Annoying creationists

[Taffer]

Finally, joobz, you are starting to think about the problem. Did you notice all the other links in that google search that also shows that multiple directional selection pressures slow evolution?

I already did this search, and showed that the first three of the "many" papers did not agree with you at all. Aren't you going to comment on this?

 

[Taffer]

...That is why real doctors use triple therapy kleinman.

Perfect. Thank you for a wonderful post.

 

[Taffer]

Ev’s helping to ‘slain it. Reptiles to birds is certainly not microevolution.

And it certainly has happened. The evidence that reptiles and birds shared a common ancestor is more then the evidence that we went to the moon.

 

[joobz]

The best hard numbers I have are based on the results from ev. Setting two of the three selection conditions to zero will allow the remaining condition to evolve 3 to 5 orders of magnitude more quickly than evolving all three selection conditions simultaneously for genome lengths in the range of HIV. For larger genomes, I expect this number to be far greater.

which number is far greater? and why do you not include population in this discussion? haven't we established as pop->inf, gen->1?

It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is your concrete basis for not worring about it?

I think this paper wouldn't have been accepted if that was the case:

Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]

I can't access the paper yet, but from the abstract:

Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios.

Seems like evolution has a mathematical basis after all.

Microevolutionary events occur, macroevolutionary events do not.

How many microevolutionary steps=macroevolution?

2.) Far too many..

AHhh, evolution doesn't occur because that's how you defined it. very interesting.

3.) The fitness landscape is used to describe the path a population subjected to a directional selection pressure must take in order to get to a new optimum. If you have a single directional selection pressure, it is much easier for the population to find this optimum.

you can't know this a priori. intensity of the selection pressure, the independant nature of the pressures will all matter.

As soon as you introduce multiple directional selection pressures, the population must find optimums for all these conditions simultaneously. This confounds the mutation and selection process where one selection pressure may cause interference with another selection pressure to find its optimum.

or it may enhance adaptation (e.g., if one pressure enhances the mutation rates.)

 

[kleinman]

Annoying Creationists

What is happening is a large number of Ka/Ks > 1 for the individual codons in a gene is a measure of the intensity of the directed selection pressure. So if a particular protease inhibitor leads to 60-70 amino acid changes in order to evolve resistance to that drug, it would be a more intense directed selection pressure than another protease inhibitor that only required 30 amino acid changes.

In other words, kleinman wants to sum the many, many selection pressures observed at the amino acid level into one, for the whole gene, but does not want to sum the gene-operating selection pressures into one for the whole organism (because that creates one selection pressure and ruins his whole multiple selection pressure argument).

This is what is so illogical about Dr Richard’s way of counting. Notice how you neglected to respond to my final quote from this post. I’ll repeat it here so we can see where your logic leads.

If you count every codon which shows the results of directional selection pressure with ev when evolving 16 binding sites, 6 bases wide (2 codons wide), you would count 32 positive selection pressures. Dr Richard, each time a particular codon in HIV changes as a result of a directed selection pressure from a protease inhibitor does mean you have additional directed selection pressures. What is happening is a large number of Ka/Ks > 1 for the individual codons in a gene is a measure of the intensity of the directed selection pressure. So if a particular protease inhibitor leads to 60-70 amino acid changes in order to evolve resistance to that drug, it would be a more intense directed selection pressure than another protease inhibitor that only required 30 amino acid changes.

Dr Richard, if you want to use your logic, ev does not have three directional selection pressures is has 32 directional selection pressures not 3. You are confusing the results of a directional selection pressure with the meaning of a directional selection pressures.

It’s time for you to answer a couple of questions. The first is what are these 60-70 directional selection pressures? The second is, there is an error in the equation in your link, what is it? If you can’t find it, perhaps the resident James Randi Educational Forum PhD in amathematics can find it.

What is really funny is his reference to a protease inhibitor as though this is the only selection pressure acting on the protease gene.

Take a look at the HIV positive selection database again klienman

Third graph down, titled "Stanford untreated dataset"

oops, multiple selection pressures measured on the genome in untreated patients

If you had read this thread carefully, you would have seen that I had said there is an immune response to HIV (how many directed selection pressures to you want to call this?) that HIV patients can mount but you appear not to know that it is insufficient to stop the disease. A single antibody directed at the protease can lead to all these amino acid substitutions, just as a single drug leads to numerous amino acid substitutions, just as ev’s 3 selection conditions leads to 32 amino acid substitutions. According to your logic, ev has 32 directed selection pressures. Which counting system do you want to work with?

5 selection pressures in HIV treated patients kleinman?

It doesn’t matter how you want to count selection pressures. If you want to count each amino acid substitution as a selection pressure then ev has 32 selection directional pressures and still gives an analogous model of combination therapy of HIV. It is better to describe directional selection pressures by the number of genes impacted, the degree of inhibition of each of the genes involved and the number of amino acid substitutions required to achieve resistance to that directional selection pressure.

What you continue to miss in this discussion Dr Richard is that the underlying mathematics does not change by changing the way you count selection pressures. The more the amino acid substitutions required, the more generations needed to accomplish these changes by mutation and selection. Stabilizing selection pressures interfere with this process. This is why as you lengthen the genome in the ev model it takes more generations to evolve your selection conditions. Ev demonstrates this with spurious binding in the non-binding site region. HIV with its short genome has a much smaller portion of it’s genome being acted on by stabilizing selection pressures than an E Coli size genome or a human size genome. This is why your theory of evolution is mathematically impossible. You don’t have the selection pressure(s) to evolve reptiles into birds and if you did, you don’t have sufficient generations and sufficient populations to accomplish the transformation my mutation and selection. You really ought to study ev, you would learn something about the mathematics of mutation and selection.

Since I have already answered a couple of questions for you, it’s time for you to answer I couple of questions for me.

The first is what are these 60-70 directional selection pressures? The second is, there is an error in the equation in your link, what is it? If you can’t find it, perhaps the resident James Randi Educational Forum PhD in amathematics can find it.

 

[Mr. Scott]

Annoying hollow assertions

There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is a fairly critical point, Dr. Alan Kleinman, because if you can't mathematically prove that assertion, then you no longer have mathematical proof that evolution was to slow to account for the origin of species.

Your failure to mathematically prove this means the entire thesis you've presented in this thread is terminally busted.

Please present this proof.

(In your response, could you refer to me as "little Tiktaalik?" Thanks!)

 

[joobz]

Microevolutionary events occur, macroevolutionary events do not.

how many microevolutionary steps = macroevolution?

2.) Far too many

5 selection pressures in HIV treated patients kleinman?

It doesn’t matter how you want to count selection pressures.

The goalpost has again changed yet again.
It has become "Evolution is impossible because Kleinman defines it as such!"

Asking for concrete values and hypotheses are not needed anymore. He's found an endzone that science can't touch. Unfortunately, in the realm of reality it is out of bounds.

 

[kleinman]

Annoying Creationists

The best hard numbers I have are based on the results from ev. Setting two of the three selection conditions to zero will allow the remaining condition to evolve 3 to 5 orders of magnitude more quickly than evolving all three selection conditions simultaneously for genome lengths in the range of HIV. For larger genomes, I expect this number to be far greater.

which number is far greater? and why do you not include population in this discussion? haven't we established as pop->inf, gen->1?

Computer memory requirements limit running large genome with large populations simultaneously. On my computer, the limit is a 1k genome length and a population of 1 meg. With smaller populations, you can run larger genome cases and these cases show that the generations for convergence proportional to about G^2. Adebz has stated that at infinite population, generation for converges goes to 1. If that is true, the data obtained from ev shows that the slope of the generations for convergence/population is so shallow with large populations that you will need unrealistically large populations to get small generations for convergence. Adebz now understands that doubling population does not double the probability of a particular mutation occurring at a particular locus. This effect is demonstrated by ev by it’s rapidly decreasing slope of the generations for convergence/population curve for the larger population series already presented here.

What you need to understand is that if you are going to propose the evolution of reptiles into birds, you don’t have infinite populations; you don’t even have the entire reptile population involved in this so called evolutionary event. If you did, why do we still have reptiles? You have large genome creatures with much longer generation times than HIV or even bacteria with much smaller populations requiring huge numbers of amino acid substitutions in order to accomplish this evolutionary event. You don’t have the selection pressure to accomplish this and you evolutionists think that directional selection pressures are not influenced by stabilizing selection pressures. The mathematics is just not there to support this concept.

It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is your concrete basis for not worring about it?

Look at this thread joobz, I present the results of Dr Schneider’s peer reviewed and published model and you all attribute this mathematics to me and instantly discredit the results. Why do you think that Dr Schneider stopped publishing on his model? He knows what his model shows. He has put himself in the position of having to retract his statements that his model represents mutation and selection realistically or that his model is showing that information acquisition on longer genomes becomes profoundly slow. There is evidence of this in his web published statements that realistic length genomes cases would take years to run.

It is the responsibility of evolutionists to prove your theory mathematically. If evolutionists think that other mechanisms of mutations will somehow accelerate evolution, put the mechanism in ev and show this. If anything, mutations which cause frame shifts will disrupt the sequences of already evolved binding sites. As it stands right now, ev shows that the rate of information gain by random point mutation and natural selection is far too slow on realistic length genomes to support the theory of evolution. However, ev does a good job in modeling how microevolution works.

I think this paper wouldn't have been accepted if that was the case:

Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]

I can't access the paper yet, but from the abstract:

Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios.

What is the Hill-Robertson effect? Here is the definition from Wikipedia which can be found at: http://en.wikipedia.org/wiki/Hill-Robertson_effect

In a finite population subject to natural selection and genetic recombination, genetic drift will create random instances of linkage disequilibrium. Some will be selectively advantageous, others will not. However, the creation of these slows down the progress of selection. Recombination breaks down the disequilibria, allowing selection to act independently on various loci.

So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm

Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).

This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.

Seems like evolution has a mathematical basis after all.

The microevolution of the HIV virus does.

3.) The fitness landscape is used to describe the path a population subjected to a directional selection pressure must take in order to get to a new optimum. If you have a single directional selection pressure, it is much easier for the population to find this optimum.

you can't know this a priori. intensity of the selection pressure, the independant nature of the pressures will all matter.

Ev is a simulation of this process and it show that the search for this optimum becomes profoundly slow with multiple selection pressures and large genomes.

As soon as you introduce multiple directional selection pressures, the population must find optimums for all these conditions simultaneously. This confounds the mutation and selection process where one selection pressure may cause interference with another selection pressure to find its optimum.

or it may enhance adaptation (e.g., if one pressure enhances the mutation rates.)

You do know that some mutations are harmful and that stabilizing selection pressures select out those creatures. Perhaps what you suggest here should be put into ev and show mathematically how one selection pressure enhances another. The problem with your logic is that you suggest when sorting a dataset, introducing another sorting condition at the same time will somehow accelerate the original sorting process. I don’t believe there is a mathematical basis for this. If you can give me a few real examples of how this happens, I’ll reconsider my position on your theory. As it stands, you are proposing an exceptional case to try to establish the rule for evolution.

 

[Mercutio]

In completely unrelated news, the first marsupial genome has been sequenced.

Overall, the genome of the opossum (Monodelphis domestica) includes roughly 18,000-20,000 genes, Graves says.

That makes it about the same size as the human genome, although the genes are arranged on a small number of extremely large chromosomes.

Most of the opossum's genes have counterparts in humans and other animals such as mice, the Nature paper shows.

Those that are opossum-specific seem to be related to immunity, sensory perception and detoxification, the researchers say.

"That's to be expected because immune genes evolve very, very fast," Graves says.

"They're under stringent selection every time we meet a new bug."

So...lots of selection pressures = fast evolution.

Like I said, just a cool article completely unrelated to the current thread.

 

[kleinman]

Annoying Creationists

It doesn’t matter how you want to count selection pressures.

The goalpost has again changed yet again.

It has become "Evolution is impossible because Kleinman defines it as such!"

Asking for concrete values and hypotheses are not needed anymore. He's found an endzone that science can't touch. Unfortunately, in the realm of reality it is out of bounds.

Joobz, unless you understand Dr Richard’s terminology you can not talk about concrete values. What Dr Richard counts as a directed selection pressure is the number of amino acid substitutions that results from a selection pressure. If you are going to count selection pressures like this, ev has 32 selection pressures (amino acid substitutions) when evolving 16 binding sites each 6 bases wide. I have counted selection pressures as the number of mathematical conditions Dr Schneider uses in ev. This concept is equivalent to the use of a drug for the treatment of HIV which can lead to 60-70 amino acid substitutions to evolve resistance to that drug. You can count the single drug therapy as a single selection pressure that leads to 60-70 amino acid substitutions. A single antibody directed against a protease can do the equivalent. There are concrete values mixed in with all the noise Dr Richard adds to this discussion. When you sort through what he is saying, ev is still a valid analogy for what is happening with combination (or monotherapy) therapy of HIV.

 

[Dr Richard]

This is what is so illogical about Dr Richard’s way of counting. Notice how you neglected to respond to my final quote from this post. I’ll repeat it here so we can see where your logic leads.

Dr Richard, if you want to use your logic, ev does not have three directional selection pressures is has 32 directional selection pressures not 3. You are confusing the results of a directional selection pressure with the meaning of a directional selection pressures.

I am saying that you can measure a selection pressure acting on the codon.

What is your definition of a selection pressure again kleinman?

You'll have a week to think of one.

It’s time for you to answer a couple of questions. The first is what are these 60-70 directional selection pressures?

Another failure in reading comprehension. But your faith is blinding you to the obvious.

I cannot say for certain, as the paper does not provide this information. But I would say they include (but are not limited to)

1. mutations within the HIV protease gene that improve the efficiency of the gene in an untreated patient

2. mutations within the HIV protease gene that improve the efficiency of the gene in an treated patient

3. mutations within the reverse transcriptase gene that improve the efficiency of the gene in an untreated patient

4. mutations within the reverse transcriptase gene that improve the efficiency of the gene in an treated patient

5. mutations within either gene that improve integration/replication in the host DNA

6. mutations that interact with other mutations in the genome to improve overall fitness

The second is, there is an error in the equation in your link, what is it? If you can’t find it, perhaps the resident James Randi Educational Forum PhD in amathematics can find it.[/SIZE][/FONT]

Which link?

If you had read this thread carefully, you would have seen that I had said there is an immune response to HIV (how many directed selection pressures to you want to call this?) that HIV patients can mount but you appear not to know that it is insufficient to stop the disease. A single antibody directed at the protease can lead to all these amino acid substitutions,

Your lack of knowledge of the immune system does not suprise me.

Are you seriously trying to contend that the whole immune response to HIV infection is due a single antibody? That is very funny.

As stated before, I would count the human immune response as about 3500 selection pressures if we use the kleinman "selection pressure acting at a gene level" method of counting.

I have never claimed that human immune system is effective in all cases at preventing HIV infection.

Although you are again sadly misguided in asserting that it cannot stop the disease: a few seconds of research will tell you that there are individuals who have sufficient immunity to HIV to have immunity: this paper will highlight some more immune mechanisms other than antibodies for you to learn about and explain why some individuals have higher natural resistance than others:

just as a single drug leads to numerous amino acid substitutions, just as ev’s 3 selection conditions leads to 32 amino acid substitutions. According to your logic, ev has 32 directed selection pressures. Which counting system do you want to work with?[/SIZE][/FONT]

You are wrong whichever system you pick: selection pressure acting at the level of the organism, the gene or base pair. Pick one.

It doesn’t matter how you want to count selection pressures. If you want to count each amino acid substitution as a selection pressure then ev has 32 selection directional pressures and still gives an analogous model of combination therapy of HIV. It is better to describe directional selection pressures by the number of genes impacted, the degree of inhibition of each of the genes involved and the number of amino acid substitutions required to achieve resistance to that directional selection pressure.

You are inching towards the light of understanding. Don't stop. But remember to update your goralpost art (getting a little crowded now) and include the other mechanisms of evolutionary change other than amino acid substitutions.

What you continue to miss in this discussion Dr Richard is that the underlying mathematics does not change by changing the way you count selection pressures.

Which why you have always been wrong

The more the amino acid substitutions required, the more generations needed to accomplish these changes by mutation and selection.

These have already been achieved. That is what the database shows. Its entire existence is a refutation of your theory.

Ev demonstrates this with spurious binding in the non-binding site region. HIV with its short genome has a much smaller portion of it’s genome being acted on by stabilizing selection pressures than an E Coli size genome or a human size genome. This is why your theory of evolution is mathematically impossible. You don’t have the selection pressure(s) to evolve reptiles into birds and if you did, you don’t have sufficient generations and sufficient populations to accomplish the transformation my mutation and selection. You really ought to study ev, you would learn something about the mathematics of mutation and selection.

Any evidence for the above list of random assertions? Other than the last 3000+ posts of mindless macro pasting?

Since I have already answered a couple of questions for you, it’s time for you to answer I couple of questions for me.

The first is what are these 60-70 directional selection pressures? The second is, there is an error in the equation in your link, what is it? If you can’t find it, perhaps the resident James Randi Educational Forum PhD in amathematics can find it.

See above.

1. Again, please tell me the minimum number of "directional "selection pressures you think must operate to prevent macroevolution by slowing microevolution to such an extent that it cannot happen within the timeframe of life on earth in the real world based on your extensive mathematical modelling.

kleinman's answer = 5 (3 modelled in ev + "a couple" more) - but less in bacteria and organisms with a longer genome

2. If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100?

4. What is your definition of a "selection pressure"

5. (for old time's sake) What is your definition of macroevolution again? (NB random lists of things you think it is are not acceptable)

 

[Dr Richard]

Joobz, unless you understand Dr Richard’s terminology you can not talk about concrete values. What Dr Richard counts as a directed selection pressure is the number of amino acid substitutions that results from a selection pressure.

Wrong

This concept is equivalent to the use of a drug for the treatment of HIV which can lead to 60-70 amino acid substitutions to evolve resistance to that drug.

Wrong

You can count the single drug therapy as a single selection pressure that leads to 60-70 amino acid substitutions.

Wrong

A single antibody directed against a protease can do the equivalent.

Wrong

There are concrete values mixed in with all the noise Dr Richard adds to this discussion. When you sort through what he is saying, ev is still a valid analogy for what is happening with combination (or monotherapy) therapy of HIV.

Wrong.

Not suprised you wrote in a small font; ashamed?

Off on holiday now, good luck with those tricky questions

 

[kleinman]

"That's to be expected because immune genes evolve very, very fast," Graves says.

So...lots of selection pressures = fast evolution.

What are these lots of selection pressures? Are you using Dr Richard’s counting scheme and counting each amino acid substitution as a selection pressure. Do you want to explain how this mechanism works with viruses, bacteria and how do you get these changes into gametes?

 

[joobz]

Computer memory requirements limit running large genome with large populations simultaneously. On my computer, the limit is a 1k genome length and a population of 1 meg. With smaller populations, you can run larger genome cases and these cases show that the generations for convergence proportional to about G^2.

only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.

Adebz has stated that at infinite population, generation for converges goes to 1. If that is true, the data obtained from ev shows that the slope of the generations for convergence/population is so shallow with large populations that you will need unrealistically large populations to get small generations for convergence.

only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.

Adebz now understands that doubling population does not double the probability of a particular mutation occurring at a particular locus. This effect is demonstrated by ev by it’s rapidly decreasing slope of the generations for convergence/population curve for the larger population series already presented here.

only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.

Look at this thread joobz, I present the results of Dr Schneider’s peer reviewed and published model and you all attribute this mathematics to me and instantly discredit the results.

I know full well you haven't done any math. Don't worry. No one has accused you of any model generation.
ev only has point mutation occuring with mutation rate and kill off rate fixed. Seems like you are making a baseless extrapolation.

Why do you think that Dr Schneider stopped publishing on his model? He knows what his model shows. He has put himself in the position of having to retract his statements that his model represents mutation and selection realistically or that his model is showing that information acquisition on longer genomes becomes profoundly slow. There is evidence of this in his web published statements that realistic length genomes cases would take years to run.

You are again confusing simulation time with evolution time. Seems like you are making a baseless extrapolation.

What is the Hill-Robertson effect? Here is the definition from Wikipedia which can be found at: http://en.wikipedia.org/wiki/Hill-Robertson_effect

So how does this work with HIV? Here is a quote from an article located at [URL="http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm"]http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm[/URL]

great. But then this completely destroys your earlier assertion

There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This statements is a baseless extrapolation.

This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.

thank you for this method of critique.
Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.

Seems like you keep adjusting the playing field to suite your needs. We used YOUR example and found it wanting. Now you claim it's a bad example.

Call the chain gang again, this goal post keeps shifting.

 

[kleinman]

Annoying Creationists

This is what is so illogical about Dr Richard’s way of counting. Notice how you neglected to respond to my final quote from this post. I’ll repeat it here so we can see where your logic leads.

Dr Richard, if you want to use your logic, ev does not have three directional selection pressures is has 32 directional selection pressures not 3. You are confusing the results of a directional selection pressure with the meaning of a directional selection pressures.

I am saying that you can measure a selection pressure acting on the codon.

What is your definition of a selection pressure again kleinman?

You'll have a week to think of one.

I don’t need a week to think about this one. I have been using the concept of a macroscopic selection pressure whether it is Dr Schneider’s selection conditions used in his model or the drugs which are used to treat HIV. These are macroscopic selection pressures. You now try to equate each amino substitution as a directed selection pressure. If you work by that definition, ev has 32 directed selection pressures.

It’s time for you to answer a couple of questions. The first is what are these 60-70 directional selection pressures?

It’s time for you to answer a couple of questions. The first is what are these 60-70 directional selection pressures?

Another failure in reading comprehension. But your faith is blinding you to the obvious.

I cannot say for certain, as the paper does not provide this information. But I would say they include (but are not limited to)

1. mutations within the HIV protease gene that improve the efficiency of the gene in an untreated patient

2. mutations within the HIV protease gene that improve the efficiency of the gene in an treated patient

3. mutations within the reverse transcriptase gene that improve the efficiency of the gene in an untreated patient

4. mutations within the reverse transcriptase gene that improve the efficiency of the gene in an treated patient

5. mutations within either gene that improve integration/replication in the host DNA

6. mutations that interact with other mutations in the genome to improve overall fitness

1. What is the selection pressure that increases protease efficiency in an untreated patient?
2. What is the selection pressure that increases protease efficiency in a treated patient?
3. What is the selection pressure that increases reverse transcriptase efficiency in an untreated patient?
4. What is the selection pressure that increases reverse transcriptase efficiency in an treated patient?
5. What is the selection pressure that improves integration/replication in the host DNA?
6. What is the selection pressure that causes mutations in the genome to interact with other mutations to improve overall fitness?

Are there any stabilizing selection pressures acting on HIV and if so, how many are there? Are there neutral selection pressures acting on HIV and if so, how many are there?

The second is, there is an error in the equation in your link, what is it? If you can’t find it, perhaps the resident James Randi Educational Forum PhD in amathematics can find it.

Which link?

It’s in The HIV positive selection mutation database link the one you said you read so carefully. Here, I’ll post the equation again for you. Once you find the error, explain to us this equation. You brought up the reference. Let’s see if you can explain to us your own links. If it is too technical for you, don’t bother. We already have enough evolutionists posting URLs on this thread that they can’t explain.

 

[kleinman]

Annoying Creationists

Computer memory requirements limit running large genome with large populations simultaneously. On my computer, the limit is a 1k genome length and a population of 1 meg. With smaller populations, you can run larger genome cases and these cases show that the generations for convergence proportional to about G^2.

only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.

Large population cases are done with unrealistically high mutation rates in order to get as fast a convergence as possible. Even under these circumstances the largest of population cases takes hundreds of hours of cpu time on a 2.3GHz machine. Do you think slowing down the mutation rate will speed up evolution? No matter what the mutation rate, half the population always survives. What do you think happens when a living thing is exposed to a mutagen?

Adebz has stated that at infinite population, generation for converges goes to 1. If that is true, the data obtained from ev shows that the slope of the generations for convergence/population is so shallow with large populations that you will need unrealistically large populations to get small generations for convergence.

only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.

If you think that other mutation mechanism will accelerate evolution, prove it. Otherwise you are the one making the baseless extrapolation. Ev shows that point mutations and natural selection doesn’t support the theory of evolution. If you contend that other mechanisms of mutations will correct what ev is showing, put this in the model and prove it. Otherwise, the theory of evolution is founded on baseless speculations and extrapolations.

Adebz now understands that doubling population does not double the probability of a particular mutation occurring at a particular locus. This effect is demonstrated by ev by it’s rapidly decreasing slope of the generations for convergence/population curve for the larger population series already presented here.

only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.

Let’s see if Adebz can show that frame shift mutations increase the probability of a particular mutation occurring at a particular location. Maybe you want to try to do this probability problem?

Look at this thread joobz, I present the results of Dr Schneider’s peer reviewed and published model and you all attribute this mathematics to me and instantly discredit the results.

I know full well you haven't done any math. Don't worry. No one has accused you of any model generation.
ev only has point mutation occuring with mutation rate and kill off rate fixed. Seems like you are making a baseless extrapolation.

What I have done is what Dr Schneider suggested to me privately and publicly suggested in his published paper on ev. That is do a parametric study with his computer simulation of random point mutation and natural selection. I guess alchemical engineers do not do parametric studies with their computer models.

Why do you think that Dr Schneider stopped publishing on his model? He knows what his model shows. He has put himself in the position of having to retract his statements that his model represents mutation and selection realistically or that his model is showing that information acquisition on longer genomes becomes profoundly slow. There is evidence of this in his web published statements that realistic length genomes cases would take years to run.

You are again confusing simulation time with evolution time. Seems like you are making a baseless extrapolation.

No joobz, I’m not confusing simulation time with evolution time. If you studied and understood ev, you would know this. Dr Schneider and Paul understand this principle even if you don’t.

What is the Hill-Robertson effect? Here is the definition from Wikipedia which can be found at:

http://en.wikipedia.org/wiki/Hill-Robertson_effect

So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htmhttp://www.cdc.gov/ncidod/eid/vol3no3/burke.htm

great. But then this completely destroys your earlier assertion

No it doesn’t, it only shows that you know how to make a baseless extrapolation.

There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This statements is a baseless extrapolation.

Simple enough; put any mutation mechanism you want in ev and prove this. Otherwise your theory of evolution started and remains without a mathematical basis. Of course, that is not a baseless extrapolation in the brainwashed mind of an evolutionist.

This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.

thank you for this method of critique.
Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.

What you continue to miss in this discussion is that recombination does not create new genes. You must still evolve the resistant gene by mutation and selection. Once you evolve the gene, recombination can spread the gene though the gene pool but recombination does not make new gene.

Seems like you keep adjusting the playing field to suite your needs. We used YOUR example and found it wanting. Now you claim it's a bad example.

I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts. Well let’s see. I started saying that the theory of evolution is mathematically impossible as shown by the results of the peer reviewed published model of random point mutation and natural selection. Then I adjusted my statement by saying that the reason why ev shows the theory of evolution is mathematically impossible is that multiple selection pressures slow the process of evolution and then shame of shames, I said it is multiple directional selection pressures which slow evolution. Do you think stabilizing selection pressures accelerate evolution?

I’ve put forth a simple mathematical hypothesis based on the results of an evolutionist written, peer reviewed and published model of mutation and selection. I have presented numerous real examples of this phenomenon. If you think that multiple directional selection pressures accelerate evolution, prove it. Complaining about moving goalposts will not win this debate.

 

[Paul C. Anagnostopoulos]

... the first marsupial genome has been sequenced.

All hail the mighty little grey, short-tailed opossum!

~~ Paul

 

[kleinman]

Annoying Creationists

... the first marsupial genome has been sequenced.

All hail the mighty little grey, short-tailed opossum!

Paul, do you know how to tell the difference between the opossum and the theory of evolution?

The opossum plays dead, the theory of evolution is dead.

 

[joobz]

For clarity, I have summarized the key points of this conversation. I think we have a new lie here.

If you studied ev, you would understand this. If you examined the real cases of combination therapy for the treatment of HIV, combination therapy for the treatment of TB, combination pesticides, combination herbicides, combination rodenticides, you would see real examples of what ev demonstrates and what the fitness landscape requires. Mutation and selection can not and does not do what evolutionists allege, it is mathematically impossible.

It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is your concrete basis for not worring about it?

I think this paper wouldn't have been accepted if that was the case:

Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]

I can't access the paper yet, but from the abstract:

Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios

Seems like evolution has a mathematical basis after all.

So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm

Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).

This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.

Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.

No it doesn’t, it only shows that you know how to make a baseless extrapolation.

I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts.

This isn't an "adjustment of a theory". This is intellectual dishonesty.

We have been discussing how multiple pressures doesn't stop evolution using HIV as an example. I give evidence that states mathematically that this isn't the case. And now you claim that it doesn't apply.
This is the worst form of professional behavior.

 

[Ichneumonwasp]

Joobz, yeah, he pulled that with me several pages ago when I pushed him into the same corner, which is why I bowed out of the debate. There is simply no sense in continuing a conversation with someone who is so dishonest.