Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."

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Multidrug-resistant (MDR) HIV-1 presents a challenge to the efficacy of antiretroviral therapy (ART). To examine mechanisms leading to MDR variants in infected individuals, we studied recombination between single viral genomes from the genital tract and plasma of a woman initiating ART. We determined HIV-1 RNA sequences and drug resistance profiles of 159 unique viral variants obtained before ART and semiannually for 4 years thereafter. Soon after initiating zidovudine, lamivudine, and nevirapine, resistant variants and intrapatient HIV-1 recombinants were detected in both compartments; the recombinants had inherited genetic material from both genital and plasma-derived viruses. Twenty-three unique recombinants were documented during 4 years of therapy, comprising ∼22% of variants. Most recombinant genomes displayed similar breakpoints and clustered phylogenetically, suggesting evolution from common ancestors. Longitudinal analysis demonstrated that MDR recombinants were common and persistent, demonstrating that recombination, in addition to point mutation, can contribute to the evolution of MDR HIV-1 in viremic individuals.
https://www.liebertpub.com/doi/10.1089/aid.2011.0383

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Recombination is an important factor in evolving multidrug resistance in HIV.

Kleinman:

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Is that all you can find is constant environment experiments with a single selection pressure.

Taq:

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The Lenski experiment used a constant environment and a single selection pressure for 50,000 generations.
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"The Kishony and Lenski experiments demonstrate exactly how descent with modification operates."--Kleinman

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That's right, in a constant environment, single selection pressure environment it takes a billion replications for each adaptive mutation. When there are multiple selection pressures and the environment is changing, it takes exponentially more replications to adapt. This is why UCD is not possible. This is your cue to claim 20 billion pre-humans, and 20 billion pre-pre-humans and 20 billion....

Kleinman:

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I've said it many times, you just don't get it. It takes 1/(mutation rate) replications in a single selection pressure environment to get an adaptive mutation.

Taq:

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Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found he

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Ah, so it was a phage that evolved a human, that's brilliant. Tell us all about it.

Kleinman:

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When recombination is a possibility, a changing environment reduces the probability because the selection condition is changing therefore, the adaptive alleles are changing.

Taq:

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Reduces the probability of what, and compared to what?

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The probability of an adaptive recombination event occurring, slow poke. You can speculate otherwise but combination therapy for HIV, weeds, and insects says you are wrong, they work.

Kleinman:

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So you dream. None of the adaptive alleles would have had a chance to increase in frequency.

Taq:

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In a constant environment, why wouldn't beneficial alleles increase in frequency in a sexually reproducing population?

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Sure they can, but it is much less likely in a varying environment with multiple selection conditions. That's why combination therapy for treating HIV, weeds, and insects works. The probability of an adaptive recombination event occurring is extremely low, that's why using combination selection pressures works. You have no experience treating populations using combination selection pressures. You should get some experience.

Kleinman:

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You should know the answer to this one dummy, even Tany blundered into this one.

Taq:

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I do know the answer. Sexual recombination doesn't change in a changing environment. It works the same way. When humans move to a different environment their gametes still work in the very same way.

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Even Tany knows that the most fit variant changes as the environment changes. But now I understand why you have this preoccupation with a constant environment, single selection pressure systems, it is the limit of your understanding. The real world isn't made of constant environments with a single selection pressure. You have very limited education.

Kleinman:

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The Lenski experiment would operate more slowly in a changing environment.

Taq:

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You said the Lenski experiment demonstrates exactly how descent with modification works, and it had 50,000 generations in the same exact environment. You reject the Desai experiment because it had a constant environment for 90 generations.
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Hypocrisy much?

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Your limited education explains why you would think that evolution occurs just as rapidly with one selection pressure as with two. Why doesn't Lenski use two selection pressures in his experiment or Kishony? Wait, Kishony has tried two selection pressures (drugs) and his experiment doesn't work. What a surprise for someone that thinks that evolution works just as rapidly with one selection pressure as with two. And I don't reject the Desai experiment, I just recognize its limitations. You don't.

Kleinman:

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The genius virologist has just proven that 3 drug combination therapy does not work for the treatment of HIV.

Taq:

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I'm not the one rejecting published science. You are.

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Oh, do you mean all the publications that explain the Kishony and Lenski experiment? Or how about what Desai said: That was written a couple of years ago. He still doesn't understand how drug resistance evolves and neither do you.

Kleinman:

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Biological evolution only gets slower with changing environments and multiple selection pressures. You really don't know anything about biological evolution.

Taq:

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Then show it in a real population. Show how an asexual and sexual population evolve in changing environments with multiple selection pressures.

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I have mental giant, with combination therapy of HIV, weeds, and insects, and with single selection pressure experiments like Kishony's, Lenski's, and Desai's. There are no examples of evolution working more rapidly when there are multiple selection pressures acting against the population. And these single selection pressure experiments operate very slowly.

Kleinman:

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I've given you many empirical examples, HIV, insects, and weeds.

Taq:

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All of which increase their rate of adaptation through sexual recombination.

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That explains why combination therapy doesn't work for treating HIV, weeds, and insects, you are one smart cookie.

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The acquired inheritable trait of plants to survive and reproduce under herbicide exposure is defined as resistance. Herbicide resistance is an extraordinary example of adaptive evolution in weed species infesting agroecosystems with clear detrimental consequences on agriculture sustainability around the globe (Palumbi, 2001; Llewellyn et al., 2016). Multiple herbicide resistance is a compelling evolutionary process in which distinct survival mechanisms are present in a population or are combined within single plants, each endowing resistance to dissimilar site of action herbicides (Hall et al., 1994; Gaines et al., 2020). These multiple mechanisms may involve either target site (TSR) or non-target site resistance (NTSR) mechanisms or any combination endowing multiple resistance. Multiple resistance can evolve through unique events that sequentially select for resistance alleles within single plants and/or genetic exchange of independently evolved resistance mutations through pollen outcrossing among plants within or between populations.
Frontiers | Editorial: Multiple Herbicide-Resistant Weeds and Non-target Site Resistance Mechanisms: A Global Challenge for Food Production

Taq:

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Wouldn't you know it, recombination can speed up the acquisition of multi-herbicide resistance.

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So you think that non-target site resistance is your answer? Do you even know what non-target site resistance is? That exists with bacteria as well. Why don't you tell us what non-target site resistance is? And let's see if that's how humans evolved.

So your only response is to quiz people on terminology? That's it?

top.Taq:

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Recombination is an important factor in evolving multidrug resistance in HIV.

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They might as well forget combination therapy for treating HIV, Taq says it will fail. You are a brilliant virologist. He is also an expert in non-target site resistance even though he doesn't know what it is.

Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMCLuria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize.There is one interesting observation in the Lederberg paper:"The culutre is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10E-7 and 10E-10 per division, respectively."In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli.Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims.If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species? It isn't exponential in sexually reproducing populations. Haven't you been paying attention? Beneficial alleles for each of those challenges can be combined into a single genetic background through recombination.You still don't understand how sexual reproduction works.

Kleinman:

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So you think that non-target site resistance is your answer? Do you even know what non-target site resistance is? That exists with bacteria as well. Why don't you tell us what non-target site resistance is?

Taq:

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So your only response is to quiz people on terminology? That's it?

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Just admit it, you don't know what non-target site resistance is. You post links you don't understand.

I am citing published science which demonstrates recombination is an important factor in evolving multidrug resistance.

Kleinman:

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That's right, in a constant environment, single selection pressure environment it takes a billion replications for each adaptive mutation.

Taq:

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Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:

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This is your link. If you think it proves UCD, go for it. And you have no idea what non-target site resistance is. Don't worry, I can explain it.

Kleinman:

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When there are multiple selection pressures and the environment is changing, it takes exponentially more replications to adapt.

Taq:

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It isn't exponential in sexually reproducing populations. Haven't you been paying attention? Beneficial alleles for each of those challenges can be combined into a single genetic background through recombination.
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You still don't understand how sexual reproduction works.

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You should publish your finding that combination treatment doesn't work for HIV, and combination therapy doesn't work for weeds and insects because you are so smart. Except you don't know what non-target site resistance is.

Still no response to the actual material????Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMCLuria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize.There is one interesting observation in the Lederberg paper:"The culutre is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10E-7 and 10E-10 per division, respectively."In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli.Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims.If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species? I'm not speculating. The scientific literature demonstrates that recombination is an important factor in multidrug resistance in HIV and multi-herbicide resistance in weeds. Apparently, you haven't been reading the papers I have cited for you.

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As stated above, Haldane (1957) argued that the costs of natural selection accumulate over loci, i.e., the reproductive cost of allele substitution at two loci would be twice the cost at a single locus. Consequently, the time required for substitution should be twice as long. In general, if it takes t generations for a gene substitution at a single locus, it should take Lt generations for substitutions at L loci. Applying this logic to our model, given that it takes 400 generations for allelic substitution at one locus, it should take 40 000 generations for substitutions at 100 loci. This prediction is in stark contrast to our finding that it takes only 400 generations for allelic substitution at all 100 loci (see Fig. 2F). How can we explain this major difference between Haldane’s prediction and our findings?
Clearly, Haldane’s scenario does not explain our simulation results as shown in Fig. 2. The reason for the discrepancy is, we believe, that Haldane’s argument assumed that the optimal genotypic combination had to be already present in the initial population and that genotypes could be considered as fixed entities that reproduce themselves from one generation to the next. But these assumptions do not hold for a sexually outbreeding population. First, the population is usually not large enough to contain even a single individual with the vanishingly rare optimal genotypic combination; this fact has already been pointed out by Ewens (1972) and Maynard Smith (1976). Second, specific genotypes are broken down by recombination each generation and replaced by other genotypic combinations (Hickey and Golding 2018). The process of recombination involves the continual disassembly of existing genotypes and reassembly of new genotypes from one generation to the next. Because of this process, however, those genotypes that are expected to be vanishingly rare when the allele frequencies are low will be automatically generated through recombination once the allele frequencies begin to rise in response to selection (Muller 1964; Hickey and Golding 2018). Consequently, there is no need for the massive culling that would be required in a very large initial population that contained an extremely rare optimal genotype. Thus, in an outbreeding sexual population, recombination solves the perceived problem of costs that are cumulative over different genetic loci. In Haldane’s scenario, it is necessary to “grow” the optimal genotypic combination from an initial, vanishingly rare frequency to fixation. In practice, however, this optimal combination is produced by recombination only near the end of the process. This avoids the huge cumulative cost of natural selection.
Canadian Science Publishing

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Sexual recombination allows multiple beneficial alleles to move towards fixation simultaneously. You keep forgetting that.

Kleinman:

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They might as well forget combination therapy for treating HIV, Taq says it will fail. You are a brilliant virologist. He is also an expert in non-target site resistance even though he doesn't know what it is.

Taq:

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I am citing published science which demonstrates recombination is an important factor in evolving multidrug resistance.

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So, stop using combination therapy for treating HIV because someone says it will fail.

I think it proves your claim about 1 adaption per 1 billion replications wrong.Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMCLuria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize.There is one interesting observation in the Lederberg paper:"The culutre is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10E-7 and 10E-10 per division, respectively."In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli.Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims.If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species? IT'S ALREADY PUBLISHED!!!

Kleinman:

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Ah, so it was a phage that evolved a human, that's brilliant. Tell us all about it.

Taq:

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Still no response to the actual material????

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You think this causes UCD, so go for it, explain how a phage makes this possible.

Kleinman:

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The probability of an adaptive recombination event occurring, slow poke. You can speculate otherwise but combination therapy for HIV, weeds, and insects says you are wrong, they work.

Taq:

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I'm not speculating. The scientific literature demonstrates that recombination is an important factor in multidrug resistance in HIV and multi-herbicide resistance in weeds.

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You think that combination therapy doesn't work because of recombination, there is far more literature that says it does work. It works for HIV, weeds, and insects. You are wrong.

Kleinman:

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Even Tany knows that the most fit variant changes as the environment changes. But now I understand why you have this preoccupation with a constant environment, single selection pressure systems, it is the limit of your understanding. The real world isn't made of constant environments with a single selection pressure. You have very limited education.

Taq:

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Apparently, you haven't been reading the papers I have cited for you.

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Show me the paper that explains how drug resistance evolves. Even Desai in his 2021 paper didn't know. Edward Tatum explained it 60 years ago. You should have read his Nobel Laureate Lecture.

Taq:

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Sexual recombination allows multiple beneficial alleles to move towards fixation simultaneously. You keep forgetting that.

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Only in a single selection pressure constant environment and that only gives a slight improvement in fitness. In a multi-selection pressure environment with multiple selection pressures, it's a different game even if you think that evolution works the same in a constant single-pressure environment as in a varying multiselection pressure environment.

Kleinman:

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This is your link. If you think it proves UCD, go for it.

Taq:

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I think it proves your claim about 1 adaption per 1 billion replications wrong.

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Tell Kishony and Lenski to use a phage and their experiments will evolve instantly.

Kleinman:

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You should publish your finding that combination treatment doesn't work for HIV, and combination therapy doesn't work for weeds and insects because you are so smart.

Taq:

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IT'S ALREADY PUBLISHED!!!

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So nobody should use combination therapy for the treatment of HIV, weeds, and insects because Taq says he read it. You are brilliant. Now tell us how a germline can get 200k retroviral infections and they do no harm, except to koalas. Do you want me to explain what non-target site resistance is?