Endogenous Retroviruses II

[BGoodForGoodSake]

Where are these scientific evidences you keep referring to, Angel? I haven't seen any just yet. What you've shown is that two distinct species have something in common. Out of some 98,000 insertion points, there happens to be 7 common ones between humans and chimps. Out of this observed commonality you conclude a common ancestor. I know analogies most often fail miserably but I will offer one anyway. Uncle Bob has 6 toes on his right foot and uncle Tom has six toes on his right foot. Therefore, uncle Bob and uncle Tom must be twins. Except they're 10 years apart and not even brothers (from 2 different parents, one on my mother's side and the other on my father's). That is the argument you are forwarding re common retroviral insertion points and common descent. I believe it is called the fallacy of the undistributed middle.

It is not simply the case that they share the same insertion points.
ERV's are the result of viral insertions. When a virus successfully inserts its genetic material into a host cell the cell will begin mass producing copies of the virus untill the host cell is full of viral particles. At this point tthe host cell will burst releasing the new viral particles to infect other host cells.

Now sometimes the viral insertion does not lead to this. If this genetic material somhow finds itself in germ cells the next generation will have this genetic material in all of their bodies cells. It has now become an ERV(endogenous retrovirus) We identify ERV's by their genetic sequence, certain proteins are known to be used specifically by retro viruses to enter their host cells. For ERV's these genes are identifiable but they are also decayed versions. Random mutations have scrambled up the sequence somewhat. Not only do closely related species share the same viral insertion points the genetic sequence of the ERV's are mostly identical. So it's not only insertion point but also shared sequence.

If it were found that guinnea pigs and humans shared an ERV which was not found in chimpanzees, it would be powerful evidence against common descent.

Scientists would have to show the section of DNA in chimpanzees which would have contained the ERV has been removed. If they were to find the section intact sans the ERV then common descent would be in trouble.

ERV's more often than not have no function in the host genome. In some cases the viral proteins have been coopted as in the case of placental development in human babies. Retroviruses are beleived to be a vehicle for horizontal gene transfer. If this mechanism of gene transfer played a large part in the development of life on earth, then ERV's become even more important in decrypting the tree of life.

The better analogy would thus be Uncle Tom and Uncle Bob both have six toes on their right foot. Their children also have six toes. The trait must be genetic. Uncle Bob and Uncle Tom are related and must have gotten this trait from a shared relative.

Although it is possible that they each got this mutation independantly the chances are low. So we will investigate, to see if the mutations are the result of independent activity. There are multiple known mutations which will cause the development of a sixth toe.

After analysis of mutations the sequences of the mutation are identical. It is most likely that they both received this genetic material from a common relative.

After a thorough search a distant relative is found in the Ural mountains. This very kind Russian gentlemen also has six toes on his right foot. The genetic sequence was determined. It is an identical sequence. The mutation cannot have occurred independently in the same manor in five separate individuals. The most likely explanation is that these men all shared a common ancestor.

[Byblos]

I decided to split this into yet another thread since the original one contains deleted posts (the poster Jbuza wished to delete them).

Ok, let's see:

Where are these scientific evidences you keep referring to, Angel? I haven't seen any just yet. What you've shown is that two distinct species have something in common. Out of some 98,000 insertion points, there happens to be 7 common ones between humans and chimps. Out of this observed commonality you conclude a common ancestor. I know analogies most often fail miserably but I will offer one anyway. Uncle Bob has 6 toes on his right foot and uncle Tom has six toes on his right foot. Therefore, uncle Bob and uncle Tom must be twins. Except they're 10 years apart and not even brothers (from 2 different parents, one on my mother's side and the other on my father's). That is the argument you are forwarding re common retroviral insertion points and common descent. I believe it is called the fallacy of the undistributed middle.

It is not simply the case that they share the same insertion points.
ERV's are the result of viral insertions. When a virus successfully inserts its genetic material into a host cell the cell will begin mass producing copies of the virus untill the host cell is full of viral particles. At this point tthe host cell will burst releasing the new viral particles to infect other host cells.

Now sometimes the viral insertion does not lead to this. If this genetic material somhow finds itself in germ cells the next generation will have this genetic material in all of their bodies cells. It has now become an ERV(endogenous retrovirus) We identify ERV's by their genetic sequence, certain proteins are known to be used specifically by retro viruses to enter their host cells.

So far so good. The virus will enter the germline and will be carried genetically through DNA.

For ERV's these genes are identifiable but they are also decayed versions. Random mutations have scrambled up the sequence somewhat. Not only do closely related species share the same viral insertion points the genetic sequence of the ERV's are mostly identical. So it's not only insertion point but also shared sequence.

Two issues I have here. 1) Since this process is random and highly unlikely then it has no known adaptive functions. And if that's the case, why hasn't natural selection gotten rid of it yet? Why is it still carried genetically? 2) If by closely related species you mean baboons, macaque, gorillas and chimps then ok. But if you're lumping humans in the mix as well, I must ask you why is that a strong case for common descent inter-specially and not a strong case for common design? Where is the proof of that? It is merely a conclusion based on an a-priori assumption of common descent. What if we find that the virus that resulted in the same sequence is actually meant to result in such, only in a number of species (because their immune systems are such that they allow for this sequencing)?

If it were found that guinnea pigs and humans shared an ERV which was not found in chimpanzees, it would be powerful evidence against common descent.

Scientists would have to show the section of DNA in chimpanzees which would have contained the ERV has been removed. If they were to find the section intact sans the ERV then common descent would be in trouble.

Oh but there is, not in guinea pigs though. It is in chimps and gorillas but oddly enough not in humans. A retrovirus that infected chimps and gorillas separately, yet it is absent from humans. It is even absent in their putative ancestry but exists in macaques and baboons. Here's the link. Here's a quote (note the highlighted):

In a new study, Evan Eichler and colleagues scanned finished chimpanzee genome sequence for endogenous retroviral elements, and found one (called PTERV1) that does not occur in humans. Searching the genomes of a subset of apes and monkeys revealed that the retrovirus had integrated into the germline of African great apes and Old World monkeys—but did not infect humans and Asian apes (orangutan, siamang, and gibbon). This undermines the notion that an ancient infection invaded an ancestral primate lineage, since great apes (including humans) share a common ancestor with Old World monkeys.

ERV's more often than not have no function in the host genome. In some cases the viral proteins have been coopted as in the case of placental development in human babies. Retroviruses are beleived to be a vehicle for horizontal gene transfer. If this mechanism of gene transfer played a large part in the development of life on earth, then ERV's become even more important in decrypting the tree of life.

So they do have a function but it's only inter-special? HGT is no more proven than inter-special ERVs.

The better analogy would thus be Uncle Tom and Uncle Bob both have six toes on their right foot. Their children also have six toes. The trait must be genetic. Uncle Bob and Uncle Tom are related and must have gotten this trait from a shared relative.

Although it is possible that they each got this mutation independantly the chances are low. So we will investigate, to see if the mutations are the result of independent activity. There are multiple known mutations which will cause the development of a sixth toe.

After analysis of mutations the sequences of the mutation are identical. It is most likely that they both received this genetic material from a common relative.

After a thorough search a distant relative is found in the Ural mountains. This very kind Russian gentlemen also has six toes on his right foot. The genetic sequence was determined. It is an identical sequence. The mutation cannot have occurred independently in the same manor in five separate individuals. The most likely explanation is that these men all shared a common ancestor.

While uncle Tom and uncle Bob may have a distant common ancestor who'll explain why his descendents all have 6 toes, it does not explain why the family dog has 6 toes as well. That's the point of my poor analogy.

[BGoodForGoodSake]

It is not simply the case that they share the same insertion points.
ERV's are the result of viral insertions. When a virus successfully inserts its genetic material into a host cell the cell will begin mass producing copies of the virus untill the host cell is full of viral particles. At this point tthe host cell will burst releasing the new viral particles to infect other host cells.

Now sometimes the viral insertion does not lead to this. If this genetic material somhow finds itself in germ cells the next generation will have this genetic material in all of their bodies cells. It has now become an ERV(endogenous retrovirus) We identify ERV's by their genetic sequence, certain proteins are known to be used specifically by retro viruses to enter their host cells.

So far so good. The virus will enter the germline and will be carried genetically through DNA.

For ERV's these genes are identifiable but they are also decayed versions. Random mutations have scrambled up the sequence somewhat. Not only do closely related species share the same viral insertion points the genetic sequence of the ERV's are mostly identical. So it's not only insertion point but also shared sequence.

Two issues I have here. 1) Since this process is random and highly unlikely then it has no known adaptive functions.

The function of these sections of RNA is to encode for viral proteins. The original purpose then is to produce more copies of the virus.

And if that's the case, why hasn't natural selection gotten rid of it yet? Why is it still carried genetically?

Because of how the genetic code works.

Generally viral particles aren't necessary for an individual to survive, if this section of the code has a copying error, there are no tears spilt. Thus being a section of the code which is not under selective pressure it will gradually accumulate mutations scrambling the original code. This mechanism of accumulating mutations has been observed and well documented.
If you mean to say the code should be removed, then by what proposed mechanism would the code be "cleaned out". As far as I am aware there are no known mechanisms which would do this. How would the system "know" that this was bad code? Would it "mark" the code which was not expressed or used in any way?

In conclusion the process of viral invasion failed, leaving inactive code in the hosts genome. As the code is passed from generation to generation there is nothing to prevent it from accumulating mutations (as the code likely has no function for the host). The position and number of mutations can be empirically meaured as a function of time.

2) If by closely related species you mean baboons, macaque, gorillas and chimps then ok. But if you're lumping humans in the mix as well, I must ask you why is that a strong case for common descent inter-specially and not a strong case for common design? Where is the proof of that? It is merely a conclusion based on an a-priori assumption of common descent.

It can be interpreted that way, however that is much less likely. Imagine a wolrd in whcih kitchen sinks reproduce. In the manufacture of your sink a spoon fell down the garbage disposal and became welded to the inside of the drainage pipe. Several generations later there are spoon like impressions in all your sinks if one examines the pipes closely. The spoon does not improve the sinks design. It does not get conserved (when an error occurs in the duplication of the spoony section it does not cause failure). The spoon doesn't need to be there at all yet it is.

ERV's are thought to be the result of viral infections. Here is a schematic of a retrovirus.

The code which encodes for proteins pol, env and gag are not found in eukaryotic cells except for ERV's. The section of code is also arranged in the same manor as it is in viral particles. Including a section of repeating code terminating the sequence, an identifing feature of retroviral genetic material. The ERV in essence is the deactivated genome of a retrovirus. Or a retroviral fossil in a way! This means that the insertion of this code must be the result of a viral infection. Otherwise the similarity of ERV's and Retroviral genome must be alternatively explained.

If we conclude that the ERV is a result of viral infection then we must then explain the distribution of ERV's found in organisms today.

What if we find that the virus that resulted in the same sequence is actually meant to result in such, only in a number of species (because their immune systems are such that they allow for this sequencing)?

Perhaps, but would this mechanisms direct the ERV to the same insertion point? In this case they would not be true othologs, i.e. not homologous. As in the example you brought up.

If it were found that guinnea pigs and humans shared an ERV which was not found in chimpanzees, it would be powerful evidence against common descent.

Scientists would have to show the section of DNA in chimpanzees which would have contained the ERV has been removed. If they were to find the section intact sans the ERV then common descent would be in trouble.

Oh but there is, not in guinea pigs though. It is in chimps and gorillas but oddly enough not in humans. A retrovirus that infected chimps and gorillas separately, yet it is absent from humans. It is even absent in their putative ancestry but exists in macaques and baboons. Here's the link. Here's a quote (note the highlighted):

In a new study, Evan Eichler and colleagues scanned finished chimpanzee genome sequence for endogenous retroviral elements, and found one (called PTERV1) that does not occur in humans. Searching the genomes of a subset of apes and monkeys revealed that the retrovirus had integrated into the germline of African great apes and Old World monkeys—but did not infect humans and Asian apes (orangutan, siamang, and gibbon). This undermines the notion that an ancient infection invaded an ancestral primate lineage, since great apes (including humans) share a common ancestor with Old World monkeys.

This is correct, read further. Further examination of the retroviral insertion point lead to the conclusion that the retroviral elements must have independently entered the germ line several times.
Thus did not infect a common ancestor but rather did so several times independently.

ERV's more often than not have no function in the host genome. In some cases the viral proteins have been coopted as in the case of placental development in human babies. Retroviruses are beleived to be a vehicle for horizontal gene transfer. If this mechanism of gene transfer played a large part in the development of life on earth, then ERV's become even more important in decrypting the tree of life.

So they do have a function but it's only inter-special? HGT is no more proven than inter-special ERVs.

No, function here is a byproduct of viral activity. It is not the same as the function you seem to be talking about. Inter-special Horozontal Gene Transfer is the idea that since viral material inserts itself into a hosts genome, it is possible that elements of the hosts genome can become incorporated into the viral genome. The mechanism is sound, and has been documented. This is one way HGT can occur. Case studies in which genetic material appears to have originated in this method have been published. Do you have a problem with theories involving HGT? I am not sure what your point is here.

[NewCreature]

Wouldn't it be neccessary to know the total actual knowledge of the biology of life in order to be able to determine that HERVs are junk DNA, or that they are present in the human Genome from historical infections of people?

Why would it be amazing or interesting that life would have some of the same genetic sequences?

There is some indication that these "HERV" sequences are functional such as placental development, also other uses can be seeb here, under the section "Biological Importance of HERVs"

http://www.pubmedcentral.nih.gov/articl ... id=1187282

These sequences are clearly a part of life; their similarity and use among life forms is not suprising. What is even more clear is that there are no scientists that are in the position to answer definitivley where they came from, or enlighten us about all the ways they are used within the human genome.

IT is not suprising that such a little known subject would be interpreted from an evolutionary assumption and argument made from conclusions that are very hypothetical.

[BGoodForGoodSake]

Wouldn't it be neccessary to know the total actual knowledge of the biology of life in order to be able to determine that HERVs are junk DNA, or that they are present in the human Genome from historical infections of people?

No,
The genetic code consists of codons, which are a set of three nucleic acids.
All active genes have a start and stop codon.
mRna uses these sequences to determine where to begin decoding and where to end.

Many of these ERV's do not have these signaling sequences.

Think of genetic code like a sentence in a bowl of alphabet soup.
The letters are strung together like below.
jahsdbiuhsdfbkuhasssthisisthemessagezzzjhsdfuhjsdhf

The mRNA goes in and looks for the start codon sss.

----------------------mRNA
jahsdbiuhsdfbkuha<color> sothisisthemessagezzzjhsdfuhjsdhf

then begins transcripting(copying in a way)

The transcription ends at the stop codon, because this will chemically cause the mRNA to disconnect from the DNA strand not because the mRNA is thinking.
jahsdbiuhsdfbkuhasss
sothisisthemessage zzzjhsdfuhjsdhf
kwyfekekyfizikklgi---mRNA

The mRNA finds it's way to a ribosome, again not actively it just gets carried along in the streaming protoplasm.
kwy fek eky fiz ikk lgi
sot thi ist hem ess age

At the ribosome it attaches the appropriate amino acids(the building blocks of proteins)
And then the message is the result.
"So this is the message"

But for many of these ERV's the code is scrambled like so:
jahsdbiuhsdfbkuhasasthisisthemessagezzzjhsdfuhjsdhf

The mRNA does not have a starting point and the code is thus never transcripted(a protein does not form off of this template).

These ERV's however share similar sequences to those of active retroviral infections.

When the HIV virus enters an immune cell in the human body, it injects it's genetic material into the hosts DNA. This genetic material is similar to those of ERV's except that they do contain the start and stop codons necessary for the proper functioning of these genes.

So on this basis among others it is determined that most ERV's are the result of failed retroviral injections of germ(reproductive) cells.

Why would it be amazing or interesting that life would have some of the same genetic sequences?

They are not identical. They are in the same location but have had sequences slightly altered. For example instead of
jahsdbiuhsdfbkuhasassothisisthemessagezzzjhsdfuhjsdhf
it's
jqhsdbiuhsdfbkuhasassothisisthemessagezzzjhsdfuhjsdhf

Just one letter different there must be a pattern to the differences.
And a pattern does indeed exist.

For example let's say you had two classes of children and they all were told to draw a butterfly.

The first class came back with all sorts of pretty anf fantastic drawings of butterflies of all colors.
Green ones, yellow ones, even some black and silver ones!

The other class had a majority of butterflys all looking similar and quite like a monarch butterfly.

There must be a reason. The second class went on a field trip where they had a butterfly presentation and got to see monarch butterflies.

Similarily with the ERV's there is a distribution of ERVS throughout the animal kingdom.

The distribution is not even nor random.

There is a pattern to this distribution.

For instance monkeys chimpanzees and goriillas share on ERV.
However another ERV is shared only between Chimpanzees and Gorillas, etc.

One can many of these ERVs.
Then take a note of all animal groups which share them.
And then plot a chart showing which animal share them.

In the resulting chart the lines will not cross.
From the scientists perspective, there needs to be an explanation for this find.

Chimpanzee *
Gorilla &
Old World Monkey @
New World Monkey %

E E E
R R R
V V V
1 2 3
* * *
& & &
@@
%

There is some indication that these "HERV" sequences are functional such as placental development, also other uses can be seeb here, under the section "Biological Importance of HERVs"

http://www.pubmedcentral.nih.gov/articl ... id=1187282

Unfortunately it takes an advanced understanding of biology to understand what may be going on here.
I can try to sumarize it as follows.
It is more illogical to find the few exceptions and say it is the rule, than it is to take the majority of cases and generalize it as an absolute principal.

In other words there are always exceptions to the rule.
In this case an active protein which binds together multiple cells into a multinucleated portion found in the placenta, is also found in retroviruses. And it has been determined that it must be retroviral in origin. An understanding that these are chemical process allows one to understand how something can become integrated into existing systems.

Not sure how to put it into laymens terms.
We can use sickle cell anemia as an example.
A mutation causes the blood cells to form into an odd shape.

But the shape is not programmed into the DNA.
What we have here is a modification in the DNA code.

This then translates into a modified amino acid sequence.

And when this amino acid sequence folds up it has different affinities and and forms a different shape than a normal one does.

All this is then results in sickle cell, if the individual has but one copy of this gene they live relatively normal lives, the mutation of modification just becomes a part of this individuals complex chemistry.

Hmm, that doesn't look plain enough...
Think of the bodies chemistry like jambalaya.
And think of the ERV involved in placental development as gummy bears.
Pop in a few gummy bears and the jambalaya is not affected adversely. If there is no harm it will then become a part of the jambalaya.

These sequences are clearly a part of life; their similarity and use among life forms is not suprising.

If you have an interest in biology, I recommend continuing your studies.
You will realize it is unimportant wether or not it is integral to life. Although the facts do not support this.
The importance lies in the pattern of sequences.

What is even more clear is that there are no scientists that are in the position to answer definitivley where they came from, or enlighten us about all the ways they are used within the human genome.

Nothing in science is definitive, it is all subject to the introduction of new observations. Science is not the Bible, it's not an authority, it's a process.
It is non-democratic and makes only negative judgements. Negative here does not mean bad, it is a process which eliminates options.

[angel]

Let me add another point to Bgood reply.

There is *another* independent way of determining junk DNA besides the one mentioned by BGood.

If you consider a DNA sequence and compare the omologous sequence from different
individuals some small differences are expected, as BGood mentioned.
By many observations done in mutations of differnet sequences they discovered that
essentially two different behaviours are observable, depending on the sequence.

1) Homogeneous Mutation frequency: the mutations are more or less random,
each mutation is equally likely to occur.

2) Non-Homogeneous mutation frequency: some mutations appear more frequently than others.
The more likely mutations are called synonimous.

Now each sequence that is known to encode for a protein behaves as (2).
This is explained by the action of selection. Proteins are very structured and random
mutations is hardly ever beneficial. So the malicious mutations tend to be suppressed by sectection
and only mutations which keep encoding the same protein are passed because they are by definition neutral mutations.
That is why they are called synonimous.

The sequences behaving as (1) are called junk DNA. It does not imply that they have no function at all.
It just means that they are not used to encode protein.

Now go back to ERV. Consider one sequence which is suspected to be an ERV.
Simply comparing the same sequence in different individuals one can decide if it junk or not by measuring the mutation frequency spectrum.

[NewCreature]

Yes I understand how evolution would interpret similar ERV sequences by claiming common decent of organisms. OF course without any way to confirm the hypothesis it wouldn't have any more weight than saying for instance that if these sequences are from a viral infection that particular viruses have a cross section of similar organisms that can provide a viable host for them. This would result in similar organisms with the same sequences. I see no clear proof that these sequences are from viral infections and not an important part of God's design, so there you have another hypothesis.

Would it be reasonable to say that since “HERVs” play a key role in placental development that animals couldn't produce offspring until they were infected with a virus? I think not. Also some hervs are thought to play an important role in protecting cells from infection by viruses (as can be seen at the link I posted earlier). IT would seem this evidence suggests that these sequences are part of a working DNA, and not mutations to a DNA.

Let me see if I understand your position. Your view is that these hervs are in the genome because a virus infected a sperm or an egg, and when the sperm or egg formed a new individual the virus was able to insert the genetic material into the new individual who then passed it on to their offspring?

[BGoodForGoodSake]

Yes I understand how evolution would interpret similar ERV sequences by claiming common decent of organisms. OF course without any way to confirm the hypothesis it wouldn't have any more weight than saying for instance that if these sequences are from a viral infection that particular viruses have a cross section of similar organisms that can provide a viable host for them. This would result in similar organisms with the same sequences.

This is true but one would not find the pattern of sequences we find. This hypothesis would not explain the location of ERV's nor the pattern of differences between species.

For instance chimpanzees can be infected first along with old world monkeys, then many mutations later gorrillas may have become infected.
If this is the case the sequence for the ERV in chimpanzees and old world monkeys would be more similar. And the gorilla less similar. Yet this is not what we find. For ERV's located in the same location the gorilla and chimpanzees sequences are always(*) more similar than that of old world monkeys.

* according to data collected so far.

Additionally the location of insertion likely would not be the same. Retro viruses are not forced to inject their material into a single location in the host genome(DNA).

Given these two factors it is highly unlikely that all ERVs are the result of separate events. The empirical evidence points away from the hypothesis you have supplied, because of the distribution of the ERV's.

In fact one should find many more ERVs if this were the case, because there would have to be a fair amount of misses for the distribution to make sence.

To clarify imagine the following.
Three students are told to pick a number between 1 and 100.
They are told to do this three times.

In the end two of the students picked the same number and one student picked two out of the three.

Not very likely, however if the students were told to pick 20 numbers each. It is very likely that we would find two student sharing three numbers and one sharing two.

Now in the alternative hypothesis a student is asked to pick two numbers.
Then a second student is given these numbers and asked to choose a third. The third student is given this new set of numbers.
Now the distribution of numbers makes sense.

I see no clear proof that these sequences are from viral infections and not an important part of God's design, so there you have another hypothesis.

They may very well be a part of God's design, but that is not what we are discussing here.
When a cell is infected by a retrovirus such as the common cold the viral DNA gets injected into the host cell.

If you check the link you'll see that the retro virus works by fusing with the host cell and injecting RNA and reverse transcriptase.
This results in the retro viral genetic material becoming part of the hosts.

Interestingly the protein which helps the viral partical fuse with the host is the same kind of protein formed in the placenta when it forms a multinucleated fused mass.

So when one compares a retro viral injection, with an ERV, it becomes clear they have the same origin. All retroviruses have a long terminating sequence (repeating segment of DNA). ERV's have long terminating sequences. All retroviruses encode for three specific proteins, gag, env and pol. ERV's encode for these proteins as well.

Would it be reasonable to say that since “HERVs” play a key role in placental development that animals couldn't produce offspring until they were infected with a virus? I think not.

You are correct. As I said earlier that biochemistry at the cellular level is not like a fine tuned machine. It's more like jambalaya. Experiments have shown that the retroviral protein involved in the creation of the placenta is a weak binding protein. In adition there are other proteins which do the same job. It appears that this protein just became a part of the mix of proteins involved in the production of the syncytiotrophoblast(the multinucleated cell in question).

Now this particular gene is highly conserved, which means it must have an important function. This can occur with modification after introduction.

For example lets say we have a recipe for crab cakes. The original recipe calls for flour and milk. Hoever one day there was insufficient flour and bread bits were added. At this point the bread bits are optional. However let us say the flour was not included when the recipe was copied. And now the bread bits are essential.

In a recent study it was found that ERV-3 (the ERV in question) may not be essential for placental formation. There may be another important function for this gene or perhaps another explanation. Further reading of this article will explain that in some of the population the gene is naturally knocked out. (A mutation causes a stop protein to occur earlier in the sequence.) These people are still able to have children.

It is very important to note that there is focus on this particular ERV because it is conserved. A conserved gene implies that it is providing a function. Most ERVs are non conserved, meaning they are susceptible to random mutation with no deleterious effects.

Also some hervs are thought to play an important role in protecting cells from infection by viruses (as can be seen at the link I posted earlier). IT would seem this evidence suggests that these sequences are part of a working DNA, and not mutations to a DNA.

Yes Some hERVs may have a function, but now you are talking about ERVs in general. Let's stick to the subject. We are discussing homologous ERVs shared between species. Whether ERV's have a function or not is unimportant. It is the pattern of distribution and sequences which concern us.

In other words it is inconsequential whether some ERVs have a function or not. For instance if the students above were picking passwords for their computers it doesn't take away from the method of password selection.

Let me see if I understand your position. Your view is that these hervs are in the genome because a virus infected a sperm or an egg, and when the sperm or egg formed a new individual

Yes good so far.

the virus was able to insert the genetic material into the new individual who then passed it on to their offspring?

No, at this point the original single cell of the fertilized egg contains the viral material. All the cells of the new individual will contain the same genetic material, thus contain the ERV.

[Byblos]

I'm still in the infancy stages of this ERV topic but I have a rather silly question nonetheless. If ERVs point to a common ancestor between chimps and humans they would also have to point to more than just a common ancestor (as common lineage), they would have to point to the SAME ancestor to the exsclusion of all other relative ancestors living at the time.

So let's say there were 100,000 living beings (potential ancestors). Considering that all humans and chimps have the same ERVs and insertion points, the scenario must be such that either all 100,000 were infected by the same virus and passed it down to humans and chimps. Or our common ancestor is only one of them who was infected, the rest didn't. And by sheer luck his lineage survived, whereas the lineage of the remaining 99,999 who were not infected became extinct (otherwise we'd have some people with different ERVs and/or insertion points). Am I making any sense? If yes, how would you explain it?

[BGoodForGoodSake]

I'm still in the infancy stages of this ERV topic but I have a rather silly question nonetheless. If ERVs point to a common ancestor between chimps and humans they would also have to point to more than just a common ancestor (as common lineage), they would have to point to the SAME ancestor to the exsclusion of all other relative ancestors living at the time.

So let's say there were 100,000 living beings (potential ancestors). Considering that all humans and chimps have the same ERVs and insertion points, the scenario must be such that either all 100,000 were infected by the same virus and passed it down to humans and chimps. Or our common ancestor is only one of them who was infected, the rest didn't. And by sheer luck his lineage survived, whereas the lineage of the remaining 99,999 who were not infected became extinct (otherwise we'd have some people with different ERVs and/or insertion points). Am I making any sense? If yes, how would you explain it?

This makes sense.
The likelyhood of the entire population becomming infected in the mannor you described is of course very unlikely.

However every individual has their own set of ERV's.
A chromosome on which a survival traits resides also contains any ERVs and other genes.
Survival traits and ERV's come as a package deal.
So in the same way an advantageous trait spreads throughout a population associated ERV's also spread.

Of course fixation of traits and associated ERV's is unlikely to occur in large populations. The ancestral population has to have been small at one point.

Let's do a very simplified calculation.
So for instance lets say that in the ancestral population an individual developed improved spacial reasoning skills. Let's say this initial population is 10,000 individuals.
So at first we have 1 individual with the trait. Let's also assume that this individual has inherited an ERV from several generations back.

After the first generation lets say this individual has 8 offspring 5 of which did not survive. 1 of which did not posess the trait.
Lets say the average pair gives birth to 10 offspring and 80% of them die.
And this trait gives them a 30% survival rate.

We will give a slight advantage in survival to those who posess this gene and associated ERV.

generation count_with_gene total_population
1_________1_____________10000
2_________2_____________10000
3_________5_____________10000
4_________11____________10000
5_________19____________10000
6_________42____________10000
7_________79____________10000
8_________154___________10000
9_________303___________10000
10________614___________10000
11________1230__________10000
12________2399__________10000
13________4756__________10000
14________9417__________10000

As you can see in this simplified example after 15 generations the entire population has this gene and it's associated ERV. Simply because the trait gave a slight survival advantage. There is no need for a rapid die off of everyone else's lineage.

[Byblos]

I'm still in the infancy stages of this ERV topic but I have a rather silly question nonetheless. If ERVs point to a common ancestor between chimps and humans they would also have to point to more than just a common ancestor (as common lineage), they would have to point to the SAME ancestor to the exsclusion of all other relative ancestors living at the time.

So let's say there were 100,000 living beings (potential ancestors). Considering that all humans and chimps have the same ERVs and insertion points, the scenario must be such that either all 100,000 were infected by the same virus and passed it down to humans and chimps. Or our common ancestor is only one of them who was infected, the rest didn't. And by sheer luck his lineage survived, whereas the lineage of the remaining 99,999 who were not infected became extinct (otherwise we'd have some people with different ERVs and/or insertion points). Am I making any sense? If yes, how would you explain it?

This makes sense.
The likelyhood of the entire population becomming infected in the mannor you described is of course very unlikely.

However every individual has their own set of ERV's.
A chromosome on which a survival traits resides also contains any ERVs and other genes.
Survival traits and ERV's come as a package deal.
So in the same way an advantageous trait spreads throughout a population associated ERV's also spread.

Of course fixation of traits and associated ERV's is unlikely to occur in large populations. The ancestral population has to have been small at one point.

Let's do a very simplified calculation.
So for instance lets say that in the ancestral population an individual developed improved spacial reasoning skills. Let's say this initial population is 10,000 individuals.
So at first we have 1 individual with the trait. Let's also assume that this individual has inherited an ERV from several generations back.

After the first generation lets say this individual has 8 offspring 5 of which did not survive. 1 of which did not posess the trait.
Lets say the average pair gives birth to 10 offspring and 80% of them die.
And this trait gives them a 30% survival rate.

We will give a slight advantage in survival to those who posess this gene and associated ERV.

generation count_with_gene total_population
1_________1_____________10000
2_________2_____________10000
3_________5_____________10000
4_________11____________10000
5_________19____________10000
6_________42____________10000
7_________79____________10000
8_________154___________10000
9_________303___________10000
10________614___________10000
11________1230__________10000
12________2399__________10000
13________4756__________10000
14________9417__________10000

As you can see in this simplified example after 15 generations the entire population has this gene and it's associated ERV. Simply because the trait gave a slight survival advantage. There is no need for a rapid die off of everyone else's lineage.

Thanks Bgood. But this didn't really address my question (unless of course I didn't understand your reasoning).

First, I didn't claim a rapid die-off. I'm simply wondering what happened to the lineage of those potential ancestors who didn't get infected or got infected with different viruses. The fact of the matter is, no matter how much ERVs differ from one individual to another, the claim (and that is your and Angel's claim) is that they are not only the exact same viruses (distinguishable from other viruses that attacked other species), but also they have the same exact insertion points. So they have enough similarities for you to come to the conclusion that those species have a common ancestor. That tells me either we all came from the lineage of one and only one ancestor or all ancestors would have been infected with the same virus. You already excluded the latter as an unlikely scenario. The former leaves us with more questions than answers.

Moreover, in your explanation you're attempting to answer HOW one individual ancestor could be the link. My question is WHY is that plausible, given that many potential ancestors must have lived contemporaneously and possibly were not infected. Where did their lineage go? Why do we not see any evidence of them anywhere either living or in the fossil record? And if every individual has their own set of ERVs, how is that an indication of common ancestry to begin with? In what areas do ERVs need to differ but still be fundamentally the same as to claim common ancestry?

[NewCreature]

Yes I understand how evolution would interpret similar ERV sequences by claiming common decent of organisms. OF course without any way to confirm the hypothesis it wouldn't have any more weight than saying for instance that if these sequences are from a viral infection that particular viruses have a cross section of similar organisms that can provide a viable host for them. This would result in similar organisms with the same sequences.

This is true but one would not find the pattern of sequences we find. This hypothesis would not explain the location of ERV's nor the pattern of differences between species.

The instance you provided didn't show how a pattern of sequences disproved, assuming the genetic material is from a viral infection, that particular viruses might by more suitable to live within similar hosts. Further mightn't the difference between ofl world monkeys and other primates be from the unique virus present in their habitat that could differ in some ways from other viral outbreaks in other parts of Earth. What about the location of ERVs and the pattern of differnces between ERVs among the species would suggest to you that species couldn't have become independently infected by a common virus. Unque sets of viruses capable of infecting a similar cross section of species in a given area would create a pattern of viral insertions; If in fact that is the cause of this genetic material.

Additionally the location of insertion likely would not be the same. Retro viruses are not forced to inject their material into a single location in the host genome(DNA).
Given these two factors it is highly unlikely that all ERVs are the result of separate events. The empirical evidence points away from the hypothesis you have supplied, because of the distribution of the ERV's.

And yet out of all the viral infections in the history of the world, and out of all the populations that have been independently infected, and all the possible locations that the genetic material could be introduced at, we see a remarkable order. At this point it should be important to point out that I was playing the part of the devil's advocate, and suggesting the possiblity of numerous infections, which of course shurely did occour. I will no longer entertain that idea, as the evidence shows it not to be true, and it is more likely that these sequences labelled however they are, are an important part of a designed DNA, and that the idea of HERVs is just silly. You have three proteins that are apparent throughout life, and they are in the Human genome as well.

In fact one should find many more ERVs if this were the case, because there would have to be a fair amount of misses for the distribution to make sence.

But we don't find many more of them, and their isn't much of a distribution, so doesn't that point to the idea that perhaps these aren't from viral infections at all.

To further complicate the matter of a female not being able to give birth before she was infected by the virus is that without the the use of another of these proteins that are present in almost all of life from the virus ot hte highest mammals, she would proably reject the fetus.

At least two of these so called ERV proteins are necessary for reproduction. At his point perhaps it would be best to just emphatically state that without somekind of actual and convincing evidence that I reject the idea of these sequences being from viral infections or that they suggest anything about common decent. At the most they show similarlity in life.

The evidence is clear that these genetic sequences are three of numerous proteins that exist within the greater complexity of the human genome.

I think I missed a couple of points. I want to post an additional message with questions and information about how this virus made it into the gene pool from your perspective.

[NewCreature]

Let me see if I understand your position. Your view is that these hervs are in the genome because a virus infected a sperm or an egg, and when the sperm or egg formed a new individual

Yes good so far.

the virus was able to insert the genetic material into the new individual who then passed it on to their offspring?

No, at this point the original single cell of the fertilized egg contains the viral material. All the cells of the new individual will contain the same genetic material, thus contain the ERV.

Ok I think I am on the same page; we shall see. So my question then becomes is it even possible for a sperm or egg that is now a virus cell to combine with the other gamate to preoduce an individual that would then have the sequence in their entire genome.

IT is general knowledge that virusal replication leads to the death of the cell which the virus entered. How can a virus take over a gamete and kill it when it is busily forming a new indivivdual?

[BGoodForGoodSake]

Thanks Bgood. But this didn't really address my question (unless of course I didn't understand your reasoning).

It would appear that way.
No lineages died off. Future generations are the result of changes in the population. The trait in question spreads throughout the population until it becomes a part of all lineages. Re-read the post above and you'll see that.

First, I didn't claim a rapid die-off. I'm simply wondering what happened to the lineage of those potential ancestors who didn't get infected or got infected with different viruses.

Their descendants aquired the slightly advantageous trait and therefore the associated ERV. The ERV became a part of all lineages.

The fact of the matter is, no matter how much ERVs differ from one individual to another, the claim (and that is your and Angel's claim) is that they are not only the exact same viruses (distinguishable from other viruses that attacked other species), but also they have the same exact insertion points.

This is correct.

So they have enough similarities for you to come to the conclusion that those species have a common ancestor. That tells me either we all came from the lineage of one and only one ancestor or all ancestors would have been infected with the same virus.

This is correct. Lets put my example above in a different way. Let us suppose your grandmother can do magic. Noone in my family can. Magic ability is genetic in this example.
Now my daughter marries your son. They have a daughter. She can do magic. Magic ability has become a part of my lineage, my lineage still lives but now has a trait which was in your lineage. Any ERV's located on the same chromosome as the trait become a part of my lineage as well.
No lineages have ended.
If magic using ability imparts a slight advantage to survival into adulthood, it will spread throughout the population. As even a slight advantage will over time become amplified.
Think interest rates. 8% and 9% over 30 years is a huge difference.

[BGoodForGoodSake]

The instance you provided didn't show how a pattern of sequences disproved, assuming the genetic material is from a viral infection, that particular viruses might by more suitable to live within similar hosts.

The fact that the viral insertion is in all individuals means that the all individuals must have a common ancestor. If the insertion points and sequences are identical in two separate species, what conclusion can you make?

Further mightn't the difference between ofl world monkeys and other primates be from the unique virus present in their habitat that could differ in some ways from other viral outbreaks in other parts of Earth.

The difference is several point mutations. Not a completely different virus.

What about the location of ERVs and the pattern of differnces between ERVs among the species would suggest to you that species couldn't have become independently infected by a common virus.

Virus are notorious for the rapid rate at which their genetic material changes. The chances of a virus simultaneously affecting multiple populations of different species without mutating and injecting the same genetic material into the exact same location is nearly impossible.
The virus cannot have the same sequence across species and be present in every individual. And be present in the same location across such a variety of species.

Unque sets of viruses capable of infecting a similar cross section of species in a given area would create a pattern of viral insertions; If in fact that is the cause of this genetic material.

Yes but this pattern would predict multiple and separate events. And in this case we would predict different insertion points. We would also be able to date the separate events because the sequences would be different. See Byblos first post. He has an example of such an occurance. And as you can see the predictions of cross-species infection does not match the observed distribution of homologous ERV's.

And yet out of all the viral infections in the history of the world, and out of all the populations that have been independently infected, and all the possible locations that the genetic material could be introduced at, we see a remarkable order.

The location of the ERV's lets us know that they are homologous, yet the pattern of differentiation is the key here. Why do the ERV's vary among species and fall into the pattern they do?

At this point it should be important to point out that I was playing the part of the devil's advocate, and suggesting the possiblity of numerous infections, which of course shurely did occour. I will no longer entertain that idea, as the evidence shows it not to be true, and it is more likely that these sequences labelled however they are, are an important part of a designed DNA, and that the idea of HERVs is just silly. You have three proteins that are apparent throughout life, and they are in the Human genome as well.

Refer back to an earlier post which describes the start and stop codons. There ERV's are deactivated. In the viral material they are active. The sequences in the ERV encode for env gag and pol. Proteins which do not generally involve themselves in a eukaryotic cell.

In fact one should find many more ERVs if this were the case, because there would have to be a fair amount of misses for the distribution to make sence.

But we don't find many more of them, and their isn't much of a distribution, so doesn't that point to the idea that perhaps these aren't from viral infections at all.

No you missunderstood. I mean the proportion to ERV's shared and those unshared must be much larger if it were just conincidence that they share the same insertion point.
I.E. there must be many more misses as compared to hits.

To further complicate the matter of a female not being able to give birth before she was infected by the virus is that without the the use of another of these proteins that are present in almost all of life from the virus ot hte highest mammals, she would proably reject the fetus.

Reptiles and Birds do fine without this protein as do marsupials. The integration of this protein may have actual lead to the development of the placenta. Refer back to the jambalaya example.

At least two of these so called ERV proteins are necessary for reproduction. At his point perhaps it would be best to just emphatically state that without somekind of actual and convincing evidence that I reject the idea of these sequences being from viral infections or that they suggest anything about common decent. At the most they show similarlity in life.

The evidence is clear that these genetic sequences are three of numerous proteins that exist within the greater complexity of the human genome.

I think I missed a couple of points. I want to post an additional message with questions and information about how this virus made it into the gene pool from your perspective.