Endogenous retroviruses

[mark kennedy]

I don't think that refutation is possible. Consider that the evidence of ERV's for common ancestry merely relies upon them being found in the same location in some species, and the same location without the virus in others.

With highly transposable elements this is not only possible it should be expected that sections would be identical. You have no idea how many of these things are littered throughout the genome do you?

If we merely consider the Lebedev et. al. 2000 paper (which is discussed at talkorigins.org here), we see 14 ERV's that are shown in the figure that are consistent with the phylogenic tree, and not one that was inconsistent.

These are all fragments, you are talking about sequences that are a few thousand nucleotides long and riddled with inversions, deletions, insertions and single nucleotide substitutions. If you want me to consider one of the papers he is baseing this statement on I will be happy to take a look. If on the other hand you want to ignore the actual scientific research in this area of study I don't know what to tell you.

Imagine, just for a moment, that there is no common descent, that all of these are merely coincidental germline infections. Now, we're only going to look at ERV's that are found in the human genome, and as such consistency with the phylogenic tree requires that each ERV only fits one of the following possibilities:
1. Human-only.
2. Human and chimp only.
3. Human, chimp, and gorilla only.
4. Human, chimp, gorilla, and orangutan only.
5. Human, chimp, gorilla, orangutan, and old world monkey only.
6. All 6 species.

I am going to need specific ERVs because generalities don't do a whole lot for me. What is more, you are working from the assumption that transposable elements make good phenotypic markers when mitocondira is questionable.

So if there is to be consistency with the phylogenic tree, each ERV must only be among the above possibilities. However, if we are to assume that these are merely coincidences, then there should be no correlation with the phylogenic tree, and thus all possible commonalities are equally likely. So, let's get to counting how many possible coincidental configurations there are:

Just one ERV: Human only (one possibility, as above)
Two ERV's: 5 possibilities (one for each non-human species)
Three ERV's: 10 possibilities
Four ERV's: 10 possibilities
Five ERV's: 5 possibilities
Six ERV's: 1 possibility
Total: 32 possible configurations.

Thus the probability that any one ERV will be consistent with the phylogenic tree is 6/32. The probability that all 14 ERV's are consistent with the phylogenic tree as inferred by other means would be (6/32)^14 = 6.6*10^-11 (that's 0.0000000066%).

There is thus no possible way that these are merely coincidental germline infections. And you may notice that nowhere in this argument did I even bother to worry about how likely such coincidental germline infections would be.

You still have no idea just how fragmentary these sections are but I think I can help you out with that. You must have missed this but that's ok, I don't mind posting it again. Let's take a little walk through some of the facts because those trees are based on fragments:

"The genomes of vertebrate species contain dozens to thousands of ERV sequences, some of which were acquired in evolutionarily recent times, whereas others derive from "ancient" times, as indicated by their identical site of integration in more than one species . Typically, ancient proviruses have sustained numerous point mutations, deletions, and insertions, rendering them incapable of expressing virus." (Constructing primate phylogenies from ancient retrovirus sequences, PNAS Vol. 96, Issue 18, 10254-10260, August 31, 1999)​

Look at the date, in 1999 these had rarely been used to construct phylogenies and after the HGP published their intitial sequence these papers suddenly stopped making sweeping statements about ERVs. Frankly, I am not entirely convinced they are the result of viruses either anymore then I am that 97% of the genome doesn't do anything.

These ERVs make up something like 8% of the human genome, if you look at enough of them you will find sequences like the LTRs a couple of thousand nucleotides that line up, big hairy deal. The HERV K is still active in the human genome and isn't even fixed yet. I find this all very interesting but only because the fascination with them is unwarranted. It is another example of fragmentary evidence passing for conclusive proof.

Don't you realize that these are highly transposable elements?

"The taxonomy of HERVs is still a source of confusion. The preferred systematic nomenclature uses the amino acid specificity of the tRNA that hybridizes to the primer-binding site. The name is defined by adding its one-letter code as a suffix to the acronym HERV (13). HERV-K, for example, uses a lysine-specific tRNA as primer for the initiation of the reverse transcription reaction. The limitations of this approach include the fact that very distantly related viruses use the same tRNAs, and that incomplete information about this short region due to deletions or mutations make classification of these retroviral sequences almost impossible. In addition, many HERV proviruses have been given arbitrary laboratory names or extensions"​

So the taxonomy of HERVs is confusing, incomplete information due to mutations make classification almost impossible and laboratory names are given arbitrarily. That sure sounds like a typical line of evidence of the single common ancestor apologists I have come to know and love.

Classification of transposable elements.

"The HERV-K113 provirus, located on chromosome 19p13.11, is not completely fixed in the human population. Genotyping of a small number of genetically diverse individuals has shown an overall allelic frequency of 19%, and the allelic prevalence seems to depend on ethnic origin. Whereas the provirus is rare in Caucasians, it is more abundant in African, Asian, and Polynesian populations."​

This one has an allelic prevelance of 19%, it's rare in caucasians and more common in other ethnic groups. I bring this up to emphasis what you are all missing, they are highly transposable and this one isn't even fixed.

"Endogenous retroviruses have proven to be especially instrumental for investigating the evolutionary separation of humans from other African great apes because some of the proviral loci appear only in distinct ape species, whereas others are exclusively human (12). However, care must be taken in the interpretation or generalization of single findings. Scenarios such as allelic segregation or loss of the proviral locus must be taken into account "

(Retroelements and the human genome: New perspectives on an old relation, PNAS October 5, 2004)​

 

[Chalnoth]

You still have no idea just how fragmentary these sections are but I think I can help you out with that.

That doesn't matter for the argument, though. Not one bit. What I posted was a maximum probability that one could possibly expect to find 14 ERV's that are all homologous in some species, and have the same DNA sections with missing ERV's in others, while remaining consistent with the phylogenic tree.

Consider that for this argument, I didn't bother to consider that the probability of having two species randomly obtaining ERV's independently at the same location was any different from the probability of three species randomly obtaining the same ERV's independently at the same location.

If you were to consider this more carefully, then, you'd go ahead and add in that probability. By any estimation, the probability of the same ERV being found at the same location due to two separate insertion events would be absolutely miniscule. The probability of finding three separate insertion events at the same location would square that probability, and so on, making it absurdly unlikely that we would ever find the same ERV existing in six separate species from completely independent insertion events.

But, just for argument, if we say that it is highly probable that the insertion events will independently occur at the same location with the same virus, we arrive at the probability estimation that I did in the previous post, which does nothing more than take the assumption that if there is no common ancestry, there should be no correlation between ERV insertions and what those studying evolution believe the family tree of these monkeys to be (if common ancestry isn't true, then how can ERV's trace something that doesn't exist?).

The only thing that this estimation relies upon is that the researchers in question didn't overlook any ERV's that failed to follow the phylogenic tree. Since no further research has found any ERV's that conflict with the phylogenic tree, the evidence is basically conclusive. After all, just this one single paper gives you a maximum probability of no common ancestry of about 0.0000000066%. What do you think would happen if we added more research to the probability estimate? Considering that no ERV's that are inconsistent with the phylogenic tree have been found?

Note: Yes, there are some that at first appeared they may have conflicted with the phylogenic tree, but upon further analysis it was obvious that there was no problem, as the ERV's in question ether existed in different parts of the genome, or existed in a portion of the genome that was deleted in some species).

 

[mark kennedy]

That doesn't matter for the argument, though. Not one bit. What I posted was a maximum probability that one could possibly expect to find 14 ERV's that are all homologous in some species, and have the same DNA sections with missing ERV's in others, while remaining consistent with the phylogenic tree.

Yes it does matter, highly transposable elements are altogether unreliable. The taxonomy of HERVs is still a source of confusion, incomplete information due to mutations make classification almost impossible and laboratory names are given arbitrarily. Now when you can actually identify specific ERVs and show me where they are and what the nucleotide sequence is we might have something here. It's all fragmentary evidence and sweeping generalities based on statistics misleading you down a blind alley in the dark.

Consider that for this argument, I didn't bother to consider that the probability of having two species randomly obtaining ERV's independently at the same location was any different from the probability of three species randomly obtaining the same ERV's independently at the same location.

We still have not identified the location or the sequence. We also know that ERVs are different for different ethnic groups of humans, some that are common in one group is rare in another. How do you explain that?

If you were to consider this more carefully, then, you'd go ahead and add in that probability. By any estimation, the probability of the same ERV being found at the same location due to two separate insertion events would be absolutely miniscule. The probability of finding three separate insertion events at the same location would square that probability, and so on, making it absurdly unlikely that we would ever find the same ERV existing in six separate species from completely independent insertion events.

The DNA between chimpanzees and humans is going to be around 95% irregardless so the probability argument is ridiculas anyway. This is fragmentary evidence at best and transposable elements are a bizzare source for evidence of somthing that supposedly happened millions of years ago.

Look, if you want to talk about the actual evidence I will but you are basing a statistical arguement on too many assumptions. Find an ERV, its location and the sequence, otherwise you are just argueing in circles.

 

[Chalnoth]

Yes it does matter, highly transposable elements are altogether unreliable.

If the elements that were measured were highly transposable, then you'd never expect them to appear in organisms in a manner consistent with the phylogenic tree. You'd expect them to be highly randomized.

If the elements that were measured were highly transposable, so much so that there was just as much probability of two species having independent insertions in the same location as three species (which is impossible, but dealing with this more rigorously would be arbitrary and would only worsen your position), then we arrive at a random chance of 14 ERV's all being, just by random chance, consistent with the phylogenic tree at 0.0000000066%.

For this calculation I have assumed three things:
1. The probability of independent insertions existing at the same location is extremely high.
2. The research group in question did not ignore any ERV's that were orthologous between different species that showed up in the chunks of DNA that they were looking at (i.e. they weren't liars).
3. If there was no common descent, then there would be no reason to expect consistency with the phylogenic tree.

Assumption one is going to be incorrect no matter what you think about how retransposable these elements are, but using this assumption provides a best-case probability for your position, and applying some probability to independent insertions existing at the same location would be arbitrary and not needed for the result. So assumption one is just there to make the calculation easy, and breaking assumption one does nothing but make things worse for your position.

Assumption two goes completely and utterly against the culture of science, as things that are 'wierd' are exciting discoveries, not things to be swept under the rug. But even if assumption two is wrong, we can check it by considering the work of other geneticists. I know you've been looking, and have yet to find a single instance of an ERV that was not consistent with the phylogenic tree.

Assumption three also is no problem, because a solid hierarchy of common infectability is every bit as strong as evidence of common ancestry as just genetic markers of common ancestry.

Edit: As far as I know, though, common infectability is conclusively ruled out by our knowledge of today's viruses: common infectability would be more related to close proximity of the species than genetic similarities.

 

[shernren]

We still have not identified the location or the sequence. We also know that ERVs are different for different ethnic groups of humans, some that are common in one group is rare in another. How do you explain that?

Firstly, your cited sources have shown at most 2 varieties of HERV-K being highly variable among humans. Not only is this argument non-generalizable (as there is no intrinsic reason given for HERVs to be highly variable), it also capitalizes on the fact that HERV-K is the most recently integrated, least mutated, and most active HERV in the genome and therefore we should not be surprised by its variability. Saying that HERV-K is variable hence ERVs are different for different ethnic groups of humans is a little like saying Kent Hovind dislikes the IRS therefore all creationists are felons.

Secondly, we have location and sequence data for at least one ERV which you have not addressed despite repeated quotings:

Unique cellular flanking-sequence probes (Fig. 1) have
been used to locate individual proviral genomes to human
chromosomes 1 and 5 and to detect unique integration sites
(13). A single 7.3-kbp fragment generated by double digestion
with EcoRI-XhoI hybridized to both the HLM-2 gag
region and the 5' unique cellular flanking-sequence probes
(Fig. 1 and SA). As in the transfectant and the human (Fig.
5A and B, lanes 1 and 2, respectively), common chimpanzee
and gorilla DNAs showed the single 7.3-kbp EcoRI-XhoI
fragment when the HLM-2 5'-flanking probe was used (Fig.
5B, lanes 3 and 4). This suggests that the genomic DNAs of
the two African apes contain the HLM-2 proviral genome at
the same site as does the human genomic DNA. Although
EcoRI-XhoI digests of orangutan DNAs resolved a 7.3-kbp
fragment, additional low-molecular-weight bands appeared
(Fig. 5B, lane 5). In contrast to those of the three large apes,
DNAs from the lesser ape lar gibbon did not cross-hybridize
to the HLM-2 gag probe (Fig. 4D) or to the HLM-2 5' unique
cellular flanking-sequence probe (data not shown) at high
stringency. This is consistent with the lack of characteristic
HLM-2 proviral internal fragments, e.g., env (Fig. 4A and B)
and pol (data not shown), and suggests that, although lar
gibbon DNA has HERVII-related sequences, it does not
contain the HLM-2 proviral genome.
The presence of the HLM-2 provirus in large apes and
humans corresponds to their phylogenetic relationships instead
of their current geographic distribution (8, 11, 12, 14,
20, 21, 25). The observed hybridization patterns suggest
either that the human HLM-2 proviral genome was inherited
from a common ancestor of all the extant large hominoids
after the divergence of the lesser ape lineage (11) or that this
region of the lar gibbon genome was lost subsequent to the
divergence of lar gibbons from large hominoids. We favor
the former possibility, since the restriction patterns of HLM-
2 proviral env, gag, and flanking sequences are consistent
with the evolutionary branching order of orangutans, African
apes, and humans (11, 21). This issue should be resolved
with studies using additional cellular DNA probes flanking
the HLM-2 provirus or other HERVII proviral genomes. In
this regard, another human endogenous proviral genome,
ERV-1, which is unrelated to the HERVII family, is known
to have entered the human germ line prior to the chimpanzee-
human branch point (3).
The possibility that the HERVII family of endogenous
retrovirus sequences entered the catarrhine lineage via an
ancient infection is suggested by the following observations:
the presence of all the HERVII internal sequences in all the
species of Old World simian primates tested, the similarity of
HLM-2 proviral patterns in humans and large apes, and the
absence of HERVII structural sequences in New World
monkeys. A HERVII infection of early catarrhines would
therefore have occurred after the geographic separation
between the Old and the New World anthropoid lineages,
i.e., approximately 40 million years ago (7, 9-11) but before
the evolutionary radiation and geographic dispersal (outside
Africa) of the ancestors of the extent large hominoids
(estimated at 17 million years ago) (1, 2, 19, 24).

 

[mark kennedy]

If the elements that were measured were highly transposable, then you'd never expect them to appear in organisms in a manner consistent with the phylogenic tree. You'd expect them to be highly randomized.

They are, even in the ones humans share. You act like it is such an incredible thing that there would be a sequence a couple of thousand nucleotides long, in transposable elements, that have the same sequence. Newsflash! 95% of the two genomes are the same the incredible thing is the 145,000,000. Once again I will tell you the problems with ERVs as phenotype markers, try to pay attention this time:

[updown] Most proviruses have been the subject of numerous amplifications and have suffered extensive deletions and mutations.

Retroelements constitute 90% of the 3 million transposable elements present in the human genome.

The taxonomy of HERVs is still a source of confusion.

Incomplete information about this short region due to deletions or mutations make classification of these retroviral sequences almost impossible.

Many HERV proviruses have been given arbitrary laboratory names or extensions.

Genotyping of a small number of genetically diverse individuals has shown an overall allelic frequency of 19%, and the allelic prevalence seems to depend on ethnic origin.
[/updown]

The recombination mechanisms that could replace integrated proviruses, their probability, as well as the population dynamics of retroelements and other mobile elements are largely unknown. The advent of genome sequencing together with highly sophisticated statistical and phylogenetic tools will help to prove or lay to rest some of the present theories concerning forces and mechanisms of dispersion, fixation, maintenance, and clearance of endogenous retroviral sequences. (Retroelements and the human genome: New perspectives on an old relation, PNAS October 5, 2004)​

If the elements that were measured were highly transposable, so much so that there was just as much probability of two species having independent insertions in the same location as three species (which is impossible, but dealing with this more rigorously would be arbitrary and would only worsen your position), then we arrive at a random chance of 14 ERV's all being, just by random chance, consistent with the phylogenic tree at 0.0000000066%.

Still hung up on the Talk Origins propaganda I see. You still have no idea how confused and random these kind of taxonomic catagories of ERVs are. You still don't want to read the actual scientific literature. You just give me some statistics based on ERVs that you cannot identify, locate or characterize.

For this calculation I have assumed three things:
1. The probability of independent insertions existing at the same location is extremely high.

Your first assumption was that they were the result of germline invasions. You do know what a germline invasion is don't you?

2. The research group in question did not ignore any ERV's that were orthologous between different species that showed up in the chunks of DNA that they were looking at (i.e. they weren't liars).

Then you should have no trouble telling me which ones they looked at and where we can find them on the Hapmap.

3. If there was no common descent, then there would be no reason to expect consistency with the phylogenic tree.

You really want to make a taxonomic tree using transposable elements when the taxonomy of HERVs is still a source of confusion. You have got to be putting me on.

Assumption one is going to be incorrect no matter what you think about how retransposable these elements are, but using this assumption provides a best-case probability for your position, and applying some probability to independent insertions existing at the same location would be arbitrary and not needed for the result. So assumption one is just there to make the calculation easy, and breaking assumption one does nothing but make things worse for your position.

I am assuming nothing, these ERVs are highly transposable and the sequences you claim as proof are only a few thousand nucleotides long. Find something specific because I know how these proviruses have been characterized by the researchers that actually study them. They have not been saying what you are since the completion of the HGP.

Assumption two goes completely and utterly against the culture of science, as things that are 'wierd' are exciting discoveries, not things to be swept under the rug. But even if assumption two is wrong, we can check it by considering the work of other geneticists. I know you've been looking, and have yet to find a single instance of an ERV that was not consistent with the phylogenic tree.

Find a specific ERV and we can talk. I will need the taxonomic name, location on both genomes and the nucleotide sequence. Other then that I have read the research and none of them are using them for taxonomic catagorizations.

Assumption three also is no problem, because a solid hierarchy of common infectability is every bit as strong as evidence of common ancestry as just genetic markers of common ancestry.

You are arguing in circles around an a priori assumption of a common ancestor, that is the only assumption at work here. Read the actual literature and try to get this Talk Origins nonesense out of your system.

Edit: As far as I know, though, common infectability is conclusively ruled out by our knowledge of today's viruses: common infectability would be more related to close proximity of the species than genetic similarities.

I am far from convinced that these ERVs are the result of viruses that happens 300 ka to 30 mya, that is the biggest assumption of all in these highly speculative scenerios. I am far from convinced that the sequences actually looked at show anything more then what we allready know, the DNA is very simular between chimpanzees and humans but the differences are not accounted for given the observed mutation rate.

You keep rehashing the same arguement and it keeps coming down to the actual ERVs and you have not even named one particular ERV, given me the location or suggested the nucleotide sequence.

 

[shernren]

Still hung up on the Talk Origins propaganda I see. You still have no idea how confused and random these kind of taxonomic catagories of ERVs are. You still don't want to read the actual scientific literature. You just give me some statistics based on ERVs that you cannot identify, locate or characterize.

Please supply a scientific paper where a cladistic analysis using ERVs was invalidated due to the ERVs in question being incorrectly identified due to arbitrary naming or confusing taxonomy. Otherwise this ends up being nothing more than a confusing conspiracy theory argument.

When I was Form 5 two years ago Mendelian laws of inheritance seemed confused, random, and arbitrary to all my classmates. Didn't stop them from being true.

 

[mark kennedy]

Firstly, your cited sources have shown at most 2 varieties of HERV-K being highly variable among humans. Not only is this argument non-generalizable (as there is no intrinsic reason given for HERVs to be highly variable), it also capitalizes on the fact that HERV-K is the most recently integrated, least mutated, and most active HERV in the genome and therefore we should not be surprised by its variability.

First of all, all ERVs are transposable elements and the older they are the more fragmentary. This is not my opinion its a known fact. This is nothing more then a homology arguement, if it's the same it's due to a common ancestor if it different it's due to natural selection. This just goes in circles endlessly and begging the question of proof is not scientific, it's a logical fallacy.

Secondly, we have location and sequence data for at least one ERV which you have not addressed despite repeated quotings:

You cut and pasted the quote from a PDF file and didn't even bother to take the time to edit out the formating. You just cut, pasted and bolded what told you what you wanted to hear. You didn't even bother to cite the source or include quotation marks. This is nothing more then quote mining without the slightest exposition of the actual scientific observations.

Why don't you try something current and characterize ERVs before you pontificate about them. The researchers certainly do, at least when they are preparing a publication.

The recombination mechanisms that could replace integrated proviruses, their probability, as well as the population dynamics of retroelements and other mobile elements are largely unknown. The advent of genome sequencing together with highly sophisticated statistical and phylogenetic tools will help to prove or lay to rest some of the present theories concerning forces and mechanisms of dispersion, fixation, maintenance, and clearance of endogenous retroviral sequences. (Retroelements and the human genome: New perspectives on an old relation, PNAS October 5, 2004)​

Saying that HERV-K is variable hence ERVs are different for different ethnic groups of humans is a little like saying Kent Hovind dislikes the IRS therefore all creationists are felons.

HERV-K elements are common in some ethnic groups and rare in others, that is what I said. I don't know anything about Kent Hovinid and I don't care anything about Kent Hovinid. I don't know what you think you just said in that last line but it didn't make a lick of sense. I can only assume you are making statements at random because you don't want to actually look at the issues involved.

 

[mark kennedy]

Please supply a scientific paper where a cladistic analysis using ERVs was invalidated due to the ERVs in question being incorrectly identified due to arbitrary naming or confusing taxonomy. Otherwise this ends up being nothing more than a confusing conspiracy theory argument.

When I was Form 5 two years ago Mendelian laws of inheritance seemed confused, random, and arbitrary to all my classmates. Didn't stop them from being true.

First of all ERVs are Transposable Elements, you need to understand that first.

Classification of transposable elements.

"Retroelements constitute 90% of the 3 million transposable elements present in the human genome...The taxonomy of HERVs is still a source of confusion...In addition, many HERV proviruses have been given arbitrary laboratory names or extensions...The recombination mechanisms that could replace integrated proviruses, their probability, as well as the population dynamics of retroelements and other mobile elements are largely unknown. The advent of genome sequencing together with highly sophisticated statistical and phylogenetic tools will help to prove or lay to rest some of the present theories concerning forces and mechanisms of dispersion, fixation, maintenance, and clearance of endogenous retroviral sequences.
(Retroelements and the human genome: New perspectives on an old relation, PNAS October 5, 2004 available online)

You are right that Mendelian laws of inheritance are not random, Mendel laid the foundation for genuine scientific laws while this Darwinian common ancestor is a modern mythology. You can argue from the facts, you can argue around the facts as far as I am concerned you can argue against the facts but get the facts straight or you don't have an arguement at all.

Grace to you and peace, through our Lord and Saviour, Jesus Christ,
Mark

 

[Chalnoth]

Not all ERV's are transposable elements. Most transposable elements are ERV's, but the converse is not necessarily the case.

But, as I've been stating, it does not matter how transposable they may or may not be for my argument.

 

[shernren]

You cut and pasted the quote from a PDF file and didn't even bother to take the time to edit out the formating. You just cut, pasted and bolded what told you what you wanted to hear. You didn't even bother to cite the source or include quotation marks. This is nothing more then quote mining without the slightest exposition of the actual scientific observations.

You're right that I didn't include the citation. Having said that, I included citation not once but twice on your ERV thread and as a result the quote was summarily ignored, here at least I got some response. Source: http://www.pubmedcentral.nih.gov/art...bmedid=2507793 ... everything I bolded was said by them, and if you think you can find anything in the context that significantly modifies it, be my guest.

Why don't you try something current and characterize ERVs before you pontificate about them. The researchers certainly do, at least when they are preparing a publication.

The recombination mechanisms that could replace integrated proviruses, their probability, as well as the population dynamics of retroelements and other mobile elements are largely unknown. The advent of genome sequencing together with highly sophisticated statistical and phylogenetic tools will help to prove or lay to rest some of the present theories concerning forces and mechanisms of dispersion, fixation, maintenance, and clearance of endogenous retroviral sequences. (Retroelements and the human genome: New perspectives on an old relation, PNAS October 5, 2004)​

Speak of the pot calling the kettle black, I don't know how you missed this:

No current transposition activity of HERVs or endogenization of human exogenous retroviruses has been documented so far. Although unlikely, the continuation of such events in our species cannot be completely excluded per se, because examples of probable ongoing endogenization processes are known from other mammals. For example, mouse mammary tumor virus (MMTV) and murine leukemia viruses in mice, Jaagsiekte sheep retrovirus (JSRV) in sheep, porcine endogenous retroviruses (PERV) in pigs, avian leukemia viruses (ALV) in chicken, and feline leukemia virus (FeLV) in cats have presently both endogenous and exogenous strains (11). Moreover, several of the known class II HERV-K proviruses are human specific and a few loci are polymorphic, indicating very recent activity in evolutionary terms (7, 12).

Researchers know what transposition looks like, have observed it occurring in other species, and have verified to a high probability that none of it is happening to HERVs. Even if some HERVs are transposing, can you say that all the HERVs used to mark phylogenetics clades have magically and simultaneously transposed in both humans and apes to miraculously coincide?

HERV-K elements are common in some ethnic groups and rare in others, that is what I said.

This is what you said: We also know that ERVs are different for different ethnic groups of humans, some that are common in one group is rare in another. How do you explain that? You did not qualify that you only meant HERV-K elements. Can I take this as a concession that the issue of variability across ethnic lines does not occur with any HERVs besides HERV-K?

I don't know anything about Kent Hovinid and I don't care anything about Kent Hovinid. I don't know what you think you just said in that last line but it didn't make a lick of sense. I can only assume you are making statements at random because you don't want to actually look at the issues involved.

I shall never use a metaphor with you again, mark, it looks like the Bible isn't the only thing you take literally.

First of all ERVs are Transposable Elements, you need to understand that first.

Classification of transposable elements.

"Retroelements constitute 90% of the 3 million transposable elements present in the human genome...The taxonomy of HERVs is still a source of confusion...In addition, many HERV proviruses have been given arbitrary laboratory names or extensions...The recombination mechanisms that could replace integrated proviruses, their probability, as well as the population dynamics of retroelements and other mobile elements are largely unknown. The advent of genome sequencing together with highly sophisticated statistical and phylogenetic tools will help to prove or lay to rest some of the present theories concerning forces and mechanisms of dispersion, fixation, maintenance, and clearance of endogenous retroviral sequences.
(Retroelements and the human genome: New perspectives on an old relation, PNAS October 5, 2004 available online)

You miss out the full statement:

The integration process of a retroviral element per se is irreversible. A principal elimination of a provirus fixed in the genome of a population is not possible unless insert free alleles are recreated by recombination processes and intrachromosomal deletions (8). The most significant impacts on fixed retroviruses are exerted by recombination events. This is clearly demonstrated by a dramatic accumulation of class I and II elements on chromosome Y due to recombination deficits caused by its genomic singularity (64). The recombination mechanisms that could replace integrated proviruses, their probability, as well as the population dynamics of retroelements and other mobile elements are largely unknown. The advent of genome sequencing together with highly sophisticated statistical and phylogenetic tools will help to prove or lay to rest some of the present theories concerning forces and mechanisms of dispersion, fixation, maintenance, and clearance of endogenous retroviral sequences.

Clearly the researchers intended to convey that absence of a retroviral element is strong evidence of its never being inserted into a genome, and that the hypothesis that a virus was integrated but then fully removed is farfetched. How does that help you?

(all emphases added)

 

[mark kennedy]

You're right that I didn't include the citation. Having said that, I included citation not once but twice on your ERV thread and as a result the quote was summarily ignored, here at least I got some response. Source: http://www.pubmedcentral.nih.gov/art...bmedid=2507793 ... everything I bolded was said by them, and if you think you can find anything in the context that significantly modifies it, be my guest.

It's not like I haven't read it, its just that you cut and pasted it with such disregard. At this point I am not entirely sure you understand what an ERV is because what is being published about them is very different now then it was before the HGP. You are showing all the signs of quote miners syndrome, I don't know that you have full blown quote miners but you are definitly infected.

Speak of the pot calling the kettle black, I don't know how you missed this:

Oh brother, here you go again...

No current transposition activity of HERVs or endogenization of human exogenous retroviruses has been documented so far. Although unlikely, the continuation of such events in our species cannot be completely excluded per se, because examples of probable ongoing endogenization processes are known from other mammals. For example, mouse mammary tumor virus (MMTV) and murine leukemia viruses in mice, Jaagsiekte sheep retrovirus (JSRV) in sheep, porcine endogenous retroviruses (PERV) in pigs, avian leukemia viruses (ALV) in chicken, and feline leukemia virus (FeLV) in cats have presently both endogenous and exogenous strains (11). Moreover, several of the known class II HERV-K proviruses are human specific and a few loci are polymorphic, indicating very recent activity in evolutionary terms (7, 12).

Oh wait, I didn't realize that they were probable ongoing endogenization processes, that explains everything. That would in fact make them human specific, polymorphic and recently active, why didn't I see it before. I must have missed the point where you had got to the point of this.

Researchers know what transposition looks like, have observed it occurring in other species, and have verified to a high probability that none of it is happening to HERVs. Even if some HERVs are transposing, can you say that all the HERVs used to mark phylogenetics clades have magically and simultaneously transposed in both humans and apes to miraculously coincide?

They don't even coincide in human populations except for framents, those LTRs as they are called. They are only a couple of thousand nucleotides long and they prove absolutly nothing. They do underscore the evolutionists fascination with the obscure and highly cryptic verbage. No one really knows what ERVs are, how to classify them or what their signifigance, none of the researchers that study them that it. They defy taxonomic catagorization themselves by they are going to be used to determine our taxonomic history. Your on a wild goose chase.

This is what you said: We also know that ERVs are different for different ethnic groups of humans, some that are common in one group is rare in another. How do you explain that?

You have got to be putting me on, these are highly transposable elements, thats how I explain it.

You did not qualify that you only meant HERV-K elements. Can I take this as a concession that the issue of variability across ethnic lines does not occur with any HERVs besides HERV-K?

You can conclude no such thing, what it demonstrates is the transposable elements are not consistant even in recent ones. The older ones are riddled with deletions, frameshifts and polymorphisms. You are rumaging through framentary evidence making bold sweeping generalities about things you know nothing about.

I shall never use a metaphor with you again, mark, it looks like the Bible isn't the only thing you take literally.

Trust me when I tell you, you don't want to go there with me.

That does it for me, you have been arugeing this in circles long enough. I'm ready to move on to something substantive. I don't usually fall for this kind of a diversionary tactic but I am looking for evolutionary mechanisms. At one point I was hopefull ERVs and alus might be involved with that but it didn't pan out.

I'm ready to move on, thanks for the quote mines but I'm no longer interested.

 

[Chalnoth]

Mark, you're failing to recognize that the existence of 14 ERV's consistent with the phylogenic tree, with the research group having found zero ERV's inconsistent, proves common ancestry to a certainty of 99.9999999934%. This is before even considering the possible mechanisms for randomizing the ERV's in the genome, which would do nothing more than make this more certain.

 

[Tomk80]

That does it for me, you have been arugeing this in circles long enough. I'm ready to move on to something substantive. I don't usually fall for this kind of a diversionary tactic but I am looking for evolutionary mechanisms. At one point I was hopefull ERVs and alus might be involved with that but it didn't pan out.

I'm ready to move on, thanks for the quote mines but I'm no longer interested.

After accusing others of dropping out of the discussion in the times' thread, this is the actual summit of hypocricy.

 

[mark kennedy]

After accusing others of dropping out of the discussion in the times' thread, this is the actual summit of hypocricy.

That's it!? All you have is a childish insult when the topic is ERVs? For one thing I'm immune to your venom and for another I know that an ad hominem approach to discussion on here is a logical fallacy. I allways know when it's time to move on to another topic when thats all the evolutionists on here have left.

Have a nice day

 

[mark kennedy]

Mark, you're failing to recognize that the existence of 14 ERV's consistent with the phylogenic tree, with the research group having found zero ERV's inconsistent, proves common ancestry to a certainty of 99.9999999934%. This is before even considering the possible mechanisms for randomizing the ERV's in the genome, which would do nothing more than make this more certain.

My sole interest in ERVs has been the fact that they are transposable elements and their effect on the functional and protein coding genes. I am not impressed with ID and creationist probability arguemtents about the origin of life nor am I concerned with the ones that have been invented as an arguement for common ancestry. I was a little puzzled that I couldn't find anything from creationists on the subject. After reading maybe half a dozen papers on the subject I'm convinced that virology is only speculating on how ERVs might be used in the future, nothing concrete is being used at this time.

The only mechanisms that really interest me are the ones that result in an adaptation. That's why I spend so much time pouring over these posts, every now and then I get a glimse of one. You have to wade through a lot of rethoric and bad manners but sooner of later you can find them.

 

[Chalnoth]

nor am I concerned with the ones that have been invented as an arguement for common ancestry.

Mark, I'm sorry that you don't understand probability. I was showing you that the probability of coincidence is just vasly too low. Thus the only possible way that you can explain these as not coming from common ancestry is to substitute another mechanism that would enforce a strict hierarchy of commonality between humans and chimps, then humans and chimps and gorillas, and so on on back.

So, Mark, do you have another mechanism that would enforce such a strict hierarchy of commonality?

 

[dad]

Mark, I'm sorry that you don't understand probability. I was showing you that the probability of coincidence is just vasly too low. Thus the only possible way that you can explain these as not coming from common ancestry is to substitute another mechanism that would enforce a strict hierarchy of commonality between humans and chimps, then humans and chimps and gorillas, and so on on back.

...

I suggest that breeding between species used to be possible, and that wicked pre flood people may have had offspring from the ape or monkey family.

 

[Chalnoth]

I suggest that breeding between species used to be possible, and that wicked pre flood people may have had offspring from the ape or monkey family.

Now that is a stretch, and it wouldn't explain the hierarchy of commonality.

 

[mark kennedy]

Mark, I'm sorry that you don't understand probability. I was showing you that the probability of coincidence is just vasly too low. Thus the only possible way that you can explain these as not coming from common ancestry is to substitute another mechanism that would enforce a strict hierarchy of commonality between humans and chimps, then humans and chimps and gorillas, and so on on back.

So, Mark, do you have another mechanism that would enforce such a strict hierarchy of commonality?

Yes I do, mitochondrial DNA:

"We then used two approaches to examine the validity of combining all of the data in a single analysis; comparative analysis of trees recovered from resampled data sets and the application of a randomization test. The results did not point to significant levels of heterogeneity in phylogenetic signal between the mitochondrial and nuclear data sets, and we therefore proceeded with a combined analysis."​

http://hydrodictyon.eeb.uconn.edu/systbiol/issues/48_2/48_2abstracts.html

Now go find out what happens when you compare the mtDNA of chimpanzees and humans.