Endogenous Retroviruses II

[BGoodForGoodSake]

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.

Yes the transcription process is not perfect. It is error prone as are all physical processes. As we mentioned earlier proteins are encoded in the DNA and have start and stop codons indicating where to begin and stop encoding.

It is possible during transcription from retro-viral RNA to the hosts DNA that one of these codons could become altered. Therefore deactivating the protein.

A frameshift would deactivte the entire viral material.
Over time as there are no selective pressures the other proteins would become deactivated as well.

As an added note the relative unreliability of transcriptase allows a virus to mutate rapidly.

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?

The virus would not form viral particles because one of the essential proteins has been rendered inactive.
This occurs all the time, an examination of your bodies cells would reveal signs of your history of cold infections. Yet your body is no longer infected.

If you need more detail on the RNA to DNA transcription process or anything else please let me know. the more you understand the material the easier this conversation will be for me.

I don't want to use terminalogy you are unfamiliar with and have that lead to a misunderstanding. That is my biggest pet peeve. Comprehension is the key to these sorts of discussions.

Thanks

[Byblos]

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.

I understand all that. This would mean any descendant of my son or the daughter of my son and your daughter will all be magicians. I get that and have no problem with it. What I'm getting at is what happened to the descendants of your other daughter and your sons who didn't marry any of my magician relatives? They married other people who were either left handed or have 6 toes. Why do we not see their lineages today? Why do we only see magicians? Would that not imply that the lineages of your other daughters and sons died off and everyone living today is a descendant of my son? What you're saying is that all non-magician descendants had to have interacted (inter-married) with magician descendants at some point for us to see the common ERVs we see today. I just don't see that as a possibility.

[BGoodForGoodSake]

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.

I understand all that. This would mean any descendant of my son or the daughter of my son and your daughter will all be magicians. I get that and have no problem with it. What I'm getting at is what happened to the descendants of your other daughter and your sons who didn't marry any of my magician relatives? They married other people who were either left handed or have 6 toes. Why do we not see their lineages today? Why do we only see magicians? Would that not imply that the lineages of your other daughters and sons died off and everyone living today is a descendant of my son? What you're saying is that all non-magician descendants had to have interacted (inter-married) with magician descendants at some point for us to see the common ERVs we see today. I just don't see that as a possibility.

Mathematics shows that it is probable and even unavoidable in a population which interbreeds thouroughly.

There is differential survivability.
Even a 1% advantage to survivability will cause the trait to spread.

Not all our descendants will marry a magician, many will die young.
As will many magician children, but we stated that magician children have a slight advantage to reaching adult hood than muggle children. So that by the time they reach adulthood a slightly disproportionate number of adults will be magical.

Remember the interest rate statement.
If the maximum population size is 100.
Lets say every pair has an average of 10 offspring.
50 x 10 gives you 500 individuals.
Due to limitations in the environment 80% of the individuals will die.
This means an average individual has a 2 in 10 chance of survival.
Lets say a trait comes along which imparts the individual a 5 in 20 chance of survival.
This means that couples with one individual with this trait will have 22 survivors out of a hundred.

Couples with both individuals with this trait will have 25 survivors out of a hundred.

And couples without will have (roughly)20 in one hundred survive.
Eventually the majority of individuals will have this trait.

As you can see the number of individuals with this trait increase each generation, in proportion to the numbers without. Eventually this trait will permeate the gene pool.

And any future isolated sub-populations of this group are almost certain to consist of only individuals with this trait.

[Byblos]

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.

I understand all that. This would mean any descendant of my son or the daughter of my son and your daughter will all be magicians. I get that and have no problem with it. What I'm getting at is what happened to the descendants of your other daughter and your sons who didn't marry any of my magician relatives? They married other people who were either left handed or have 6 toes. Why do we not see their lineages today? Why do we only see magicians? Would that not imply that the lineages of your other daughters and sons died off and everyone living today is a descendant of my son? What you're saying is that all non-magician descendants had to have interacted (inter-married) with magician descendants at some point for us to see the common ERVs we see today. I just don't see that as a possibility.

Mathematics shows that it is probable and even unavoidable in a population which interbreeds thouroughly.

It may show it today with the advent of travel (even that can be questioned but I'll give you that for now). But does mathematics show that in the pre-human age with the different populations interspersed on different continents with no way of connecting? I don't think so.

There is differential survivability.
Even a 1% advantage to survivability will cause the trait to spread.

Now you've added another advantageous function to ERVs (that of the tendency for survivability over other non-ERV infected species). Those so-called junk DNA sure are doing a whole lotta stuff. Besides, how can you prove that? How do you show empirically that magicians had an advantage over non-magicians when you have no non-magicians to test against?

Not all our descendants will marry a magician, many will die young.

Which goes back to my assertion that the common ancestor must be one and only one individual.

As will many magician children, but we stated that magician children have a slight advantage to reaching adult hood than muggle children. So that by the time they reach adulthood a slightly disproportionate number of adults will be magical.

Again, where is the proof of that? How do you compare that to non-magicians? We've never found any.

Remember the interest rate statement.

BGood, If there's anything I know it's interest calculations in all its forms (I write financial software for banks), but I digress.

If the maximum population size is 100.
Lets say every pair has an average of 10 offspring.
50 x 10 gives you 500 individuals.
Due to limitations in the environment 80% of the individuals will die.
This means an average individual has a 2 in 10 chance of survival.

By that token and going back to my example, out of 100,000 potential ancestors, the lineage of 20,000 should have survived. The common ancestry you are proposing allows for the lineage of only 1 of them to survive (yes, albeit over time). That's a staggering margin of error.

Lets say a trait comes along which imparts the individual a 5 in 20 chance of survival.
This means that couples with one individual with this trait will have 22 survivors out of a hundred.

Couples with both individuals with this trait will have 25 survivors out of a hundred.

And couples without will have (roughly)20 in one hundred survive.
Eventually the majority of individuals will have this trait.

As you can see the number of individuals with this trait increase each generation, in proportion to the numbers without. Eventually this trait will permeate the gene pool.

And any future isolated sub-populations of this group are almost certain to consist of only individuals with this trait.

It's a nice theory and all but it is fundamentally untestable.

[BGoodForGoodSake]

It may show it today with the advent of travel (even that can be questioned but I'll give you that for now). But does mathematics show that in the pre-human age with the different populations interspersed on different continents with no way of connecting? I don't think so.

Very good, now you're thinking like a scientist! No if pre-human populations had no way of connecting we would have divergent populations and speciation would have occured. A breeding population is defined as a group of individuals which share a common gene pool. In the past this would have been restricted to a much smaller geographic area. The original population from which modern humans derived from would most likely have been an isolated population in a single geographic location. Thus the out of Africa hypothesis. But this is off topic.

There is differential survivability.
Even a 1% advantage to survivability will cause the trait to spread.

Now you've added another advantageous function to ERVs (that of the tendency for survivability over other non-ERV infected species).

No, as I clearly stated earlier the ERV is packaged with the advantageous trait.

Those so-called junk DNA sure are doing a whole lotta stuff.

No.

Besides, how can you prove that? How do you show empirically that magicians had an advantage over non-magicians when you have no non-magicians to test against?

Simply showing that any advantageous trait will dominate a population over time suffices. We can then show that the mechanism is plausible. This is how science works.

Any breeding program shows clearly that selection will eventually lead to a population devoid of those selected against, but again this seems to be going off topic.

Which goes back to my assertion that the common ancestor must be one and only one individual.

Yes and no,
The genetic material will consist of the entire original populations gene pool. However all individuals in the resulting population will at least share one common ancestor.

Remember we all have 2 parents and 4 grandparents and 8 great grand parents.
After ten generations we are the result of the mixing of genes from at most 1,024 ancestral individuals from the first generation, only one of which has to be your magical son.

Again, where is the proof of that? How do you compare that to non-magicians? We've never found any.

Again we can surmize this by running experiments where we do in fact give certain a slight selective advantage. The results of these experiments is that after a certain number of generations has passed, the entire population will consist of individuals with this trait even if the selective advantage is very very small.
The only exception to this is if the trait somehow failed to make it past the first few generations.

Remember the interest rate statement.

The results expectedly agree with the mathmatical predictions.
So any trait which confers a selective advantage will eventually make it's way through the entire population.

Of course most traits don't confer a selective advantage, they are simply alternate traits.

BGood, If there's anything I know it's interest calculations in all its forms (I write financial software for banks), but I digress.

If the maximum population size is 100.
Lets say every pair has an average of 10 offspring.
50 x 10 gives you 500 individuals.
Due to limitations in the environment 80% of the individuals will die.
This means an average individual has a 2 in 10 chance of survival.

By that token and going back to my example, out of 100,000 potential ancestors, the lineage of 20,000 should have survived. The common ancestry you are proposing allows for the lineage of only 1 of them to survive (yes, albeit over time). That's a staggering margin of error.

No the lineage of 20,000 do indeed survive. There is no margin of error.
After 15 generations each individual is the result of the mixing of genes from at most 32,768 individuals from the first generation. Only one of these ancestors has to have had the trait.

In fact it is possible, and even with a fair likelyhood depending on the amount of interbreeding occurring, that after 16 generations a single individual could represent all 20,000 lineages!

Of course for a population as large as 20,000 individuals it will take longer than 15 generations to fix this trait. Unless it confers a great advantage. Such as disease resistance.

Populations which reproduce asexually will take a far longer time to consist of only individuals with the selected mutation. Given similar selective advantages and population size an asexually reproducing population could take up to 300 generations to reach a population with the same distribution of traits.
Of course asexually reproducing organisms have the advantage in that they can fix a trait in a single generation.

Lets say a trait comes along which imparts the individual a 5 in 20 chance of survival.
This means that couples with one individual with this trait will have 22 survivors out of a hundred.

Couples with both individuals with this trait will have 25 survivors out of a hundred.

And couples without will have (roughly)20 in one hundred survive.
Eventually the majority of individuals will have this trait.

As you can see the number of individuals with this trait increase each generation, in proportion to the numbers without. Eventually this trait will permeate the gene pool.

And any future isolated sub-populations of this group are almost certain to consist of only individuals with this trait.

It's a nice theory and all but it is fundamentally untestable.

This is not the case we can test selective advantage in any laboratory around the world. Many choose mice or bacteria or fruit flys because of their short generation span.

In all cases a slight advantage in survivability will eventually lead a trait to become ubiquitous.

[NewCreature]

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.

Yes the transcription process is not perfect. It is error prone as are all physical processes. As we mentioned earlier proteins are encoded in the DNA and have start and stop codons indicating where to begin and stop encoding.

It is possible during transcription from retro-viral RNA to the hosts DNA that one of these codons could become altered. Therefore deactivating the protein.

A frameshift would deactivte the entire viral material.
Over time as there are no selective pressures the other proteins would become deactivated as well.

Ok that is all fine and good, but I don't see how it addresses my question. I understand that a virus can infect a cell and alter its DNA, but I am looking for actual evidence that this viral insertion and common decent hypothesis has any validity whatsoever.

Would it be safe to say that the idea is that a gamete became infected by a virus, and was the benefactor of some kind of a phase shift or coding error that caused it to still be a viable gamete while still containing the infectious DNA?

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?

You could concluded that they don't exhibit the characteristics of being the result of random viral infections. IF we took the time we could come up with a large number of conclusions.

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.

Which indicates that these sequences are not from viral insertions. Viral insertions would exhibit quite different genomes. For instance; IF any individual in the line from the common ancestor could have had any number of different viral insertions we should still see numerous different distributions of these genetic sequences. You can't just take a snapshot from some common ancestor and freeze frame there and point out all the HERVs. IT seems reasonable if this process works that we should see any number of viral instances that would diverge groups of individuals showing more of a distribution of insertion points and sequences.

[NewCreature]

a discussion including quite a bit on retroviruses

http://www.twoorthree.net/2006/04/students_doubt_.html

[BGoodForGoodSake]

Would it be safe to say that the idea is that a gamete became infected by a virus, and was the benefactor of some kind of a phase shift or coding error that caused it to still be a viable gamete while still containing the infectious DNA?

This is correct the viral DNA did not make it into the host genome intact.

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.

What instance are you talking about, the only example I brought up is the one Byblos brought up.
It show how analysis can lead to the conclusion of multiple infection events.
This was determined because the insertion sites were disparate.
Is this the example you are talking about?

I have not yet provided an example of homologous ERV analysis, wanting to avoind the posibility of it being misunderstood, but here is one.

You could concluded that they don't exhibit the characteristics of being the result of random viral infections. IF we took the time we could come up with a large number of conclusions.

Come up with other alternative hypothesis, and we will examine each.

Which indicates that these sequences are not from viral insertions.

How so? Why does the fact that it is not random among multiple individuals indicate that it is not a viral infection?
Is there a fundamental problem with the theories behind inheretance?
I think you need to provide further explanation.

Viral insertions would exhibit quite different genomes. For instance; IF any individual in the line from the common ancestor could have had any number of different viral insertions we should still see numerous different distributions of these genetic sequences. You can't just take a snapshot from some common ancestor and freeze frame there and point out all the HERVs. IT seems reasonable if this process works that we should see any number of viral instances that would diverge groups of individuals showing more of a distribution of insertion points and sequences.

I don't think I completely understand what you are trying to say here.
If you could restate it more clearly I would appreciate it.

It would seem you are trying to say that descendants should display different genetic sequences. If this is the case I would agree. And the more time goes on the genetic seqiences should vary more.

Not sure what your point is with the snapshot.
What process are you speaking of?
I'm sorry this is very frustrating can you send me a private message elaborating what you are trying to say here.
I don't understand what you are trying to say.

[godslanguage]

Since the topic revolves around common ancestry, here is a few words from an article regarding common descent:


"The presented examples challenge the idea that alignment of mutations is compelling evidence of common descent at the molecular level. Rather, shared mutations may be the result of common mechanisms. Up to 50 percent of all mutations of homologous DNA sequences of distinct species may line up due to such mechanisms and create a genetic mirage — the illusion of common descent. How these mechanisms operate is not yet
understood, but the elucidation poses an excellent challenge for the scientific community concerned with alignment of mutations. In the meantime, the principle of Occam's razor— also known as the principle of parsimony — dictates that scientific explanations must be simple; they should not contain unnecessary assumptions. The simplest explanation for
shared mutations between humans and the great apes is not common descent, but rather a common mechanism that introduced the mutations on the same spot in the DNA sequence. Non-random mutations may not only explain alignment of mutations, they could also be the basis to understand linkage disequilibrium, convergent evolution and
the recent observation that selection appears not to act on genes with a high mutation rate"


To elaborate briefly here, for example, Ford and Mercedes both manufacture automobiles, they use very "common" mechanisms and some vary based on design principles such as machinery, people and technology (computers, robots etc...). In no way is ford and mercedes related to each other, they may indeed use some of the same machinery, but the design principles and finished product vary extensively.
To go further, lets say you take apart an engine from a ford and a mercedes, lay it out on a table and have a automotive expert look at each of the parts, an automotive expert determined that most of the parts were very similar and in some instances felt there was completely no differance, however, this is not the case. This is not to say that the originating "function" and the mechanics of the automobile is differant, both cars in essence have the same function, but they are entirely differant at the same time. Though the concept or idea of the car was invented at one point, Ford and Mercedes have no relation to one another (this is theorectically speaking since I am clueless whether Ford has any relation to Mercedes, if not Mercedes and Ford, replace with Honda and Ford).

[NewCreature]

Sorry for not being clear.

What I am saying is that from what we now know viral insertions appear to happen at quite random points, and with varied sequences. Since these "HERVs" don't appear to follow the pattern of viral activity that we observe it seems that a likely conclusion is that these sequences are not viral in origin.

I would also add that there is some evidence in the literature that some viruses may "prefer" particular insertion points. Nevertheless many of these HERVs seem to run contrary to what we see for the distribution of viral insertions in the genome.

[BGoodForGoodSake]

Sorry for not being clear.

What I am saying is that from what we now know viral insertions appear to happen at quite random points, and with varied sequences. Since these "HERVs" don't appear to follow the pattern of viral activity that we observe it seems that a likely conclusion is that these sequences are not viral in origin.

Explain your reasoning, start with your assumptions and show clearly how you reached this conclusion. It may help to clearly answer the following questions.
1. How do HERV's not appear to follow the pattern of viral activity? It's not at all clear how you can possibly make this statement.
2. Are you confusing HERV's with homologous ERV's? HERV are human endogenous retrovirus. They are not all found interspecially, so why change the topic?
3. What is the expected pattern? Lay out your reasoning and I can help you to determine an expected pattern.

I would also add that there is some evidence in the literature that some viruses may "prefer" particular insertion points. Nevertheless many of these HERVs seem to run contrary to what we see for the distribution of viral insertions in the genome.

How? On what basis are you making this statement?
No offense but from my knowledge of ERV's these statements seem completely baseless, so I would like an explanation based on facts.

Also why did the conversation turn to HERV's? Are we confusing subjects here?

[BGoodForGoodSake]

Since the topic revolves around common ancestry, here is a few words from an article regarding common descent:

"The presented examples challenge the idea that alignment of mutations is compelling evidence of common descent at the molecular level. Rather, shared mutations may be the result of common mechanisms. Up to 50 percent of all mutations of homologous DNA sequences of distinct species may line up due to such mechanisms and create a genetic mirage — the illusion of common descent. How these mechanisms operate is not yet
understood, but the elucidation poses an excellent challenge for the scientific community concerned with alignment of mutations.

The presumed mechanism is natural selection, but now this thread is going way off topic.

In the meantime, the principle of Occam's razor— also known as the principle of parsimony — dictates that scientific explanations must be simple; they should not contain unnecessary assumptions. The simplest explanation for
shared mutations between humans and the great apes is not common descent, but rather a common mechanism that introduced the mutations on the same spot in the DNA sequence.

How is this the simplest conclusion? Occam's razor would not lead to this conclusion, the mechanism you speak of hasn't even been demonstrated. Occam's razor cannot ever point to a phantom mechanism.

Non-random mutations may not only explain alignment of mutations, they could also be the basis to understand linkage disequilibrium, convergent evolution and
the recent observation that selection appears not to act on genes with a high mutation rate"

Again what mechanism cause non-random mutations?!? This has never been observed, so how can it be presented as a posibility? This is story-telling, it is not science.
Mutations may be random but selection is not. Just like engineering, test-results drive development. Prototypes to product, selection drives development. The only difference is that in engineering there is also a mechanism for targeted change.

To elaborate briefly here, for example, Ford and Mercedes both manufacture automobiles, they use very "common" mechanisms and some vary based on design principles such as machinery, people and technology (computers, robots etc...). In no way is ford and mercedes related to each other, they may indeed use some of the same machinery, but the design principles and finished product vary extensively.

Completely disagree, no matter what two companies you choose all car manufactures benefit from the initial invention of the combustion engine. All developments stem from that. The fact that they do not have the biological restrictions to be fully functional at each iteration does not change the fact that the blueprint was passed from one to the other. DNA is natures blueprint.

DNA acts like a set of molds from which the parts are created. The only analogy in our technology to this are the ideas themselves. And I can guarantee that the idea for combustion engines came from that initial development.

Actually I can think of a better analogy, die casts for minting coins. But the problem here is that the die cast cannot be modified. Unlike DNA.

[godslanguage]

The link to the "entire" article is here, that was only part of it:

http://www.iscid.org/papers/Borger_Shar ... 061506.pdf


That "presumed" mechanism, natural selection, does not work.

[NewCreature]

I don't think it would be wise to start with my assumptions to show my conclusions that would be quite circular. What shall I say I assume this to be true so I will conlude this. Sort of silly. I agree lets just stick to the facts.

While it was once thought that insertion points were quite random viruses show insertion site preference. A lot has been studied about this in particular with HIV.

This fact could easily account for viable hosts showing the same viral fragments in the preferred insertion sites. Now I don't have time to do your research on this, but if you like I am sure you can frind lots of information on human virus insertion site preference.

Some scientists are coming to the conclusion that numerous repeats of viral fragments is actually the virus searching for the best insertion point.

I am not seeking to prove any particular thing, I am just doubting the conventional wisdom on HERVs. The idea of a few bits of this DNA proving common decent is quite silly to me. But I guess if people want something to be true bad enough they will see proofs all around them. Here is a reasoning that I think you can follow.

Viruses are increasingly being shown to NOT insert randomly

The human genome has about 30,000 of these virus like bits of code

The Chimp genome has about 30,000 of these virus like bits of code

They share about 7 of these bits of code.

The "viral" signature of chimps and humans is way over 99% different.

IT is likely that viruses with particular insertion point affinities may line up from time to time.

IT is also likely that since these bits of code do have use to the organisms that these shared bits could be designed.

I would think a major struggle for the conventional wisdom on ERVs and common decent would be to show how every individual got the genetic material of a single member of a breeding population. The breeding population should have bred out the individual not the individual breeding out the entire gene pool. Even the offspring of the common ancestor would not all have gotton the infected area. Perhaps the mate had the same insertion.

But perhaps you have started with your assumptions the way you encouraged me to. IF you do that you know you will even skew the results of a tiny segment of DNA as prooving that your assumptions are true.

[BGoodForGoodSake]

I don't think it would be wise to start with my assumptions to show my conclusions that would be quite circular. What shall I say I assume this to be true so I will conlude this. Sort of silly. I agree lets just stick to the facts.

While it was once thought that insertion points were quite random viruses show insertion site preference. A lot has been studied about this in particular with HIV.

Let us expand this fact. A retroviral insertion prefers certain base sequences. But of course a virus is not restricted to this, only more likely to insert here. The way you presented it in your posts you made it seem that the preference leads to few possible insertion sites.

This is not the case. Read on to find out why.

This fact could easily account for viable hosts showing the same viral fragments in the preferred insertion sites.

I asked for scientific assumptions because of statements such as this. It would appear you assumed that preffered sites would limit the number of possible insertion points to the point where this sort of statement can be made.
This is simply not the case. The chances of two disparate insertion events occurring at the same site AND THEN finding it's way into every individual in two separate species is highly unlikely.

Now I don't have time to do your research on this, but if you like I am sure you can frind lots of information on human virus insertion site preference.

Believe me I am aware of this topic. Again preference is based on structure at the integration sites, it could be anywhere along the genome. For example out of lets imagine 1 billion possible insertion points 10 million may be preferred. This is the sort of preference we are talking about here.

Think of this virus as a home hunter. His preference is a house painted blue, not 123 Flanders Ave. There are many many houses painted blue, and this man is not restricted to them, just three times more likely to select one.

Some scientists are coming to the conclusion that numerous repeats of viral fragments is actually the virus searching for the best insertion point.

Come again? Please point me to the source. I am not sure this statement retained the original content.

I am not seeking to prove any particular thing, I am just doubting the conventional wisdom on HERVs. The idea of a few bits of this DNA proving common decent is quite silly to me.

That is quite evident, and you are entitled to your opinion. Perhaps they don't point to common descent.

But I guess if people want something to be true bad enough they will see proofs all around them. Here is a reasoning that I think you can follow.

Viruses are increasingly being shown to NOT insert randomly.

Nothing is truly random, no one assumed this. Because the insertion is chemically based it is assumed that there could be a preference. But again preference is by structure of the host genome.
Not once has a virus been shown to insert into the same spot in the genome.

The human genome has about 30,000 of these virus like bits of code

The Chimp genome has about 30,000 of these virus like bits of code

They share about 7 of these bits of code.
The "viral" signature of chimps and humans is way over 99% different.

IT is likely that viruses with particular insertion point affinities may line up from time to time.

No, they share more than 7. They share 7 ERV's not shared by any other primate. That's where the number 7 came from.

Also why are you ignoring the patterns of differentiation in these shared bits?

If viral material is shared cross-species the sequences of more closely related species always are more similar than distantly related ones. Chimp sequences are always more similar to the Gorilla than that of the Orangutan at shared ERV's.

ERV's are never shared between Gorillas and Humans which are not also shared with Chimps and Humans.

Imagine we have a dozen philatelists. They each have quite large collections. However we observe some peculiarities.

Those with a rare German Stamp always have a rare French stamp.
Half of them have a rare Italian stamp. These men all have 50 or so stamps in common which no other collector has. In fact all similarities wrap nicely within each other.

Meaning that if collector A shares a stamp with collector B and not with Collector C, then collector A and C do not share a stamp which is also not found in Collector B's collection.

Collector A
1,2,3,4,5
Collector B
2,3,4,8
Collector C
2,3,7

Not
Collector A
1,2,3,4,7
Collector B
2,3,4,8
Collector C
2,3,7

Something strange is going on with these stamp collectors.

IT is also likely that since these bits of code do have use to the organisms that these shared bits could be designed.

This is not a fact. Based on what can you make this conclusion?

I would think a major struggle for the conventional wisdom on ERVs and common decent would be to show how every individual got the genetic material of a single member of a breeding population.

Read the conversations I have had with Byblos in this same thread.

The breeding population should have bred out the individual not the individual breeding out the entire gene pool.

Another assumption. The experiments, mathematics and theories do not support this assumption. Actually I don't know where this idea came from.

Let us assume you are correct.
Any different trait will be removed from the gene pool.
Over time a population will consist of genetic clones.
If this were true then every individual would be a clone of the next identical in every way.

A quick look at the natural world, and this is falsified immediately.

Even the offspring of the common ancestor would not all have gotton the infected area. Perhaps the mate had the same insertion.

Impossible, or close to it. And unecessary, refer to the Byblos conversation. Both mates do not need to share the same insertion for an offspring to have the ERV.

But perhaps you have started with your assumptions the way you encouraged me to. IF you do that you know you will even skew the results of a tiny segment of DNA as prooving that your assumptions are true.

No, I am only presenting facts.

The only thing I am doing here is cleaning up the mess. People skew the facts to fit their assumptions.

I haven't even stated that common descent is what I beleive. Only that the facts being presented here are sometimes not facts at all.