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

Although HIV doesn't reproduce sexually, it's RNA genome in the cell cytoplasm can recombine between viral genomes. Here is a study that Kleinman and others might find interesting:

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Viral recombination has been postulated to play two roles in the development of human immunodeficiency virus (HIV) resistance to antiretroviral drugs. First, recombination has the capacity to associate resistance mutations expressed by distinct viruses, thereby contributing to the development of viruses with improved drug resistance. In addition, recombination could preserve diversity in regions outside those subject to strong selective pressure. In this study, we sought direct evidence for the occurrence of these processes in vivo by evaluating clonal virus populations obtained from the same patient before and after a treatment change that, while unsuccessful in controlling viral replication, led to the emergence of viruses expressing a different profile of resistance mutations. Phylogenetic studies supported the conclusion that the genotype arising after the treatment change resulted from the emergence of recombinant viruses carrying previously existing resistance mutations in novel combinations, whereas alternative explanations, including convergent evolution, were not consistent with observed genotypic changes. Despite evidence for a strong loss of genetic diversity in genomic regions coding for the protease and reverse transcriptase, diversity in regions coding for Gag and envelope was considerably higher, and recombination between the emerging viruses expressing the new pattern of resistance mutations and viral quasispecies in the previously dominant population contributed to this preservation of diversity in the envelope gene. These findings emphasize that recombination can participate in the adaptation of HIV to changing selective pressure, both by generating novel combinations of resistance mutations and by maintaining diversity in genomic regions outside those implicated in a selective sweep.
Just a moment...

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They found that recombination played an important part in adaptation to challenges with HIV drugs by joining different drug resistance mutations (instead of clonal interference). They also found that genetic diversity was preserved after selective sweeps. Hmm, interesting.

So you think the entire field of population genetics is inadequate? Hubris much? Why should we care about your uninformed opinion? You have strode in here without even understand how sexual reproduction works, and you think in your vast ignorance of biology you can claim the entire field is just wrong? I can think about it just fine. The results are pretty spectacular. Why don't you think about it?Just for reference, I am going from this paper:Spatiotemporal microbial evolution on antibiotic landscapes - PMCIn this paper, Bahm et al. (Kishony is last author) set up an experiment where there are multiple layers of agar with increasing concentrations of antibiotic. What happens is that at the interface between these different antibiotic concentrations you see something like a fan. This is due a mutation that happens in a bacteria that allows it to expand out into the new environment with higher antibiotic. This happens all along the interface. You can see it in Fig 1 in the paper above.What is interesting is that these fans intersect each other. Since the bacteria are reproducing asexually you get competition between lineages, and the most fit clone wins out. This is clonal interference. There can also be differences in timing, such as one fan starts before another.What would happen if there was sexual reproduction? As those fans of migrating organisms meet each other you get mating. This would combine the beneficial mutations (assuming they are unlinked) from each population and you would have offspring with both beneficial mutations. You wouldn't have clonal interference.In addition, at the very start of the fan you would have some hitchhiking in the initial population due to the strong bottleneck in the population. In an asexual population there is no way to get rid of the deleterious mutations that hitchhike with the beneficial mutation. You just have to live with it. However, if these were sexual organisms then the deleterious mutation could be selected out while keeping the beneficial mutation.So you get two things with sexual reproduction that you don't see with asexual reproduction in the Kishony experiment: 1. lack of clonal interference, 2. removal of hitchhiking deleterious mutations.

Did Lenski?I have shown you an experiment where sexual reproduction negates clonal interference. Are you going to continue to ignore this or not? No. Did I ever say that?First, HIV doesn't reproduce sexually. That's just silly. Second, I have already posted a paper above discussion how recombination increases adaptation to multi-drug treatments in HIV. Perhaps you should read it.

No, it isn't. In sexual reproduction you get the combination of many beneficial mutations in to the same genetic background. Under the conditions of sexual reproduction. That competition is removed by sexual reproduction when beneficial mutations that happen in different individuals are placed in the same genetic background.

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For example, recombination can relieve clonal interference, bringing together beneficial mutations that arise on different genetic backgrounds and would otherwise compete5,6,18,19,20. Sex can also rescue beneficial mutations from deleterious backgrounds7,8.
Sex speeds adaptation by altering the dynamics of molecular evolution | Nature

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They don't have to be at high frequency in order to get mating between carriers.Also, the model we are both working from already assumes that they exist. You are arguing that if A and B exist then there will be competition between them which will drive one of the mutations to extinction. I am telling you that sexual selection will combine those mutations into the same genetic background so that they no longer compete. Both experiments and simulations back my conclusion. And that challenge was met in this message:https://www.evcforum.net/dm.php?control=msg&m=900849#m900849 There will be clonal interference until it is relieved by sexual reproduction. That's false. You said that the first law of thermodynamics demands clonal interference. So you are either wrong, or sexual reproduction violates the first law of thermodynamics. Which is it? Yes, when a population faces several simultaneous and severe challenges it might quickly go extinct, and sexual reproduction can't change that. That doesn't change the fact that sexual reproduction can speed adaptation and remove clonal interference in other situations, such as in human evolution. There are situations other than microorganisms dealing with drugs meant to kill them. That's also false. It's the strength of the selection pressures that will drive extinction, not the number of them. If all of these multiple selection pressures are weak then it is rather easy to find multiple beneficial alleles to deal with each and move them into the same genetic background through sexual reproduction, just as happened in the Desai experiment. The lack of self awareness is dumbfounding. A million irony meters just exploded from overload.Who is the one who has been trying to apply the Lenski and Kishony experiment to everything in biology? That would be you. You even think that asexual evolution can be equally applied to sexual evolution, which is completely false. My goodness, man. Look in a mirror. It removes them in one generation. That's not a selective sweep, and it has little to do with sexual or asexual reproduction since you get removal of a big part of the population in less than a generation. All you are testing is standing variation. If both mutations are beneficial in a given environment won't they both be increasing in frequency? If so, doesn't the frequency of mating between carriers increase with time? It seems rather inevitable that crosses will happen. How did you calculate the number of cases where it works and doesn't work? Before, you claimed that it doesn't happen at all.You are the one who keeps limiting this discussion to extremely rare cases, not I. You insist everyone only focus on drug resistance in E. coli, for example. Take your advice and branch out a bit.

Multidrug resistant phenotypes have arisen through recombination which violates the multiplication rule.

Get back to us when you understand how sexual reproduction works. Because we don't make stupid mistakes like saying sexual reproduction violates the first law of thermodynamics. I understand those concepts way better than you do which is why I don't think sexual reproduction violates the first law of thermodynamics. I suspect your explanation of descent with modification and the 2LoT is just as ignorant. Yes, I read the paper.Are you going to address anything I said? Are you going to address the combination of multiple beneficial alleles into the same genetic background that would happen if there were sexual organisms in the experiment? Are you going to address how clonal interference would be alleviated by sexual reproduction in this experiment? Yes, when you have a two drug challenge you need drug resistance for both drugs to occur in the same individual in the same generation in order to overcome both challenges because non-resistant bacteria will die off in one generation without both mutations. No amount of recombination can overcome a multiple selective pressures that wipe out the population in one generation.In what way do you think this applies to how species are adapting out in the wild? Do you remember who said this?"You are trying to extrapolate the results of this experiment to all examples of adaptive evolution by recombination."--KleinmanWhy are you trying to extrapolate the results of the Kishony experiment to evolution in all species?

There you go with the strawmen again. Where did I ever say that sexual reproduction was an unlimited process? NOWHERE!!!! Please address what I say, not what you want me to say. Absolutely there is a limit, but those limits don't include clonal interference. I'm not saying that sexual reproduction is some unstoppable superpower. I am saying that it alleviates clonal interference. In situations where clonal interference would pose problems for evolution those problems can be solved through sexual reproduction. THAT'S WHAT I'M SAYING. Will you address it? Probably not. You will probably continue attacking strawmen. No, they aren't. They are adapting to a new environment which poses several simultaneous pressures, and offers several possible adaptations. No, I'm not. The only person being stubborn is the one refusing to admit that sexual reproduction alleviates clonal interference. In many, many situations, yes. The further you away you are from a fitness peak the quicker evolution usually proceeds. As you near a fitness peak there are fewer and fewer possible adaptations which slows evolution. This is what was seen in the Lenski experiment where the population approached a local fitness peak which slowed its evolution.

I've already shown you examples where it does work. Because sexual selection puts different beneficial mutations into the same genetic background, unlike asexual reproduction. I agree that clonal interference happens in asexual populations. Why 40%? If each beneficial mutation is at 5% in the population then 2.5% of births will have a chance of inheriting both mutations. If 5% of an asexual population has one of two beneficial mutations then there will be far fewer than 2.5% of offspring that have both mutations, if any at all.We've been over this multiple times already. Clonal interference would have been much more prominent. I agree. I have agreed all along that asexual reproduction drives clonal interference while sexual selection alleviates it. More asexual reproduction and less sexual production would swing the needle towards clonal interference.Is that the case in human evolution? Do we go 300 generations without sexual reproduction? How many generations do humans go before they participate in sexual reproduction? Do we clone ourselves for 90 or 300 generations? What about lions, or bears? Do they clone themselves for 300 generations? You are forgetting about selection. Over time, those frequencies will increase for both mutations if they are beneficial. They may start out as rare mutations, but if they are beneficial then they won't stay rare. That's correct. Desai had to introduce sexual selection to avoid clonal interference. That's my entire point. I have already given you scenarios where it can. What would you expect? Would you expect a near absence of clonal interference since it is only the rounds of asexual reproduction that introduce clonal interference? Why wouldn't beneficial mutations increase in frequency in a completely sexual population? No, it isn't.My model for human evolution would be sexual reproduction in every generation which would greatly alleviate clonal interference for unlinked genes. This same model would apply to the vast majority of obligate sexual species. Different models would have to be used for species that switch between sexual and asexual reproduction, and yet a different model for obligate asexual species. Unlike you, I don't think there is a one-size-fit-all model. My models adjust to the mechanisms that are in action. I already told you:"Yes, when you have a two drug challenge you need drug resistance for both drugs to occur in the same individual in the same generation in order to overcome both challenges because non-resistant bacteria will die off in one generation without both mutations. No amount of recombination can overcome a multiple selective pressures that wipe out the population in one generation."Please read my posts. I'm getting tired of repeating myself. This is why I keep telling you to go read my previous posts. The answer is sexual reproduction as long as the population is able to survive the initial challenge. How many times do I need to keep repeating this? What happens to the frequency of a beneficial allele over time in a sexually reproducing population? Does it increase? As that beneficial allele increases in frequency, is there an ever increasing probability of a carrier of that beneficial allele mating with someone who has a beneficial allele for a different gene?

I don't resist them at all. They are on my side. What I resist is lies that come from creationists.

That rule doesn't apply in the case of recombination.Your multiplication rule is based on the claim that the second mutation for resistance to the second drug must occur in an individual that already has the first mutation. Recombination removes this requirement, so the multiplication rule doesn't apply. With recombination, the mutation can occur in an individual who doesn't have the first mutation for the first drug.

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The potential contribution of recombination to the development of HIV-1 resistance to multiple drugs was investigated. Two distinct viruses, one highly resistant to a protease inhibitor (SC-52151) and the other highly resistant to zidovudine, were used to coinfect T lymphoblastoid cells in culture. The viral genotypes could be distinguished by four mutations conferring drug resistance to each drug and by other sequence differences specific for each parental virus. Progeny virions recovered from mixed infection were passaged in the presence and absence of both zidovudine and SC-52151. Dually resistant mutants emerged rapidly under selective conditions, and these viruses were genetic recombinants. These results emphasize that genetic recombination could contribute to high-level multiple-drug resistance and that this process must be considered in chemotherapeutic strategies for HIV infection.
Recombination leads to the rapid emergence of HIV-1 dually resistant mutants under selective drug pressure.

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That doesn't spell it out at all. Care to explain? If the strain carrying drug resistance to two drugs recombines with a strain carrying resistance to a 3rd drug, what then?

Why would it need to? Yes, you are lying. You keep claiming that clonal interference is a driving force in sexually reproducing populations. Yes, you are lying. You keep claiming that your addition rule applies to any group of mutations in the human genome when it clearly doesn't. Why is that a problem? Your next lie is that this is a problem. Yet another lie. Look in a mirror, bud. That is a yet another lie. I have never argued for universal common descent based on the Desai experiment.

The correct terminology here would be de novo mutations, not descent with modification. Species can be physically modified by recombining existing variation, so that isn't the correct term. Wouldn't sexual reproduction in every generation be quicker?You also haven't shown that the evolution in the asexual organisms in the Kishony experiment would be faster compared to the same experiment with sexually reproducing organisms. If there are beneficial mutations in different genes then sexual reproduction could combine those beneficial mutations into the same genetic background and speed up adaptation, just as happened in the Desai experiment. You could also remove deleterious mutations at unlinked sites, further increasing adaptation and fitness. Let's remember what the Desai paper stated:

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One potential evolutionary advantage of sex is that recombination can speed adaptation4. Several distinct mechanisms could drive this effect. For example, recombination can relieve clonal interference, bringing together beneficial mutations that arise on different genetic backgrounds and would otherwise compete5,6,18,19,20.
Sex speeds adaptation by altering the dynamics of molecular evolution | Nature

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This is the hypothesis they were testing, and the hypothesis they confirmed. Sexual reproduction takes beneficial mutations that happened in different individuals and combines them into the same individual. That's what sex does, and that is what happened in the Desai experiment. As I have repeated multiple times now, sexual reproduction alleviates clonal interference.The step you may be overlooking is that you are getting a mixture of alleles from different individuals, not just mixing of alleles within the same individual. Lineages merge so that they are not competing with one another. Each human has one copy of the genome that is from their father and one that is from their mother. This is a merger of the father's and mother's lineage. This is what doesn't happen in asexual populations, and this is what alleviates clonal interference by putting different beneficial mutations into the same individual.This also means that each beneficial mutation will increase in frequency independent of other beneficial mutations. This is again stated in the Desai paper:

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To investigate how sex improves the efficiency of selection, we analysed the dynamics of adaptation. As in earlier studies21,22, asexual populations exhibit signatures of hitchhiking and clonal interference (Fig. 2a–d). Groups of functionally unrelated mutations, linked within the same genetic background, change in frequency together as clonal cohorts. The outcomes of evolution are determined by competition between these cohorts. In contrast, sexual populations are not characterized by cohorts of linked mutations (Fig. 2e–h). Instead, the dynamics of each mutation is largely independent of other variation in the population. In these populations, mutations that occur on different backgrounds fix independently, while others briefly hitchhike to moderate frequencies where they persist or are eliminated from the population.
Sex speeds adaptation by altering the dynamics of molecular evolution | Nature

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It is also stated in the computer simulation paper I cited earlier:

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These results show that, in a sexually outbreeding population, the frequency of favorable alleles at many loci can respond simultaneously to independent selection at rates that are very similar to the predicted rate at a single locus (compare Figs. 2F and 1B). This implies that the rate of response to selection at any given locus is not greatly impeded by selection at other loci. In other words, many loci can respond simultaneously to independent selection—but only in a sexually reproducing population.
Sex Solve Haldane's Dilemma

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This isn't something I am just making up. This is real. This is supported by both mathematical simulations and real world experiments.For this discussion to move forward we should be focusing on helping you understand why this is happening, not if it is happening. It is happening. This is how evolution works in sexually reproducing species.Instead of going through the rest of your post, which can result in some rather long and untidy messes, I would like to pause right here. I think it is much more important that we both understand this reality of sexual reproduction. Do you agree?

In the name of finding a better understanding of how sexual and asexual reproduction works and how it affects evolution . . .Playing cards may offer us a useful analogy. Don't get me wrong, there are many problems with this analogy, but no analogy is perfect. For example, we can't use this analogy to model hetero- or homozygosity. In fact, I'm going to leave true diploidy out so it doesn't get too complicated. However, I'm hoping it creates a bit of an "Aha!" moment that may lend itself to better understanding the actual biological system. Please don't torture the analogy beyond a very surface level comparison. I know it's imperfect.We are going to use playing cards to represent genes. This doesn't have to be a standard deck, and it certainly won't be as the analogy progresses. All we need to understand is that some cards are better than others, and these represent genes with higher fitness. An Ace is more fit than a Queen, for example.As time progresses, we will change the value of one card at random at some given rate. The rate will be long enough that we won't see that many changes in any given deck at any given generation. Just once in a long while. The change may not change the value of the card (e.g. a 5 for a 5), it may increase the value, or it may decrease the value. It's random.To measure fitness at any point in time we compare the total value of cards. For example, we could assign 13 to 1 for Ace to Deuce, respectively. We would then add up the total value of the deck and compare that total to the total of other decks. That gives us the relative fitness between decks.Now let's set up our reproduction strategies.Asexual population:You start with 1,000 decks that are all the same. Each deck is passed on to the next generation as a whole. In each generation 5 decks are removed and replaced by a deck with higher fitness. The probability of replacement is determined by the relative fitness of different decks and their frequency, so a deck with 1.2 higher fitness and 0.5 frequency would have a better chance of replacing one of those 5 decks than a deck with 1.1 higher fitness and a 0.1 frequnecy. Since the decks stay together, we get lineages that compete with one another. We will tend to see one deck that tends to dominate to the exclusion of others.Sexual population:This situation is a bit different. First, we shuffle the deck, and then we split the deck into two piles. Two random people will then donate 1 half deck each to the next generation. No longer are we passing on a whole deck. We separate cards from one another and mix them with other shuffled and halved decks. Selection works the same as before, as do mutations. The random shuffling and random mating means that we get a whole bunch of different combinations of cards, some of which would have been mutations at some point in our little analogy. The process of random mixing and selection means that each card is essentially being judged on its own when we look at the population as a whole. This is because decks that have a higher than average number of lower value cards are eliminated from each generation, and those with higher than average high value cards have a higher chance of replacing them. This process will slowly eliminate the lower ranked cards, not the lowest ranked whole decks.Does this analogy help explain why we see differences in how evolution is different in asexual and sexual populations?

Through de novo mutations. I will be glad to address all of this once we deal with how alleles behave.Like I said before:This isn't something I am just making up. This is real. This is supported by both mathematical simulations and real world experiments.
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For this discussion to move forward we should be focusing on helping you understand why this is happening, not if it is happening. It is happening. This is how evolution works in sexually reproducing species.
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Instead of going through the rest of your post, which can result in some rather long and untidy messes, I would like to pause right here. I think it is much more important that we both understand this reality of sexual reproduction. Do you agree?