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Annoying creationists

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Can I just see if I've got this straight? Is Kleinman really now arguing that the evolution of drug resistance proves that evolution doesn't happen? I didn't think it was possible to prove yourself quite so spectatularly wrong without actually imploding.
 
Can I just see if I've got this straight? Is Kleinman really now arguing that the evolution of drug resistance proves that evolution doesn't happen? I didn't think it was possible to prove yourself quite so spectatularly wrong without actually imploding.

As far as I can tell, he is arguing that using three drugs on one microbe culture at once causes them to evolve resistances to all three drugs slower then if the drugs were applied one-by-one.

This is, of course, complete bollocks.
 
Wait, I thought he was saying that multiple selection pressures causes evolution to stop. Well, with a sufficiently large genome, anyway.

~~ Paul
 
Wait, I thought he was saying that multiple selection pressures causes evolution to stop. Well, with a sufficiently large genome, anyway.

~~ Paul
Well, yes and no. He claims "stop", but when he speaks of specific examples like HIV treatment, reality creeps in a bit:
Kleinman said:
This is exactly analogous to the strategy used in the treatment of HIV. By using multiple drug regimens, you apply multiple selection pressures and reduce the ability of the virus to evolve. Monotherapy treatment markedly increases the likelihood of evolving resistant strains of the virus.
[color highlighting mine]

In the real world, he cannot demonstrate evolution coming to a stop. His interpretation of evolution in ev is made possible by an a priori definition of success; certainly, if there is only one way into a room, and you block the door, you have stopped entry. But in the real world, evolution cannot be stopped by some Maginot line; there is more than one way to respond to any given selection pressure. Some interesting reading here, about TMTOWTDI (There's More Than One Way To Do It). An appropriate excerpt:
TMTOWTDI said:
This is why a lot of computer programmers, mathematicians, and engineers seem to have a hard time intuitively grasping both evolution and the possibility of abiogenesis. They think that things have to be just one way in order to work, and then they wonder how evolution can possibly find such a tiny target in such a large field of possibilities. This is also a point harped on by evolution's critics, and I am willing to believe that at least some of them honestly think they are onto something here (especially the mathematicians and computer scientists for the aforementioned reasons).
 
In the real world, he cannot demonstrate evolution coming to a stop... But in the real world, evolution cannot be stopped by some Maginot line...
It can be stopped by complete extinction. If you wipe out all of the relevant life, there won't be anymore evolution.
 
It can be stopped by complete extinction. If you wipe out all of the relevant life, there won't be anymore evolution.
True--thus the "Maginot Line" reference (if not a great analogy). If there is a way around, over, under, or through, then blocking one of those routes is not enough. Nor two, nor three. While there is life, there is the possibility that something will stumble upon the solution. If, instead of the Maginot Line, the French had simply exterminated the Germans...
 
Annoying Creationists

Kleinman said:
Because he doesn’t realize that setting a mistake weight to 0 is equivalent to turning off that particular selection condition.
kjkent1 said:
What you don't recognize is that an ev "perfect creature" is defined as a genome substantially absent missed or spurious bindings. So, when you turn off a selection condition, ev reports a perfect creature when no perfect creature has yet evovled according to the ev definition of perfection. Thus, the report is an error -- as is your conclusion based on the error.
“Perfect creature” is only a label used by Paul and Dr Schneider to indicate a creature that has satisfied all three of their selection conditions. If you turn off two of the three selection conditions then a “perfect creature” is one that satisfies that selection condition.
Taffer said:
One specific point, though. The time to create a triple-resistant mutant is the same in both cases you provided. If you disagree, provide evidence and citations. Until you do, I will trust my own studies, thank you.
Taffer, read the guidelines for treating HIV and why triple medications are used. I posted a specific quote from the guidelines and I repost it again here:
Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents said:
Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.

With respects to your argument that you can achieve triple resistance as quickly using triple antimicrobials in parallel as when the antimicrobials serially, provide your evidence and citations. You argue that 1+1+1=3 give the same results as 1*3=3. Do you think this argument extends to millions of selection conditions? If so, you are in disagreement with the results from ev.
Kleinman said:
When you have one selection condition, ev evolves for that one condition, when you have two or more conditions, ev will evolve for those selection conditions if the genome is short enough. What is interesting is that you cling on to this Rcapacity concept when you admit it only has application to Dr Schneider’s selection process. Why don’t you define Rcapacity for Unnamed’s selection process.
Paul said:
I did not say it was relevant only to Ev's selection process. I said it was only relevant when the width of the binding sites are fixed, as they are in Ev. Rcapacity works the same with Unnamed's selection process, assuming that the mistake counts are all positive.
Really? I don’t recall Unnamed running any cases with a short site width.
Kleinman said:
Paul, your observation that with Dr Schneider’s selection conditions lead to a point where ev stops converging when Rfrequency approaches 2*binding site width is an interesting coincidence but does not explain why ev stops converging.
Paul said:
It explains why it has stopped converging in all the experiments I've seen. You claim to have two experiments that stop converging even when Rcapacity is not an issue. Please present the parameters of those experiments.
Rcapacity doesn’t explain why ev converges when you eliminate two of the three selection conditions no matter what the site width is.
Kleinman said:
I’ve already done two cases that demonstrate this. I’m checking with kjkent1 to see if we can use his company’s computer to do the 3 gigabase case.
Paul said:
Please present the parameters of those experiments.
1st case: Population 64, gamma=16, site width=6, G=16384, mutation rate=1/G/generation, weight width=5, Rfreq=10, Paul’s infamous Rcapacity=2*site width=10. With the weights for each mistake, (missed site, spurious binding in gene, spurious binding outside gene), set to 1, this case fails to converge. But for varying weights you get the following results:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233

2nd case: G=100,000, binding site width=4, weight width is 3, Rfrequency is 13.61, Rcapacity=8, gamma=8, mutation rate=1/G/generation.
Missed sites/spurious gene/spurious non-gene/gens to perfect creature

1/0/0/1
0/1/0/54
0/0/1/2192
Kleinman said:
Paul, Rfrequency is dependent on gamma and G. gamma and G are independent of the selection process. Unless Dr Schneider improperly defined Rfrequency, this value is independent of the selection process.
Paul said:
Alan, what is Rfrequency? Could you define it for us?
Rfrequency=-log2(gamma/G) where gamma is the number of binding sites and G is the number of sites in the genome. Do you want to define Rcapacity for us?
Kleinman said:
A binding site width of 1 means that particular base will always be recognized as a binding site. What ev should do is evolve so that all binding sites will be of that base in the binding site region and eliminate that base from causing spurious binding inside and outside the gene.
Paul said:
And so as Rfrequency climbs above Rcapacity (2 in this case), the number of bits required to distinguish binding sites from other sites exceeds the available number of bits in the binding sites. This happens quickly when Rcapacity = 2.
Paul, run those cases I’ve listed above. Single step through the cases and watch what happens to the mistake counts.
Kleinman said:
Paul, that’s what these examples do. These examples do not evolve when all three selection conditions are turned on yet when you set two of the three to 0, the non-zero condition evolves sequences that satisfy the remaining selection condition.
Paul said:
Which examples? Please present the parameters.
I’ve presented them above for the third time. Do you want me to post the parameters again?
Kleinman said:
Paul, I never said I demonstrated the 3 gigabase case.
Paul said:
I know you haven't. What I want to see are the two examples you claim "stopped."
And the reason they “stopped” is that there was only one selection condition acting. This condition was achieved by setting to of the three weight factors to 0 thereby eliminating two of the three selection conditions. Once you run these cases, it should become clear to you that the reason these cases are able to converge is there is only a single selection condition.
Kleinman said:
The 16k case was one from a series I did last year and it did not converge. The 100k case, I chose parameters much worse than many of the other cases which failed to converge. I chose a small site width of 4 and a larger genome length than many of the other cases which failed to converge. Feel free to burn up some clock cycles on your computer on this 100k case and prove me wrong and that this case will converge with all three selection conditions acting.
Paul said:
I can't burn any cycles until you specify the parameters.
Don’t worry; you won’t burn very many clock cycles with these cases. If fact, you should run the 16k case using the step button.
Kleinman said:
Just what good is your Rcapacity concept? Let’s see you apply it to Unnamed’s selection process.
Unnamed said:
It isn't any good! It just explains why certain Ev experiments will not converge. You claim evolution stops for a different reason. I just want you to demonstrate your claim. Is this really so hard to understand?
Paul, I have posted the parameters three times now. If you don’t run the cases after reading this post, you have no other excuse than denial.
Kleinman said:
Because he doesn’t realize that setting a mistake weight to 0 is equivalent to turning off that particular selection condition.
kjkent1 said:
He doesn't?
He seems to think that you can only have a perfect creature when you satisfy all three of your selection conditions. Who knows what is going on in his mind, he thinks string cheese explains evolution.
Cuddles said:
Can I just see if I've got this straight? Is Kleinman really now arguing that the evolution of drug resistance proves that evolution doesn't happen? I didn't think it was possible to prove yourself quite so spectatularly wrong without actually imploding.
You didn’t get it quite right Cuddles. What I said was that multiple selection processes slow and then ultimately stop evolution. This is what ev shows and it is this principle which is used to treat HIV. Monotherapy treatment of HIV quickly leads to resistant strains of the virus to that drug, so standard of care now for HIV is triple antiviral drugs to reduce the evolution of drug resistance strains. Multiple selection processes slow and ultimately stop evolution. This is a mathematical fact revealed by ev and it occurs in reality.
Paul said:
Wait, I thought he was saying that multiple selection pressures causes evolution to stop. Well, with a sufficiently large genome, anyway.

Paul, that is in fact what your model shows.
Paul said:
Wait, I thought he was saying that multiple selection pressures causes evolution to stop. Well, with a sufficiently large genome, anyway.
Mercutio said:
Well, yes and no. He claims "stop", but when he speaks of specific examples like HIV treatment, reality creeps in a bit:

The mutations that give drug resistance in HIV are usually single base substitutions which are much simpler than the evolution example described by ev and therefore don’t require multiple mutations to a sequence of bases yet three drugs (selection pressures) are enough to prevent the evolution of resistant strains for years. If resistant strains do start appearing, I suspect the strategy will be to add a fourth drug. To you want to explain how you can have a selection processes evolving the ancestral insulin gene, the ancestral hemoglobin gene, the ancestral genes for the DNA replicase system… all acting simultaneously?
Kleinman said:
This is exactly analogous to the strategy used in the treatment of HIV. By using multiple drug regimens, you apply multiple selection pressures and reduce the ability of the virus to evolve. Monotherapy treatment markedly increases the likelihood of evolving resistant strains of the virus.
Mercutio said:
In the real world, he cannot demonstrate evolution coming to a stop. His interpretation of evolution in ev is made possible by an a priori definition of success; certainly, if there is only one way into a room, and you block the door, you have stopped entry. But in the real world, evolution cannot be stopped by some Maginot line; there is more than one way to respond to any given selection pressure. Some interesting reading here, about TMTOWTDI (There's More Than One Way To Do It). An appropriate excerpt:
Add a fourth drug to the HIV treatment regimen, it will only slow the evolution of resistant strains more so. As Paul said previously, there are millions of selection pressures acting simultaneously on living things. Ev shows that three selection pressures are enough to stop evolution. Ev presents you with a humungous mathematical problem. The reason why ev takes so many generations to evolve binding sites is that the three selection conditions in the model interfere with each other. This principle is used to treat HIV to prevent the evolution of drug resistant strains of the virus.
Mercutio said:
In the real world, he cannot demonstrate evolution coming to a stop... But in the real world, evolution cannot be stopped by some Maginot line...
Delphi ote said:
It can be stopped by complete extinction. If you wipe out all of the relevant life, there won't be anymore evolution.
Is the HIV virus relevant?
Delphi ote said:
It can be stopped by complete extinction. If you wipe out all of the relevant life, there won't be anymore evolution.
Mercutio said:
True--thus the "Maginot Line" reference (if not a great analogy). If there is a way around, over, under, or through, then blocking one of those routes is not enough. Nor two, nor three. While there is life, there is the possibility that something will stumble upon the solution. If, instead of the Maginot Line, the French had simply exterminated the Germans...
Your “Maginot Line” is a perfect analogy. The Maginot line was a single selection pressure. The French might have done better if they used multiple selection pressures such as an Air Force and mobile armor.
 
“Perfect creature” is only a label used by Paul and Dr Schneider to indicate a creature that has satisfied all three of their selection conditions. If you turn off two of the three selection conditions then a “perfect creature” is one that satisfies that selection condition.
Nope. You're wrong, and you need to drop your superiority complex and recognize that you're wrong, so we can move on, because you're spewing out nonsense with this current argument.

A perfect creature in ev is a creature which is substantially free of missed and/or spurious bindings, and which has evolved information such that Rseq is approaching Rfreq. There's an easy way to prove this:

1. Use the default settings, and pick a random seed that produce a perfect creature. Whenever you do this, the perfect creature will also show that Rseq is approaching Rfreq, because that is the measure of an evolved genome that ev uses to prove that evolution is possible by RMNS.

2. Use the same settings, but set one of the mistake weights to zero, and pick a random seed that produces a perfect creature. Under no circumstances will Rseq come anywhere near Rfreq.

Under your required conditions, with mistake weights at zero, there is no requirement that the final genome represent anything remotely resembling an evolved genetic sequence. You will consistently obtain a perfect creature in one generation with a genome that's random gibberish.

All you need do is look at the sequence to see that it's still filled with errors. So, just open your eyes and look.
 
Kleinman said:
“Perfect creature” is only a label used by Paul and Dr Schneider to indicate a creature that has satisfied all three of their selection conditions. If you turn off two of the three selection conditions then a “perfect creature” is one that satisfies that selection condition.
This is arguable, but not really worth the effort to argue it.

Really? I don’t recall Unnamed running any cases with a short site width.
What does this have to do with whether Rcapacity is relevant to Unnamed's selection process? Rcapacity is relevant when all three mistake counts are nonzero.

Rcapacity doesn’t explain why ev converges when you eliminate two of the three selection conditions no matter what the site width is.
That is correct. As I have now said a half dozen times: Rcapacity is irrelevant when any mistake counts are zero.

1st case: Population 64, gamma=16, site width=6, G=16384, mutation rate=1/G/generation, weight width=5, Rfreq=10, Paul’s infamous Rcapacity=2*site width=10. With the weights for each mistake, (missed site, spurious binding in gene, spurious binding outside gene), set to 1, this case fails to converge.
Actually, Rcapacity = 12. How do you know it fails to converge, or simply takes a long time?

Rfrequency=-log2(gamma/G) where gamma is the number of binding sites and G is the number of sites in the genome. Do you want to define Rcapacity for us?
I know the math. I want you to define what Rfrequency means.

And the reason they “stopped” is that there was only one selection condition acting. This condition was achieved by setting to of the three weight factors to 0 thereby eliminating two of the three selection conditions. Once you run these cases, it should become clear to you that the reason these cases are able to converge is there is only a single selection condition.
On and on you go, without actually demonstrating what you claim: Evolution stopping with all mistake counts nonzero and Rcapacity not an issue.

Paul, I have posted the parameters three times now. If you don’t run the cases after reading this post, you have no other excuse than denial.
I don't need to run the cases. I am not claiming that you are lying. How do you know your experiment won't produce a perfect creature?

He seems to think that you can only have a perfect creature when you satisfy all three of your selection conditions. Who knows what is going on in his mind, he thinks string cheese explains evolution.
Alan, this is simply a question of the definition of perfect creature, isn't it? As the person who coined the term, I get to specify the definition. Would you like it to mean (a) a creature who perfectly distinguishes binding sites from other sites; or (b) a creature with zero mistakes?

Paul, that is in fact what your model shows.
Demonstration, please.

~~ Paul
 
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Annoying Creationists

Kleinman said:
“Perfect creature” is only a label used by Paul and Dr Schneider to indicate a creature that has satisfied all three of their selection conditions. If you turn off two of the three selection conditions then a “perfect creature” is one that satisfies that selection condition.
kjkent1 said:
Nope. You're wrong, and you need to drop your superiority complex and recognize that you're wrong, so we can move on, because you're spewing out nonsense with this current argument.
Well, Paul is going to run the cases I have suggested so prepare yourself for a shock.
kjkent1 said:
A perfect creature in ev is a creature which is substantially free of missed and/or spurious bindings, and which has evolved information such that Rseq is approaching Rfreq. There's an easy way to prove this:
You need to take a few courses in mathematical modeling of physical systems.
kjkent1 said:
All you need do is look at the sequence to see that it's still filled with errors. So, just open your eyes and look.

So what? The ev model won’t converge with all three selection conditions imposed. Turn off two of the three selection conditions and you can evolve that condition in the genome. It is the competing selection conditions which slow and ultimately stop evolution in ev. This effect is seen in reality. This principle is used to slow if not stop the evolution of resistant strains of HIV viruses. Not only do you not have a selection process to evolve a gene from the beginning, multiple selection pressures slow and ultimately stop evolution. This is what ev shows mathematically and this is what is seen in the treatment of HIV. This is why the theory of evolution is mathematically impossible.
 
Taffer, read the guidelines for treating HIV and why triple medications are used. I posted a specific quote from the guidelines and I repost it again here:

I have read enough of that document to know it does not say what you are claiming. Multiple drugs are used, primarily as far as I can tell from your source, because if resistance to one drug evolves, you can replace it with another drug while continuing treatment.

Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.

They are talking about specific drugs, and not he overall drug regeme. Did you even read your own source? Just doing a word search isn't going to cut it, especially if you do not understand microbiology.

Secondly, it is stating that there is an increased risk of resistance arrisal because of the increased half-life of those specific drugs. Read your own bloody source.

With respects to your argument that you can achieve triple resistance as quickly using triple antimicrobials in parallel as when the antimicrobials serially, provide your evidence and citations.

My own experiments. Provide your citations and evidence that they are wrong. Can't? Didn't think so.

You argue that 1+1+1=3 give the same results as 1*3=3. Do you think this argument extends to millions of selection conditions?

Yes. In fact, I think multiple selective pressures increase variation within a population, and ultimately lead to more diversity (and thus more evolution).

If so, you are in disagreement with the results from ev.

I'm in disagreement with a model of one specific section of evolution when it is compared to the whole of evolution? Oh noes, the horror! :rolleyes:
 
Paul, you better check your arithmetic, that 16384 base case has an Rfrequency of 10 according to your computer model.
 
Kleinman said:
Well, Paul is going to run the cases I have suggested so prepare yourself for a shock.
If I run anything, it will be the experiment with all three mistakes counts set to 1. I don't care about the other cases.

You need to take a few courses in mathematical modeling of physical systems.
Cripes, Alan, you're such a condescending jerk. The term perfect creature is just one I made up. There is no mathematical/scientific definition of the term.

So what? The ev model won’t converge with all three selection conditions imposed.
Demonstration, please.

~~ Paul
 
Annoying Creationists

Kleinman said:
Paul, you better check your arithmetic, that 16384 base case has an Rfrequency of 10 according to your computer model.
Paul said:
Yes, Alan, it does. What I said was that Rcapacity = 12.
Oh, I’m sorry, so let’s do the case of G=16384 and site width=4, all other parameters the same:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/104
0/1/0/114
0/0/1/14

Rfrequency=10, and your famous Rcapacity value =8. Let’s try a site width of 3.
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/12
0/1/0/1
0/0/1/36

Rfrequeny=10, Rcapacity=6
Paul, it is the competing selection processes that prevent ev from evolving all the selection conditions simultaneously.
 
Kleinman said:
Paul, it is the competing selection processes that prevent ev from evolving all the selection conditions simultaneously.
Alan, read my fingers: I don't care about experiments with mistake counts of zero. The only reason you've moved the goalpost to that red herring is because you can contrast it with experiments in which you claim that evolution stopped completely. But that isn't interesting if it didn't actually stop, is it? And you don't have no compelling data to show they stopped, do you? So we don't give a crap, do we?

Prove that evolution stops in the normal case and then we have something to talk about.

Edited to add: And you can do it with high mutation rates, because if evolution stops, then it stops no matter the mutation rate.

~~ Paul
 
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Your “Maginot Line” is a perfect analogy. The Maginot line was a single selection pressure. The French might have done better if they used multiple selection pressures such as an Air Force and mobile armor.

Ok, then let me expand on it a bit. Suppose the French did use an Air Force and mobile armor, and nerve agents, blister gases, poisoned saurkraut, and a hermetically sealed geodesic dome over the entire country. Let us further suppose that these successfully kept the Nazis out of France. Have they stopped the Third Reich from successfully evolving? Not as long as there are other countries--other sources of energy to exploit.

If we define success as "invading France", and our selection pressures prevent that outcome, we can "stop evolution". But in the real world, we don't get to define an outcome a priori. We have to come up with a new flu vaccine each year, because even though we provided a selection pressure in the form of last year's vaccine, we could not predict which direction(s), if any, the Nazi Flu Germs would take around our Maginot Line, or even whether they would give up on France and head for Canada instead. Ev does not model that. Sorry.
 
Annoying Creationists

Kleinman said:
Paul, it is the competing selection processes that prevent ev from evolving all the selection conditions simultaneously.
Paul said:
Alan, read my fingers: I don't care about experiments with mistake counts of zero. The only reason you've moved the goalpost to that red herring is because you can contrast it with experiments in which you claim that evolution stopped completely. But that isn't interesting if it didn't actually stop, is it? And you don't have no compelling data to show they stopped, do you? So we don't give a crap, do we?
You forgot your strawman argument as well. Only two of the three selection conditions are set to zero. There are no moving goalposts here Paul. I started this discussion stating that your computer model shows that evolution is mathematically impossible. The only thing that has been added is the explanation why your computer model shows it is impossible. It is the competing selection processes that slow down and ultimately stop ev from converging. It is not due to the weight matrix not being able to match (surpass the threshold). The last two cases I presented had Rcapacity values much less than Rfrequency yet they rapidly converge if you have only one selection condition. In fact all three selection conditions will converge if done one at a time. This accurately models the situation of using three drugs (three selection conditions) to prevent the evolution of resistant strains of the HIV virus. You are in denial about what the data from ev shows. With respects to having compelling data to show that ev slows down and stops converging with the three selection conditions imposed, the G=8192 case took over 700,000 generations to converge. The G=16,384 case takes only about 100 generations to converge each of the individual selection conditions and that is with small site widths than what your Rcapacity condition would allow.
Paul said:
Prove that evolution stops in the normal case and then we have something to talk about.
Paul, there is no “normal” case. You have three selection conditions defined in ev and can weight each condition from 0 to what ever value you have allow. If you think that it requires your three selection conditions to be imposed in order to have a “normal” case, what do you think would happen to your model if you evolve two different sets of binding sites simultaneously? In this case you would have 6 selection conditions, 2 selection conditions for missed binding sites, 2 selection conditions for spurious binding in the gene and 2 selection conditions for spurious binding outside the gene. Do you think this model will converge more quickly than your present model? Paul, it is the competing selection conditions that slow down and ultimately stop ev from converging. This effect would be worse with more selection conditions.
Paul said:
And you can do it with high mutation rates, because if evolution stops, then it stops no matter the mutation rate.

Paul, it is the multiple selection conditions which slows down the convergence of ev. I’ll start posting series of cases which make it more apparent to you. This is a real phenomena that Dr Schneider’s model has captured. Why don’t you put a two binding site set model on your to do list? Then you can evolve perfect creatures that satisfy 6 selection conditions. This would make kjkent1 happy except I doubt this model would ever converge no matter what the genome length.
Kleinman said:
Is the HIV virus relevant?
Delphi ote said:
Definitely. If you can find any treatment to which it cannot adapt, do let the world know. A cure for HIV/AIDS would probably be a big deal.
There already is a good strategy for treating this disease. 3 drug therapy can extend life for years. The biggest problem with these multi-drug regimens is the adverse reactions from the drugs. If more low side effect drugs can be developed that target more viral proteins then you can put more selective pressure on the virus than just 3. The more selective pressures you can put on the virus, the less likely resistant strains will evolve. Multiple selective pressures slow the evolutionary process.
 
So what? The ev model won’t converge with all three selection conditions imposed. Turn off two of the three selection conditions and you can evolve that condition in the genome.
No, you can't, because the other condition is physically present and its hosts are never selected against. You can produce a "perfect creature," but it's not evolved in any meaningful sense, according to the mathematics upon which ev is postulated.

It is the competing selection conditions which slow and ultimately stop evolution in ev.
Laughably incorrect conclusion.
This effect is seen in reality.
BZZZZ! Incorrect!
This principle is used to slow if not stop the evolution of resistant strains of HIV viruses.
Is it? Let's test this spectacular logic. In the real world there are countless environmental stresses on every creature, and evolution is generally slow but inexorable. Along comes the mighty Alan Kleinman and he subjects one of these creatures, the HIV virus, to one more selective pressure, and the creature starts to evolve more slowly. Then he does it with one more stress, and the creature's evolution really starts to slow. Finally, he applies the third stroke, and HIV's evolution comes to a practical halt. Remarkable -- the first 10 billion odd environmental stresses had no perceivable effect, and in fact, HIV evolved OUT of this huge number of stresses. Then suddenly, just by coincidence, the application of three more stresses brings evolution to a dead stop -- just like Mr. Logic says that it should.


Makes sense huh? Of course a reasonable person might just conjecture that the reason why HIV was slowing down in the lab is because the anti-virals were killing most of the virus off entirely, or that the drugs were targeted in a manner which would be more likely to destroy the virus -- not necessarily because of the coincidence of environmental stresses.

I'm sure you'll have a startling explanation for why my logical analogy is wrong and your ridiculous conclusion is correct -- and I can't wait to read it in the next episode of: "When the wine cork turns."
 
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