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Another poor response to ERV evidence for common ancestry by a creationist.

Zaius137

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LoudMouth…


“In both cases, LTR sequences evolved in sequence independently from, and obviously more rapidly than, the proviral bodies. Reasons for apparently different evolutionary rates of LTRs and proviral bodies are currently not clear.”

From Blayz…
“This is the only valid observation you have made so far”.

Still no responses on this… want to toss in your two cents. There should be no reason for the lower mutation rates in proviral bodies except maybe they hold more importance than just being fossil infections.


Now your ~5% would be expected since your figure of ~5% chimp human variance (another argument altogether because I think it is higher) but where is all the other variances from the active retrovirus infection times.


Perhaps you could cite these figures instead of claiming that there is no change?


I did not claim ~5% Blayz did. There should be massive changes in the retrovirus which is not observed in the proposed infections of HERV-K because as I noted earlier the mutation/ evolution rate is enormous…

“Thus, oncogenes seem to exemplify a general feature of genome evolution: the rate of evolution of RNA genomes can be more than a million times greater than that of DNA genomes because of a high mutation rate in the RNA genome.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC397963/


How can you trivialize the lack of mutations in the retrovirus over long periods of time with a mutation rate hundreds of times if not thousands of times that of supposed evolution?


“You have not shown a lack of retroviral evolution,” and you have also ignored the effect of selection on the mutation rate. The lack of evolution is?


“Reasons for apparently different evolutionary rates (faster) of LTRs and proviral bodies are currently not clear.”

I guess not clear…

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC479102/?tool=pubmed




What about the outrageous time frames between those supposed infection times (Orders of millions of years) but only 10 families of HERV-Ks were identified. I really like your argument against evolution in the following..


Please cite any data showing that there should be more than 10 families.


“ Phylogenetic analysis of HERV reverse transcriptase sequences have identified 10 HERV-K families in the human genome which were termed human MMTV-like (HML-1 to HML-10) because of homologies to the betaretrovirus mouse mammary tumor virus (MMTV) (1, 32). Repbase Update also lists 10 HERV-K families.”

That is what has been found… You can explain why there should not be more than 10 families… And a retrovirus can have an evolution rate 1 million times faster than DNA.

Chimp human divergence time ~5 million years so retrovirus evolution time would be 5 million times 1 million ~ 5x10^12 years or about a thousand times the age of the universe according to the Big Bang. Again:

“Thus, oncogenes seem to exemplify a general feature of genome evolution: the rate of evolution of RNA genomes can be more than a million times greater than that of DNA genomes because of a high mutation rate in the RNA genome.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC397963/





Neither is the fairytale of evolution…
Ignoring the evidence is not helping your argument.

That’s right ignoring the evidence is a trait of evolutionists.

 
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Zaius137

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Look at what you are complaining about . . . Apes changed into another species; wait a minute that's not right the apes remained apes . . .

Humans are apes. Chimps are apes. Their common ancestor was an ape. So where is the problem?


From an ape point of view I am insulted…

I recall a conversation with an old friend.

“You are right, I have always known about man. From the evidence, I believe his wisdom must walk hand and hand with his idiocy. His emotions must rule his brain. He must be a warlike creature who gives battle to everything around him, even himself.” (Dr. Zaius)
 
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Loudmouth

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Still no responses on this… want to toss in your two cents. There should be no reason for the lower mutation rates in proviral bodies except maybe they hold more importance than just being fossil infections.


What is there to respond to? LTR's evolved at a different rate than the viral protein genes. You have given no reason why this can't occur.


I did not claim ~5% Blayz did. There should be massive changes in the retrovirus which is not observed in the proposed infections of HERV-K because as I noted earlier the mutation/ evolution rate is enormous…


You have yet to support this argument with anything other than your say so. You have also not established just how many differences there are between these viruses, nor the integration time between the viruses in the comparison. You keep saying that there is not enough change, but I have yet to see you cite any comparisons. Where are they?

Until you do there is really nothing to discuss.
 
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Loudmouth

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Perhaps you could actually address what I said? You complained that fruit flies stay fruit flies. Well, apes remained as apes. So where is the problem?
 
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Zaius137

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LoudMouth...

“What is there to respond to? LTR's evolved at a different rate than the viral protein genes. You have given no reason why this can't occur.”

Again you are backwards on the evidence. Look, the LTRs are being used to produce the mutation rate in the calculations (they are not the problem). The question is not why the LTRs are mutating faster than the core Provirus; the question is why the provirus cores aren’t mutating at the same rate as the LTRs. The provirus mutation is suppressed in its rate.

You came up with a lame excuse earlier for the LTRs being changed faster but they are supposed to be the same upon insertion and thusly comparing the mutations of the two LTRs they can come up with a mutation rate.


You evolutionists have the same problem with all fossil evidence whichever it may be, a vertebrate or a virus. There is not evolution from one species to another. Evolutionists have to invent a new definition of a species (about 24 now) to try and prove speciation. Adaptation is essential to life and is built into a virus or a vertebrate and that is all that has ever been observed. Variation around a mean…
 
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Blayz

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You came up with a lame excuse earlier for the LTRs being changed faster but they are supposed to be the same upon insertion and thusly comparing the mutations of the two LTRs they can come up with a mutation rate.

Like I said, it is an issue, though quite what fantasy land you got the idea its proviral body supression rather than LTR acceleration, and why it would matter, is a mystery.

You evolutionists have the same problem with all fossil evidence whichever it may be, a vertebrate or a virus.

Naaah, it's you creationists that all think alike. Us evolutionists are quite varied. I for instance, couldn't care less about fossils, since they add 0.1% to evolution evidence, and the theory gets on fine without them.

There is not evolution from one species to another. Evolutionists have to invent a new definition of a species (about 24 now) to try and prove speciation.

Feel free to provide some evidence for this fluff too. Seriously, your argument now is "nomenclature ambiguous therefore evolution false!"

Yer an unintentionally funny guy Z. Lets take a moment to talk about the definition of a "kind"

Adaptation is essential to life and is built into a virus or a vertebrate and that is all that has ever been observed. Variation around a mean…

Please provide a molecular mechanism
 
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Zaius137

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As a LoudMouth says...

“You have yet to support this argument with anything other than your say so. You have also not established just how many differences there are between these viruses, nor the integration time between the viruses in the comparison. You keep saying that there is not enough change, but I have yet to see you cite any comparisons. Where are they?”

“Until you do there is really nothing to discuss.”

The idea is ludicrous that I need provide in depth data for a deductive assertion. I am posing an inductive argument that supports a probable conclusion. I do not need to cite comparisons but only to propound a reasonable argument.

It is reasonable that if evolution is true changes in the provirus insertions will show rapid evolution of retroviral infections seen as fossils in the DNA.

There is an elaborate taxonomy of retroviruses so that any of the noted changes can reflect a reclassification of the infecting retrovirus.

Retroviral Taxonomy, Protein Structures, Sequences, and Genetic Maps

http://www.ncbi.nlm.nih.gov/books/NBK19417/

In those HERV-K insertions we should see some recognizable change in that infection that reflects a retroviral evolution rate nearing a million times that of evolution buried as fossils in the human genome. We do not….
 
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Zaius137

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Blayz you crack me up…

“Naaah, it's you creationists that all think alike. Us evolutionists are quite varied. I for instance, couldn't care less about fossils, since they add 0.1% to evolution evidence, and the theory gets on fine without them.”


Actually evolution gets along fine without “any” evidence…
 
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sandwiches

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I like how you ignored the rest of his post and still didn't back up your claims.
 
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Loudmouth

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The idea is ludicrous that I need provide in depth data for a deductive assertion.


Since when is it ludicrous to expect people to back their assertions with evidence? You claim that not enough evolution has occurred. In order to make this claim you should, at a minimum, show a comparison of the insertions and their insertion times.

In those HERV-K insertions we should see some recognizable change in that infection that reflects a retroviral evolution rate nearing a million times that of evolution buried as fossils in the human genome. We do not….

Evidence please.
 
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Loudmouth

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The question is not why the LTRs are mutating faster than the core Provirus; the question is why the provirus cores aren’t mutating at the same rate as the LTRs. The provirus mutation is suppressed in its rate.

Or the LTR rate is being accelerated. Why is either a problem?

You came up with a lame excuse earlier for the LTRs being changed faster but they are supposed to be the same upon insertion and thusly comparing the mutations of the two LTRs they can come up with a mutation rate.

Comparison of the 5' and 3' LTR's within a single insertion gives the mutation rate in the host since the LTR's are identical at the time of insertion.

There is not evolution from one species to another.

Evidence please.

Evolutionists have to invent a new definition of a species (about 24 now) to try and prove speciation.

The definitions are based on the observations of reproductive isolation in living populations. The most obvious difficulty is speciation in sexual species vs. asexual species. For sexual species you can define speciation in terms of gene flow between two populations. If there is limited gene flow then it is defined as incipient speciation. If gene flow is completely stopped then it is complete speciation.

You obviously can't do this for asexual species. So at what point is a bacterial population sufficiently different from the parent population in order to be classified as a new species? That decision is completely arbitrary, and it is even further muddied by horizontal genetic transfer. This doesn't mean that evolution doesn't occur in asexual species. Obviously it does.

The third problem is fossil species. We can't look at gene flow in fossil species, so that definition is out. We are stuck with something akin to the bacterial problem. We can see that changes have occurred by comparing morphology, but how much changed is needed in order to classify them as separate species? Again, this can be arbitrary. This doesn't mean that no change has occurred because obviously it has. A comparison of Australopithecines, older Homo species, and modern humans shows obvious changes, but where do we put the dividing line in the continuum of change?

Adaptation is essential to life and is built into a virus or a vertebrate and that is all that has ever been observed. Variation around a mean…

Evidence please.
 
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Zaius137

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Originally Posted by Zaius137 http://www.christianforums.com/t7567545-post59210887/#post59210887
The question is not why the LTRs are mutating faster than the core Provirus; the question is why the provirus cores aren’t mutating at the same rate as the LTRs. The provirus mutation is suppressed in its rate.

Or the LTR rate is being accelerated. Why is either a problem?

If the LTR mutation is being accelerated (implied by your responses) and it is the basis for dating insertions in the genome; the insertion is younger than concluded by the evolution. I will go with that conclusion and maybe the human genome is 6 thousand years old.


You came up with a lame excuse earlier for the LTRs being changed faster but they are supposed to be the same upon insertion and thusly comparing the mutations of the two LTRs they can come up with a mutation rate.

True…


Comparison of the 5' and 3' LTR's within a single insertion gives the mutation rate in the host since the LTR's are identical at the time of insertion.

Stated this several times…

There is not evolution from one species to another.

Evidence please.


The entirety of the fossil records shows no transitional forms. Paleontology and now paleovirology have come to the same dead end in evolution.

Evolutionists have to invent a new definition of a species (about 24 now) to try and prove speciation.

Your answer is not worth the reply.
 
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Loudmouth

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I think you are confusing two things. LTR evolution as part of the viral genome and LTR evolution as part of the host genome. Frankly, it isn't all that clear in the papers. Perhaps you could show us exactly where this accelerated evolution is taking place.


There is not evolution from one species to another.
Evidence please.

The entirety of the fossil records shows no transitional forms.


I didn't ask for a restatement. I asked for evidence that backs the assertion. Please show, with evidence, that there are no transitional forms.

Your answer is not worth the reply.

Oh please. If you can't deal with biology then you might as well bow out now.
 
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Zaius137

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LoudMouth....

“I think you are confusing two things. LTR evolution as part of the viral genome and LTR evolution as part of the host genome. Frankly, it isn't all that clear in the papers. Perhaps you could show us exactly where this accelerated evolution is taking place.”

“Third, sequence divergence between the LTRs at the ends of a given provirus provides an important and unique source of phylogenetic information. The LTRs are created during reverse transcription to regenerate cis-acting elements required for integration and transcription. Because of the mechanism of reverse transcription, the two LTRs must be identical at the time of integration, even if they differed in the precursor provirus (Fig. 1A). Over time, they will diverge in sequence because of substitutions, insertions, and deletions acquired during cellular DNA replication”.

http://www.pnas.org/content/96/18/10254.full


You claimed accelerated LTRs. Do you wish to withdraw that statement?
 
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Split Rock

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I will go with that conclusion and maybe the human genome is 6 thousand years old.
Please show us the genetic data that infers humans are only 6,000 years old. Oh... wait.. you didn't get that number from some dead bishop.... did you?


The entirety of the fossil records shows no transitional forms.
Absolute rubbish.
Horse Evolution
Philip D. Gingerich
Mysticeti - Palaeocritti - a guide to prehistoric animals



Evolutionists have to invent a new definition of a species (about 24 now) to try and prove speciation.
Speciation has been observed both in the lab and in nature. Would you like a list?

The problem with identifying a species exists in many cases because nature doesn't create species. Nature creates populations of organisms that evolve, and are related by heredity. Taxonomy is a way for us humans to try and make sense of it all. Now, "Kinds" on the other hand should be simple to define, since by definition they were all created separately by a divine act. Strangely enough, creationists cannot come up with useful definition of "kind." Maybe you could be the first?
 
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Loudmouth

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You claimed accelerated LTRs. Do you wish to withdraw that statement?

I claimed accelerated LTR evolution as part of a viral genome prior to insertion, not as evolution of the ERV after insertion into the host genome. Those are two different different things. Remember, "proviral" indicates the viral sequence prior to insertion.

Phylogenetic analysis of LTR sequences associated with proviral bodies revealed several apparent LTR families. However, phylogenetic analysis of proviral body sequences yielded monophyletic tree topologies for most examined regions. Only a region between reverse transcriptase and RNase H displayed branches with higher bootstrap support. Clearly, proviral bodies appear much more homogeneous in sequence than the associated LTR sequences. Thus, almost homogeneous proviral bodies were associated with clearly different LTR variants at the time of provirus formations.
Human Endogenous Retrovirus Family HERV-K(HML-5): Status, Evolution, and Reconstruction of an Ancient Betaretrovirus in the Human Genome

The increased evolution of LTR's occurred in the replicating virus prior to endogenization into the host genome. This does NOT mean that the endogenized retrovirus (ERV) experienced higher evolution in the LTR's compared to the proviral body. They do offer two mechanisms:

It is currently not known whether the different LTR variants were already present in the exogenous precursor(s) or represent derivatives from a germ line-fixed LTR founder family.
IOW, there may have been recombination between the LTR's from ERV's and actively replicating viruses. However, even in this case the LTR's will be the same at the time of insertion because that is how the process of insertion works. Also from the paper:

Owing to the retroviral reverse transcription strategy, both LTR sequences are identical in sequence at the time of provirus formation. Without selective pressure, both LTRs independently accumulate mutations over time. Thus, sequence differences between a provirus' LTRs are an approximate measure of provirus age (8). We determined the degree of sequence divergence between 5′ and 3′ LTRs with larger overlapping portions for 53 HML-5 proviruses. We obtained sequence divergences ranging from 6 to 24% (mean, 12.9%; standard deviation, 3.87). These numbers equal an approximate age of 50 (±15) million years for the HML-5 proviruses (Table ​(Table2).2). We furthermore calculated the average ages of proviral sequences from Kimura-2-parameter corrected distances to the HML-5 consensus sequence for five different proviral regions, excluding gaps and CpG dinucleotides (16). Here, an average evolutionary age of about 60 (±27) million years was indicated. The age of roughly 55 million years from both analyses thus corresponds to a HML-5 integration time into the genome clearly before the evolutionary split of Old World from New World monkeys that took place about 40 million years ago.
Clearly, they are not talking about accelerated LTR evolution once the virus has been inserted into the genome. They are talking about the evolution of the virus outside of the host. Therefore, your argument that LTR divergence can not be used is not supported by this paper.

 
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Zaius137

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Split Rock...

“Please show us the genetic data that infers humans are only 6,000 years old. Oh... wait.. you didn't get that number from some dead bishop.... did you?”

"Mitochondrial DNA appears to mutate much faster than expected, prompting new DNA forensics procedures and raising troubling questions about the dating of evolutionary events. ...Regardless of the cause, evolutionists are most concerned about the effect of a faster mutation rate. For example, researchers have calculated that "mitochondrial Eve"--the woman whose mtDNA was ancestral to that in all living people--lived 100,000 to 200,000 years ago in Africa. Using the new clock, she would be a mere 6000 years old."

  • Gibbons, Calibrating the Mitochondrial Clock, Science, Vol 279, No. 5347, Jan 1998, pp. 28 – 29
 
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Zaius137

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LoudMouth…


“In both cases, LTR sequences evolved in sequence independently from, and obviously more rapidly than, the proviral bodies. Reasons for apparently different evolutionary rates of LTRs and proviral bodies are currently not clear.”

From Blayz…
“This is the only valid observation you have made so far”.

Still no responses on this… want to toss in your two cents. There should be no reason for the lower mutation rates in proviral bodies except maybe they hold more importance than just being fossil infections.


From you…

Originally Posted by Zaius137 http://www.christianforums.com/t7567545-75/#post59209680
Still no responses on this… want to toss in your two cents. There should be no reason for the lower mutation rates in proviral bodies except maybe they hold more importance than just being fossil infections.


You being deliberately obtuse is equivalent with a lack of honesty on your part.

And this….

“Originally Posted by Zaius137 http://www.christianforums.com/t7567545-post59210887/#post59210887
The question is not why the LTRs are mutating faster than the core Provirus; the question is why the provirus cores aren’t mutating at the same rate as the LTRs. The provirus mutation is suppressed in its rate.

Or the LTR rate is being accelerated. Why is either a problem?”

I reserve the right to respond to intellectually honest participants.

 
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Blayz

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You say "no response on this" but I don't know what you are expecting. I agree it is a surprising and unaccounted for result, but one for which a number of hypotheses could be generated, including the one you put forward, as well as those in the paper.

What's the issue again?


Tsk tsk Z, haven't we had the conversation about you posting on topics you don't understand? Gibbon's work, from 1998 (and only someone ignorant of science would look at human sequence literature prior to the advent of high throughput whole genome sequencing) is based on the fundamentally flawed assumption that the mtDNA control region mutation rate is representative of the whole, and that heteroplasmy mutations can be included.

heck, this PRATT is nicely rebutted here
CB621.1: Young mitochondrial Eve

and more in full here
Mitochondrial Eve

You have to remember Z, that not everyone sets in the stone of ultimate truth some book written along time ago. Most of us like to look at more recent data generated with more advanced techniques.

Anyway, a nice little goalpost shuffle there Z. One wonders what irrelevant-to-the-original-argument topic you'll sneak in next.


 
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Loudmouth

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I can name two mechanisms: recombination events with other retroviruses or with LTR's from ERV's. I still don't understand why you have a problem with higher evolution of LTR's in actively replicating and actively infecting retroviruses. Care to explain?



I reserve the right to respond to intellectually honest participants.

Too bad it is not a two way street. You still have not said why this is a problem or why it puts the evidence in doubt. In fact, you still have not evidenced the lack of evolution that you claim exists. Before you start accusing others of being dishonest perhaps you should start backing your own assertions with evidence. The mtDNA example was not a good first step.
 
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