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

Bacteriophage do contribute to antibiotic resistance. Bacteriophages Contribute to the Spread of Antibiotic Resistance Genes among Foodborne Pathogens of the Enterobacteriaceae Family – A ReviewOf course, phage aren't ERV's, but integrated virus nonetheless.

Please show me how my math is wrong for computing the chances of independent retroviral insertions creating orthologous insertions at 99+% of 200,000 ERV's.

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Verily, you have no clue what you are talking about!Please pull your head out from your auto-proctological exam and learn something (despite it being against your religion): Endogenous retrovirus (ERV)So in your medical school you never learned the difference between viruses and bacteria? Was that because your medical school was of such poor quality? Or because even back then you were so self-absorbed in auto-proctology?

Kleinman:

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Really, then why do you have to make up so much?

Taq:

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I didn't make up anything.

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Sure you do. You make up populations, you imagine alleles increasing infrequencies, none of your ideas is based on real examples.

Kleinman:

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What makes you think that competition doesn't exist?

Taq:

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Competition does exist, but it only exists between alleles at the same loci, or loci that are close to one another on a chromosome (i.e. linkage disequilibrium).

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What are you talking about? You can have competition between different species let alone competition in a species. The only requirement is that the replicator uses the same resources.

Kleinman:

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Now Taq is under the delusion that joint probabilities are not computed by multiplication.

Taq:

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Now Kleinman is under the delusion that sexual recombination doesn't happen.

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That's a stupid thing to say. I wrote the mathematics of recombination, dummy.

Kleinman:

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You are a math genius, get it published.

Taq:

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Please note how you treat people when they do the math you request of them.

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You make up some kind of story and then do the math. I do the mathematics of real problems. You are doing the mathematics of an imaginary problem.

Kleinman:

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Taq will now tell us all about infectious diseases. He knows all about how bacteria evolve resistance, it's ERVs.

Taq:

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Bacteriophage do contribute to antibiotic resistance.
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Bacteriophages Contribute to the Spread of Antibiotic Resistance Genes among Foodborne Pathogens of the Enterobacteriaceae Family – A Review
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Of course, phage aren't ERV's, but integrated virus nonetheless.

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See, Taq knows all about how bacteria get antimicrobial resistance, he's a genius. Of course, he never explains how the phage gets the resistance allele.

What the hell are you talking about? Populations exist. Alleles increase in frequency. Are you really saying none of these things exist in nature?I just showed you that your addition rule allows two variants at different loci to increase in frequency together. This is all you have in return? I am talking about competition within a species. For sexually reproducing species, variants at different loci do not compete with one another. And yet you still can't figure out how alleles at different loci can increase in lockstep with one another, and why there is no clonal interference in sexually reproducing populations.

Why should I give you an explanation when all you have is mockery in return?

Kleinman:

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It certainly doesn't apply to your magical world of ERVs.

Taq:

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Please show me how my math is wrong for computing the chances of independent retroviral insertions creating orthologous insertions at 99+% of 200,000 ERV's.

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You can believe that 8% of the human genome is ERVs, I don't. That's garbage just like the biologist claim that most of the DNA is junk DNA.

I accept the findings in the human genome paper. Why don't you? What is wrong with their methods for counting ERV's?

Kleinman:

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You make up populations, you imagine alleles increasing infrequencies, none of your ideas is based on real examples.

Taq:

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What the hell are you talking about? Populations exist. Alleles increase in frequency. Are you really saying none of these things exist in nature?
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I just showed you that your addition rule allows two variants at different loci to increase in frequency together. This is all you have in return?

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You make up populations, you make up advantageous alleles, and you don't do real examples. And when I do real examples, you say they don't apply. You let your imagination run amok.

Kleinman:

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What are you talking about? You can have competition between different species let alone competition in a species. The only requirement is that the replicator uses the same resources.

Taq:

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I am talking about competition within a species. For sexually reproducing species, variants at different loci do not compete with one another.

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In the real world, competition exists between species, not just within species. What do you think insects are doing when they eat a crop grown for humans? You really don't understand competition at all.

Kleinman:

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That's a stupid thing to say. I wrote the mathematics of recombination, dummy.

Taq:

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And yet you still can't figure out how alleles at different loci can increase in lockstep with one another, and why there is no clonal interference in sexually reproducing populations.

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This is your imagination speaking. Why don't you give us a real example? What alleles are increasing in frequencies in lockstep with humans?

Since you have been incapable of refuting any of my math, I see no reason to discuss it any further. Any claims by you in the future will be rerouted to the post containing the python script. Competition also exists between alleles within a population. The Desai experiment.

Kleinman:

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See, Taq knows all about how bacteria get antimicrobial resistance, he's a genius. Of course, he never explains how the phage gets the resistance allele.

Taq:

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Why should I give you an explanation when all you have is mockery in return?

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Try giving a real example rather than one you make up.

There are real world examples of existing retroviruses creating new ERV's in modern populations. The Koala genome is currently undergoing an invasion of retroviral sequence into their genome.

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Endogenous retroviruses are a common ancestral feature of mammalian genomes with most having been inactivated over time through mutation and deletion. A group of more intact endogenous retroviruses are considered to have entered the genomes of some species more recently, through infection by exogenous viruses, but this event has never been directly proved. We have previously reported koala retrovirus (KoRV) to be a functional virus that is associated with neoplasia. Here we show that KoRV also shows features of a recently inserted endogenous retrovirus that is vertically transmitted. The finding that some isolated koala populations have not yet incorporated KoRV into their genomes, combined with its high level of activity and variability in individual koalas, suggests that KoRV is a virus in transition between an exogenous and endogenous element. This ongoing dynamic interaction with a wild species provides an exciting opportunity to study the process and consequences of retroviral endogenization in action, and is an attractive model for studying the evolutionary event in which a retrovirus invades a mammalian genome.
Retroviral invasion of the koala genome - PubMed

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I gave you a review article with numerous real world examples of bacteriophage moving antibiotic resistance genes between species of bacteria.

Kleinman:

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You can believe that 8% of the human genome is ERVs, I don't.

Taq:

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I accept the findings in the human genome paper. Why don't you? What is wrong with their methods for counting ERV's?

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The idea of hundreds of thousands of viruses infecting cells and yet not causing disease is nonsense, especially in the initial stem cell of a replicator. You can believe it if you want but I think it is hogwash. This is the kind of garbage suitable for Tany while he is chasing bugs.