Endogenous Retroviruses: Evidence for Human Evolution

Loudmouth

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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:

bishop_image01_full_1.jpg


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?
 
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Loudmouth

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How about first, you explain how the structure and shape was discovered and the scientific process used for the virus below (its supposedly the hiv virus):

Could you please get rid of that photo? It is way too big for the page.

Also, this is a discussion on how ERV's are used as genetic markers when testing for common ancestry, not the history of retroviral discoveries.
 
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morse86

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Could you please get rid of that photo? It is way too big for the page.

Also, this is a discussion on how ERV's are used as genetic markers when testing for common ancestry, not the history of retroviral discoveries.


Actually, it's very relevant. If the photos of the HIV virus are bs....how can you even trust the research on ERV?!?!?!?
 
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CabVet

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Actually, it's very relevant. If the photos of the HIV virus are bs....how can you even trust the research on ERV?!?!?!?

Yes, just like "if you don't know how life started, how can evolution have happened?", right?
 
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Loudmouth

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Actually, it's very relevant. If the photos of the HIV virus are bs....how can you even trust the research on ERV?!?!?!?

Are you challenging the claim that retroviruses exist? If so, I would love to see your evidence. Don't forget the red portion of the opening post.

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

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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:

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.
I am not disputing this but I have questions.

There are over 200,000 ERV's in the human genome.
How was this determined, I mean, how do geneticists recognize an ERV?
Aren't some of the ERV's, in whole or in part, actually being used to produce functional proteins for the cells or are part of the "instructions" for our current body shape and function?
 
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Loudmouth

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I am not disputing this but I have questions.

There are over 200,000 ERV's in the human genome.
How was this determined, I mean, how do geneticists recognize an ERV?

They search the genome for repetitive DNA, and then further screen the hits to determine if they share homology with known ERV's and retroviruses.

The repetitive DNA is found in the LTR's (long terminal repeats) of the viral genome which are like the bookeneds of the viral genome.

Aren't some of the ERV's, in whole or in part, actually being used to produce functional proteins for the cells or are part of the "instructions" for our current body shape and function?

A handful are being used, most famously in the case of viral proteins that are important for placental development and embryo attachment.

Abbie Smith has a nice blog entry on it.

ERMAHGERD! ERVALANCH! ERVs and Placentas – erv

It is worth mentioning at this point that ERV's are useful genetic markers even if they are functional. It is the retroviral origin of ERV's that makes them useful genetic markers. However, more fine detailed evidence, such as LTR divergence, may rely more on a lack of function, but the species distribution of ERV's, functional or otherwise, is ample evidence.
 
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CabVet

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I am not disputing this but I have questions.

There are over 200,000 ERV's in the human genome.
How was this determined, I mean, how do geneticists recognize an ERV?

An ERV is recognized because the retroviral genome is flanked by a characteristic long terminal repeat (LTR).

Aren't some of the ERV's, in whole or in part, actually being used to produce functional proteins for the cells or are part of the "instructions" for our current body shape and function?

Yes.
 
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Loudmouth

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Question: Are these 200,000 ERVs in the exact same location for all humans?

Answer: No. A handful of ERV's are insertionally polymorphic, meaning that only some of the population has the insertion. However, the ones who do have a specific ERV share that ERV at the same location in their genomes. Think of it as an allele.

http://www.ncbi.nlm.nih.gov/pubmed/11591322

Also, the ERV's that happen to not be found in everyone are in the HERV-K family which are the youngest family of ERV's in the human genome. That part of the ERV evidence meshes quite well.
 
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StormanNorman

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Answer: No. A handful of ERV's are insertionally polymorphic, meaning that only some of the population has the insertion. However, the ones who do have a specific ERV share that ERV at the same location in their genomes. Think of it as an allele.

http://www.ncbi.nlm.nih.gov/pubmed/11591322

Also, the ERV's that happen to not be found in everyone are in the HERV-K family which are the youngest family of ERV's in the human genome. That part of the ERV evidence meshes quite well.

Thanks.

In other words, population genetics has not had enough time to fix them in one location throughout the population. For the HERV-K ERVs, will each eventually disappear from the human genome or eventually fix itself to one location for all humans?
 
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Loudmouth

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Thanks.

In other words, population genetics has not had enough time to fix them in one location throughout the population. For the HERV-K ERVs, will each eventually disappear from the human genome or eventually fix itself to one location for all humans?

It is impossible to tell whether or not a neutral mutation will become fixed. I believe that the odds of any single neutral mutation reaching fixation is 1/n where n is the population size. Obviously, it is hard for alleles to reach fixation in a large population, but genetic bottlenecks can result in a wave of fixation.
 
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StormanNorman

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It is impossible to tell whether or not a neutral mutation will become fixed. I believe that the odds of any single neutral mutation reaching fixation is 1/n where n is the population size. Obviously, it is hard for alleles to reach fixation in a large population, but genetic bottlenecks can result in a wave of fixation.

That makes sense, e.g., the larger the population the less likely a neutral mutation will become fixed within the entire population.

I don't mean to derail your thread as I'd like to know more about this stuff. So, is the thinking that the majority of the ERVs common to all humans are the result of population bottlenecks, in most cases from quite some time ago?
 
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Loudmouth

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That makes sense, e.g., the larger the population the less likely a neutral mutation will become fixed within the entire population.

I don't mean to derail your thread as I'd like to know more about this stuff. So, is the thinking that the majority of the ERVs common to all humans are the result of population bottlenecks, in most cases from quite some time ago?

I don't know if a majority are due to population bottlenecks, but I think it is safe to say that a population of billions would be the least likely scenario for these ERV's reaching fixation.
 
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Loudmouth

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I'm afraid this will go over the heads of most on here. I certainly expect a specific group to completely ignore the information. Specifics cause them to hide.

The concepts so far are very simple. Viruses insert into the genome. Those insertions can be passed on like any other chunk of DNA in the genome. We find many instances of viral DNA in the human genome. These are all facts.

How many times have we seen creationists demand that we observe life emerging in a petri dish in the lab? Well, we observe viruses inserting DNA into the host genome and producing ERV's right in the lab, and even in petri dishes. Surely they can't ignore this evidence, can they?
 
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