must be small to be passed one from one generation to the next by propagation?

In a small or large population, 50% of any offspring's DNA will come from each parent.
 
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The IbanezerScrooge

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Not in the least. It's one of evolutionist's arguments they share common decent because they target specific sites.

http://www.evolutionarymodel.com/ervs.htm

So just what am I to believe now??????

Did you actually read the article that you posted as an example of contradiction of "evolutionist" claims??

from the article:
When we examine the collective genome of Homo sapiens, we find that a portion of it consists of ERVs (IHGS Consortium, 2001). We also find that humans share most of them with Chimpanzees, as well as the other members of Hominidae (great apes), the members of Hylobatidae (gibbons), and even the members of Cercopitheciodae (old world monkeys) (Kurdyukov et al., 2001; Lebedev et al., 2000). Since humans don't and/or can’t regularly procreate and have fertile offspring with members of these species, and thus don’t make sizable contributions to their gene pools, and vice versa, their inheritance cannot have resulted from unions of modern species. As previously mentioned, parallel integration is ruled out as an explanation for the many shared ERVs by the highly random target selection of integrase.

??

On the contrary - specific virus devise specific ways of getting past cell defenses - which are passed on to their offspring - are they not even in evolutionary theory? Which is why they are always found targeting specific sites in the genome. Not because of any shared ancestory. The loci is shared because they have mechanism's already in place to bypass the defenses at those specific loci. The data is correct - it is just the flawed interpretation that it means familial decent that is wrong. So flawed we are now told that there is no pattern , even if they used that very pattern to argue their case...

Contradiction after contradiction is all I see before me.

How viruses counteract the defenses of the cell in order to get inside the cell has nothing to do with it. We're talking about inserting viral DNA into whatever host cell is being attacked once the virus has defeated those defenses. Specific DNA loci do not have specific defenses, the cell membranes do. These are 2 different things.

So, what of the 200 or so ERV's shared by humans and no other organism. Were these also the result of multiple separate infections in multiple human hosts that just happened to all insert in the same location or do you accept that these were the result of shared common ancestors among humans?
 
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Justatruthseeker

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No, it isn't. You have the entire argument backwards.

"Given the size of vertebrate genomes (>1 × 10^9 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14)."
http://www.pnas.org/content/96/18/10254.full



"As previously mentioned, parallel integration is ruled out as an explanation for the many shared ERVs by the highly random target selection of integrase."

That's from the website you are citing. It clearly states that there is no target specificity.



They are not found targeting specific sites to any significant extent, certainly not enough to produce the same insertion 99.9% of the time.



That is 100% made up.


I read just fine - do you?

And yet it is those exact same location insertions you claim support you to, because suddenly their isn't any targeting. My how the story switches from evolutionist to evolutionist tale as it's told.

http://www.evolutionarymodel.com/ervs.htm#Layer_1

"the presence of ERVs in identical loci among species of various degrees of taxonomic separation, and of the nested hierarchies they fall into.

Since they’re passed on through sexual reproduction, the many ERVs fixed in identical loci in different species necessitates the past presence of a species ancestral to both, that has since diverged into the two modern ones. And the patterns of their distribution indicate a specific sequence of divergence."

No it doesn't, and there's the highlighted data you can never seem to read when you read things.

So now this evolutionist is wrong and you are right, what am I to believe? How about we all just accept the truth - that that shared point is the point when the foreign genome was inserted - always in the loci in which those foreign genomes are found on top of that. Or we wouldn't be here discussing ERV's at all.
 
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The IbanezerScrooge

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I read just fine.

Well, I'm at a loss. Perhaps Loudmouth can make sense of what you're trying to say, but you appear to be interpreting the words you're quoting exactly opposite of what they are clearly saying based on the meanings of words.

Maybe on more little try, but I am not hopeful.

The passages you are quoting are saying that the most parsimonious explanation for ERV insertions in identical locations in different organisms is common ancestry expressly because of the random nature of those insertions.
 
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Loudmouth

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I read just fine - do you?

You don't read just fine.

"It's one of evolutionist's arguments they share common decent because they target specific sites."--Justatruthseeker

They don't target specific sites. The references we have given you state that they don't target specific sites. The references you tried to use also say that they don't target specific sites.

We all make mistakes. It's ok to fess up with you make a mistake. However, your use of bald face lies to cover up these mistakes does not make you look good.

And yet it is those exact same location insertions you claim support you to, because suddenly their isn't any targeting.

The insertion only happened once in a common ancestor. That is why it is found at the same spot, because it was vertically inherited from a common ancestor. It is the same reason that you and your siblings were born with the same exact ERVs at the same exact spots in your genomes, because you vertically inherited them from your parents.

http://www.evolutionarymodel.com/ervs.htm#Layer_1

"the presence of ERVs in identical loci among species of various degrees of taxonomic separation, and of the nested hierarchies they fall into.


Yes, from a single insertion that happened just once in a common ancestor. No one is arguing that these shared ERV's are from many independent insertions by a target specific retrovirus. In fact, we are arguing against that explanation.

No it doesn't, and there's the highlighted data you can never seem to read when you read things.

IronyMeter1.gif


The website you are quoting and what I am saying are one in the same. Learn to read.
 
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Loudmouth

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Well, I'm at a loss. Perhaps Loudmouth can make sense of what you're trying to say, but you appear to be interpreting the words you're quoting exactly opposite of what they are clearly saying based on the meanings of words.

Maybe on more little try, but I am not hopeful.

The passages you are quoting are saying that the most parsimonious explanation for ERV insertions in identical locations in different organisms is common ancestry expressly because of the random nature of those insertions.

Justatruthseeker has really poor reading comprehension. At some point, even hand holding doesn't work.
 
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SkyWriting

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ERV's are not target specific, meaning that the DNA insertions that result from those infections are random and could be anywhere within the host genome. The likelihood of 2 different organisms being infected by the same virus and having viral DNA inserted into the same place within their genomes is infinitesimally small.

Sure. I am not suggesting that the offspring need to experience the
same exposure to get the same result. I'm not sure why you are.
 
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