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

[sfs]

(sfs)...
Thanks for the graphs.

“In the case of hard selection, the fitness is just given by the number of deleterious mutations carried: (1-s)m. For soft selection, the fitness is relative to the fittest individual in the population, which has fitness = 1.0. (As soft selection goes, this is still pretty hard: the introduction of a single fitter individual reduces the fitness of the entire population by the amount he's better than the previous best, which is pretty weird biologically.)

Under hard selection, the population always becomes extinct if the reproductive rate per individual is lower than 1/e-U, consistent with Kimura's formula. For example, if U = 4.2, O = 6 offspring/pair and s = 0.01 (i.e. each mutation hurts fitness by 1%), the number of offspring per generation looks like this:”

I believe the formula is not 1/e^-u but 2e^u… hope you did not use it in the simulation.

No, it's not used in the simulation. The formula for the reproductive capacity required of a breeding pair of diploids is 2e^U. Since a breeding pair consists of two individuals, the capacity required of a single individual is e^U = 1/e-U, which is what I wrote (and which is what you quoted a few posts earlier from the Nachman and Crowell paper).

Your population does not just decline it crashes. Yes, I guess you can say this is not close to reality… because it is not.

Hey, it's the model you're claiming applies to humans.

 

[sfs]

(sfs)

Really I am trying to be polite here. Your program has so many issues, besides being off point, which I can not begin to reply kindly.

Call me skeptical, but I don't think politeness is what's preventing you from criticizing the simulation.

You need to convince me that “soft selection” is a real argument to Haldane.

Why would I need to do that? Leaving aside the fact that we're discussing the genetic load imposed by deleterious mutations, rather than Haldane (something you might remember, since you brought the subject up), I don't need to convince you of anything. I like to correct errors about genetics when I see them so that others aren't misinformed, but I'm under no obligation to convince you of anything.

By the way you could graph this in Excel and circumvent the ancient compiler.

Gag. I dare say I could program it in Excel. I could also program it in R, in Perl, in Java, in C++ or in Fortran. I could probably even do it in Javascript, although I've been fortunate enough not to have to touch that language for ten years. I knew somebody who would program in postscript, and do calculations on the lab printer, just for fun. I think I'd choose Excel over postscript, but it would be a tough call. Otherwise, no. The right tool for the job.

 

[Naraoia]

Obviously, no real population experiences only soft selection. so this is not a realistic picture. (On the other hand, the ideal genotype that hard selection is measured against is also unreal, and has never existed. Like every other complex organism, humans have evolved while carrying many deleterious alleles, and it's not clear to me what exactly the perfectly fit individual represents in reality.)

If you add hard selection on top of soft selection, wouldn't it be fundamentally the same as having only hard selection?

Population genetics is really not my thing...

 

[Zaius137]

(sfs)

Hey, it's the model you're claiming applies to humans.”

With O=6 a crash sounds about right. With the U=4.2 your O would require a 131 value just to stay level. That is of course you correct the birth rate formula.…

 

[Zaius137]

LoudMouth..

Not going to follow you down that rabbit hole again until you want to talk about my outrageous claim from an earlier post. Every time it looks like dinner the rabbit vanishes.


“The HERV fossils in the human genome show no to little change from the original infection yet a monkey changes into a man…”

How do you explain the viral fossils in our genome not showing evolution?

 

[Naraoia]

How do you explain the viral fossils in our genome not showing evolution?

Where did you get that they didn't show evolution? LM was just telling you how scientists reconstructed the ancestral version from a bunch of these viral fossils. Why exactly would you need to reconstruct anything if the ancestral version hadn't evolved?

Also, a retrovirus has a few kilobases of genome containing a handful of genes. A monkey has 3 million kilobases with ~20 000 protein-coding genes plus a large amount of non-coding sequence with a variety of functions. All of that extra genetic complexity adds up to a much more complex phenotype. Don't you think that a monkey has just a wee bit more traits to evolve than a virus?

 

[sfs]

If you add hard selection on top of soft selection, wouldn't it be fundamentally the same as having only hard selection?

Population genetics is really not my thing...

Depends on how you're adding. If some mutations undergo hard selection and some undergo soft selection, then as far as population fitness is concerned, you might just as well have only the hard-selected mutations. If individual mutations undergo selection that is partly soft and partly hard, then you can get almost anything. What the mixed selection means is that the mutation's effect on relative fitness is different than its effect on the population fitness; the two effects can even have different signs. Here's an example I've posted elsewhere:

Consider a species of unicorn, living on a single mountain. Their population size is limited by their food supply, which consists solely of onion grass. In this species, some males mate multiple times and some males don't mate at all; mating success is determined by battles between males, carried out using their horns.

In this species, a new allele arises that increases horn length by 25% (50% for two copies of the allele). The new allele spreads rapidly through the population, because males who have a copy of it win most of their battles and sire colts, while those who don't are left to retire to their dens and read email spam about horn enhancement products. The larger horn requires more protein to grow and more calories to carry around, so those with the new allele have to eat more, but the mating advantage outweighs the lower probability of surviving to mate. Positive selection therefore drives the new allele to fixation.

This is a case of a beneficial allele that is positively selected for, but that lowers the overall fitness of the population, since the food supply can support fewer unicorns after the mutation has fixed. After fixation, back mutations to the smaller horn phenotype will be deleterious, but will actually reduce the genetic load rather than increasing it.

 

[sfs]

(sfs)

Hey, it's the model you're claiming applies to humans.”

With O=6 a crash sounds about right. With the U=4.2 your O would require a 131 value just to stay level.

Yes, that's what it requires. A little more, actually, since if you're just above replacement level, random fluctuations will eventually kill you. All assuming hard selection, of course.

That is of course you correct the birth rate formula.…

There was nothing to correct.

 

[Loudmouth]

LoudMouth..
How do you explain the viral fossils in our genome not showing evolution?

They do show evolution:

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.
Constructing primate phylogenies from ancient retrovirus sequences

​

The authors were able to show just that, divergence of LTR sequences due to lineage specific mutations (i.e. evolution). In fact, the authors were able to evidence a specific mutational mechanism:

Some authors have suggested that methyl-CG deamination has evolved as a specific defense against colonization of the genome by ERVs (38). Existence of such a mechanism should be manifest as a bias toward C-G → T-A transitions within CG dinucleotides. Tracing the pattern and direction of shared derived substitutions on each of the HERV trees revealed such a bias.
​

The very fact that a consensus sequence produced a viable retrovirus indicates that ERV's evolved once they became endogenized.

 

[Naraoia]

Thanks again, sfs

 

[Zaius137]

LoudMouth…

They do show evolution:
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.


The paragraph you cited says nothing except the LTR’s are the same at time of insertion. Nothing is really said about the rapid evolution of the virus itself. How would you recognize the virus over a period of 5 million years! Retroviruses mutate at an astounding rate often just within the same host.

“ In addition, the HIV reverse transcriptase enzyme makes many mistakes while making DNA copies from HIV RNA. As a consequence, many variants of HIV develop in an individual, some of which may escape destruction by antibodies or killer T cells. Additionally, different strains of HIV can recombine to produce a wide range of variants or strains.”

http://www.bloodindex.org/mutation_hiv.php

In the case of HERV-k it is claimed that the infection happened just after the chimp human divergence and continued up until 100,000 years ago. That is on the order of about 5 million years according to the tale. You literally have an ape like hominid turn into a human but the HERV-k stays literally intact, enough so as to be put back together???

Evolutionists are nuts…


“The authors were able to show just that, divergence of LTR sequences due to lineage specific mutations (i.e. evolution). In fact, the authors were able to evidence a specific mutational mechanism:”


Sorry the LTR did not change until after insertion (your own source). No allowance was made for the evolution of the retrovirus prior to insertion except the LTR’s are the same.

The very fact that a consensus sequence produced a viable retrovirus indicates that ERV's evolved once they became endogenized.

Viruses don’t change host to host??? “NO WAY”

Evolution does not even work for a virus let alone a human….

 

[Zaius137]

(sfs)

Thanks for the graphs. I did work as a programmer at one time so I can appreciate the effort.

 

[Zaius137]

“Some authors have suggested that methyl-CG deamination has evolved as a specific defense against colonization of the genome by ERVs (38). Existence of such a mechanism should be manifest as a bias toward C-G → T-A transitions within CG dinucleotides. Tracing the pattern and direction of shared derived substitutions on each of the HERV trees revealed such a bias.”

Well what if the insertions were not done by retroviruses. What if these patterns were laid down in a dynamic way with some variances to provide a memory to guard against future invasions by a retrovirus (a defense of one generation to the next). Well I guess we may never find out if we do not give up the paradigm of evolution as it relates to these sequences.

 

[Blayz]

The paragraph you cited says nothing except the LTR’s are the same at time of insertion. Nothing is really said about the rapid evolution of the virus itself. How would you recognize the virus over a period of 5 million years! Retroviruses mutate at an astounding rate often just within the same host.

“ In addition, the HIV reverse transcriptase enzyme makes many mistakes while making DNA copies from HIV RNA. As a consequence, many variants of HIV develop in an individual, some of which may escape destruction by antibodies or killer T cells. Additionally, different strains of HIV can recombine to produce a wide range of variants or strains.”

http://www.bloodindex.org/mutation_hiv.php

I am rarely surprised by the level of ignorance and misinformation held by creationists, but you have managed to do it Z. How can you be this many pages into this discussion and not know the difference between the mutation rate experienced by live virus during replication caused by its own RT and the mutation rate its DNA copies experience once they are a part of the genome caused by host polymerases.

Silly conflation much?

And that you'd use rapid evolution of retroviruses as an argument against evolution...words fail me.

 

[Blayz]

Well what if the insertions were not done by retroviruses. What if these patterns were laid down in a dynamic way with some variances to provide a memory to guard against future invasions by a retrovirus (a defense of one generation to the next). Well I guess we may never find out if we do not give up the paradigm of evolution as it relates to these sequences.

Of course we can find out. That's the whole point of science. You have provided an hypothesis: "ERVs were placed by a designer to provide a memory guard against future invasions by a retrovirus"

Now all you have to do is design an experiment to test it.

I have a question though, since most DNA is identical from human to human, which is to say we all have pretty much the same sets of these alleged memory guards:
1) How do you intend to test it, without a null population
2) Since humans get infected by retroviruses anyway, are we allowed to fire this incompetent designer that created these memory guards, perhaps even sue?

 

[Loudmouth]

The paragraph you cited says nothing except the LTR’s are the same at time of insertion. Nothing is really said about the rapid evolution of the virus itself. How would you recognize the virus over a period of 5 million years! Retroviruses mutate at an astounding rate often just within the same host.

Deleterious mutations can occur in viral genomes as well. There are conserved regions in every viral genome that, if changend, will result in a non-viable virus. You can use these conserved regions to find HERV's in the genome. You can also use algorithms that detect repetitive DNA to find LTR's which are later confirmed through direct comparison to known viral LTR's. I found this paper which compared HERV-K insertions and discusses the evolution of the virus itself:

Human Endogenous Retrovirus Family HERV-K(HML-5): Status, Evolution, and Reconstruction of an Ancient Betaretrovirus in the Human Genome

Pay close attention to figure 3. They did a phylogenetic analysis on HERV-K LTR's and found several subfamilies. That is, they were able to track the evolution of the LTR's in the viral genome.

In the case of HERV-k it is claimed that the infection happened just after the chimp human divergence and continued up until 100,000 years ago. That is on the order of about 5 million years according to the tale. You literally have an ape like hominid turn into a human but the HERV-k stays literally intact, enough so as to be put back together???

Where have you ever shown that the HERV-K insertions show no evolution or change? Perhaps you could cite this evidence?

Sorry the LTR did not change until after insertion (your own source).

Where did they say that? It says that the LTR's within each insertion were the same, not that the LTR's between all insertions were the same. When a retrovirus inserts it copies one of the LTR's to produce the other LTR. This creates identical "bookends" for each insertion. However, this doesn't mean that the bookends are the same between different insertions. In fact, the paper I cite above found differences between the LTR's in different HERV-K, the very thing that you claim doesn't exist.

No allowance was made for the evolution of the retrovirus prior to insertion except the LTR’s are the same.

Evolution does not even work for a virus let alone a human….

Evidence please.

You have made the claim that all HERV-K insertions were the same at the time of integration. It is time for you to back up this assertion or withdraw the claim.

 

[Loudmouth]

Well what if the insertions were not done by retroviruses. What if these patterns were laid down in a dynamic way with some variances to provide a memory to guard against future invasions by a retrovirus (a defense of one generation to the next). Well I guess we may never find out if we do not give up the paradigm of evolution as it relates to these sequences.

This is like claiming that fingerprints at the scene of a crime were put there by mischevious leprechauns.

 

[Zaius137]

“ 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.”

“Pay close attention to figure 3. They did a phylogenetic analysis on HERV-K LTR's and found several subfamilies. That is, they were able to track the evolution of the LTR's in the viral genome.”

Excuse me but the LTR’s are generated upon insertion…. Get that fact threw your head. They belong to the provirus only by the action of reverse transcription. They are not in the central viral genome. You missed that point altogether.

“Owing to the retroviral reverse transcription strategy, both LTR sequences are identical in sequence at the time of provirus formation.”

That’s from your article… Remember the LTRs are removed to produce the phony resurrected virus… snip, snip.

Ten families were identified? If you believe they can not evolve outside 10 families in 30 million years (remember they are retroviruses) I guess you can also believe in evolution. By the way where do you Darwinists meet for fellowship?

Evolution is religion not observable science. You still pay homage to mischievous leprechauns and magic (central to your origin fairytales).

Remember I showed where the HERV-k con (as in conman) does not insert like MMTV and does not have the functionality of the MMTV. So forget about claiming that it is a viable reconstructed virus in that genus.

Your citation still does not show how a retrovirus can survive virtually unchanged 5-30 million years and still be identified as HERV-K; the suggestion of that happening is absurd.

“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.”

It will not be clear until they drop that fossil virus nonsense.

 

[Blayz]

Excuse me but the LTR’s are generated upon insertion…. Get that fact threw your head. They belong to the provirus only by the action of reverse transcription. They are not in the central viral genome. You missed that point altogether.

“Owing to the retroviral reverse transcription strategy, both LTR sequences are identical in sequence at the time of provirus formation.”

LOL. So if the LTRs are not in the "central viral genome", then what template does the RNA-dependent DNA polymerase AKA reverse transcriptase use to generate them? conjures them out of thin air?

You have no idea how polymerases work either

proviral LTRs arise from duplications of internal viral sequences.

 

[Zaius137]

I only maintain that the LTRs are equal at the time of insertion and thus they are independent of the core virus to that degree. You are claiming that the LTRs being examined are included in the core retrovirus?