Exposing the evolution theory. Part 2

Kleinman:

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Are you going to post a link to a thread in this forum where you explain how drug resistance evolves and why cancer treatments fail?

Taq:

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Sure. Here you go:
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https://www.evcforum.net/dm.php?control=msg&t=20319

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And

Kleinman:

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You might as well tell Kishony and Lenski how their experiments work since you have figured out how descent with modification and adaptation works.

Taq:

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They understand their own findings just fine.

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Neither you, Kishony, nor Lenski, have ever published how drug resistance evolves or why cancer treatments fail mathematically. Nor have you, Kishony and Lenski published or explained how their experiments work mathematically.

Kleinman:

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Neither you, Kishony, nor Lenski, have ever published how drug resistance evolves

Taq:

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Card KJ, Thomas MD, Graves JL Jr, Barrick JE, Lenski RE. Genomic evolution of antibiotic resistance is contingent on genetic background following a long-term experiment with Escherichia coli. Proc Natl Acad Sci U S A. 2021 Feb 2;118(5):e2016886118. doi: 10.1073/pnas.2016886118. PMID: 33441451; PMCID: PMC7865137.
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Lenski RE. Bacterial evolution and the cost of antibiotic resistance. Int Microbiol. 1998 Dec;1(4):265-70. PMID: 10943373.
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Article Source: Historical contingency in the evolution of antibiotic resistance after decades of relaxed selection
Card KJ, LaBar T, Gomez JB, Lenski RE (2019) Historical contingency in the evolution of antibiotic resistance after decades of relaxed selection. PLOS Biology 17(10): e3000397. Historical contingency in the evolution of antibiotic resistance after decades of relaxed selection | PLOS Biology
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Stracy M, Snitser O, Yelin I, Amer Y, Parizade M, Katz R, Rimler G, Wolf T, Herzel E, Koren G, Kuint J, Foxman B, Chodick G, Shalev V, Kishony R. Minimizing treatment-induced emergence of antibiotic resistance in bacterial infections. Science. 2022 Feb 25;375(6583):889-894. doi: 10.1126/science.abg9868. Epub 2022 Feb 24. PMID: 35201862; PMCID: PMC7612469.
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Baym M, Lieberman TD, Kelsic ED, Chait R, Gross R, Yelin I, Kishony R. Spatiotemporal microbial evolution on antibiotic landscapes. Science. 2016 Sep 9;353(6304):1147-51. doi: 10.1126/science.aag0822. PMID: 27609891; PMCID: PMC5534434.i

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None of these papers explain how drug resistance evolves. That's why you don't quote from these papers.

Kleinman:

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What percent certainty do you say that any deities don't exist?

Taq:

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Less than absolutely certain. There's no percentage involved.

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And

Kleinman:

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And what is your evidence for this claim?

Taq:

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My claim for what I do or don't believe? I guess you will have to take my word for it.

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Sure, it is your religious belief.

Kleinman:

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Are you claiming that all vertebrate DNA sequences that have similarities to viral sequences came from insertions of viruses?

Taq:

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Either directly or indirectly, yes. Viral sequences can still hop around through transposon activity without an active infection.

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Do you have any scientific proof for such a belief, that is all vertebrate DNA sequences that have similarities to viral sequences came from viruses?

Kleinman:

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How do viruses cause vertebrate cells to initiate the transcription of viral proteins?

Taq:

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The LTR's bind transcription factors which drives transcription of the provirus.

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Is the virus causing the host cell to produce viral components rather than the host cell doing its own metabolic processes?

Kleinman:

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Are you saying that the DNA sequences that code for the viral proteins have not been identified in their entirety, only fragments?

Taq:

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Depends on the ERV. Different ERV's have retained different amounts of sequence as they have evolved in the host genome. Across the many HERV-K insertions there is enough sequence between them that a functional retrovirus can be reconstructed from their consensus sequence.

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Of the 203,000 ERVs you claim that humans have, how many DNA sequences of viral proteins have been identified?

Kleinman:

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Are the only DNA replications seen in vertebrates due to ERVs?

Taq:

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The entire genome is replicated, last I checked.

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That's not the question. I'll rephrase it. Are the only DNA repeats seen in vertebrates due to ERVs?

Kleinman:

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Why are DNA repeats identifiable but the protein-coding portions of viral insertions are only seen in fragments?

Taq:

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For the same reason that we can't identify the type of tires on this truck.

There's little doubt that this is a truck. In the same way, there is little doubt that we are looking at insertions from retroviruses even if a few of the parts are missing. In case you aren't aware, DNA deletions happen. It's a normal type of occurrence. Homologous recombination is also a very natural process that will delete everything in the protein coding regions and only leave one LTR.

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Are you claiming that the protein-coding portion of viral insertions can get mutations and other forms of genetic transformations but DNA repeats remain constant and never change? And if so, why? By the way, the truck is decomposing as well as the tires are missing.And I ask you again. Do DNA repeats only occur with viral insertions? Do vertebrate genomes have DNA repeats not associated with viral insertions?

Kleinman:

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Atheists seem to think that they know. Do you want to tell us what evidence they have to make their assertion?

Taq:

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When you have to start putting words in other peoples' mouths, perhaps you should take a step back and rethink your argument.
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Atheists are telling you that they can't be absolutely certain that deities exist. They are atheists because they don't believe deities exist. That's our position.

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Go ahead and be as illogical as you want. If you want to say you are an atheist that doesn't know whether deities exist or not, that is fine. However, some might say that you are confusing the meaning of "atheist" and "agnostic".

So you are both an atheist and agnostic. But you still haven't told us whether a vertebrate cell can have DNA repeats not associated with a viral insertion.

Kleinman:

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Do you have any scientific proof for such a belief, that is all vertebrate DNA sequences that have similarities to viral sequences came from viruses?

Taq:

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"We used the PCR to screen for the presence of endogenous retroviruses within the genomes of 18 vertebrate orders across eight classes, concentrating on reptilian, amphibian, and piscine hosts. Thirty novel retroviral sequences were isolated and characterized by sequencing approximately 1 kb of their encoded protease and reverse transcriptase genes. Isolation of novel viruses from so many disparate hosts suggests that retroviruses are likely to be ubiquitous within all but the most basal vertebrate classes and, furthermore, gives a good indication of the overall retroviral diversity within vertebrates. "
Retroviral Diversity and Distribution in Vertebrates - PMC

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Did they identify 203,000 retroviruses in these genomes?

Kleinman:

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Is the virus causing the host cell to produce viral components rather than the host cell doing its own metabolic processes?

Taq:

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First of all, a cell can do both at the same time.
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Second, there are mechanisms that shut down transcription of viral DNA.
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"TRIM28 is a corepressor that mediates transcriptional silencing by establishing local heterochromatin. Here, we show that deletion of TRIM28 in neural progenitor cells (NPCs) results in high-level expression of two groups of endogenous retroviruses (ERVs): IAP1 and MMERVK10C. We find that NPCs use TRIM28-mediated histone modifications to dynamically regulate transcription and silencing of ERVs, which is in contrast to other somatic cell types using DNA methylation. We also show that derepression of ERVs influences transcriptional dynamics in NPCs through the activation of nearby genes and the expression of long noncoding RNAs. These findings demonstrate a unique dynamic transcriptional regulation of ERVs in NPCs. Our results warrant future studies on the role of ERVs in the healthy and diseased brain."
TRIM28 represses transcription of endogenous retroviruses in neural progenitor cells - PubMed

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What happens if a germ cell has more than one retrovirus active in the cell at a time?

Kleinman:

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Of the 203,000 ERVs you claim that humans have, how many DNA sequences of viral proteins have been identified?

Taq:

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As stated multiple times already, 90% are solo LTR's that don't have any protein coding regions. About 10% have remnants of genes for proteins.

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Is your claim that the LTRs remain but the protein-coding region has disappeared? Do the LTRs ever get a mutation when they are replicated?

Kleinman:

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Are the only DNA repeats seen in vertebrates due to ERVs?

Taq:

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There are many different types of DNA repeats, retroviral LTR's being one of those types.

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Are all LTRs associated with retroviruses?

Kleinman:

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Are you claiming that the protein-coding portion of viral insertions can get mutations and other forms of genetic transformations but DNA repeats remain constant and never change?

Taq:

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The repeats evolve as well. However (for the upteenth time), it is common for homologous recombination to occur between the LTR's because they have identical sequence. This loops out the protein coding genes so that all you are left with is a single LTR.

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If you don't have the viral protein-coding genes in the genetic sequence, and the LTRs have evolved, how can you be sure this genetic sequence is from a retrovirus?

Kleinman:

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By the way, the truck is decomposing as well as the tires are missing.

Taq:

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Just as ERVs take on substitutions, deletions, insertions, and near complete removal by homologous recombination.

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How do you determine that this piece of genetic material is the remnant of a retrovirus rather than host DNA when the viral protein-coding DNA is gone? Can the host vertebrate genome have its own LTRs that are not from a virus?

Kleinman:

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Do DNA repeats only occur with viral insertions?

Taq:

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DNA repeats do occur outside of viral insertions, but the sequence is different. Retroviral LTRs are recognized by their sequence.

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Can vertebrates have retrotransposons not associated with retroviruses?

Kleinman:

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None of these papers explain how drug resistance evolves.

Taq:

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What a fucking moron. This is why people see no need to respond to your posts on this subject. Even when shown exactly what you are asking for you deny what is right in front of you.

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It appears you are having difficulty posting a quote from any of your papers that you think describes the mathematics of the evolution of drug resistance. The fact is that biologists have failed to describe the physics and mathematics of biological evolution and the evolution of drug resistance. I'm familiar with most of those papers you listed and none give the correct mathematics. None of these papers explain why it takes a billion replications for each adaptive mutation in the Kishony and Lenski experiments. You are wrong Taq and you are angry because you know it.

AZPaul3:

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This discussion has left any science topic behind and is now nothing more than an intransigent Kleinman pushing a religious agenda.

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None of Taq's references explain how drug resistance occurs and why it takes a billion replications for each adaptive mutation for a single selection pressure in the Kishony and Lenski experiments. I realize it is difficult for you and biologists to understand the mathematics of evolution but here it is.
For a single selection pressure:
The basic science and mathematics of random mutation and natural selection
And for multiple simultaneous selection pressures:
The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance
And here is the correct probability equation for a single adaptive step in a single selection pressure environment:
P(X) = (1-(1-P(Beneficial)μ)^N
where P(X) is the probability of the beneficial mutation occurring, P(Beneficial) is the probability that of all the mutations that may occur at that site that it is the beneficial mutation, μ is the mutation rate, and N it the number of replications that the particular variant does.I don't post this for you AZPaul because you refuse to learn about probability theory and the "at least one" rule. This is for any of those that know a little about probability theory. That is how you do the mathematics of descent with modification and adaptation, a stochastic process.

AZPaul3:

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An intransigent Kleinman pushing a religious agenda.

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You are confuse AZPaul3, these papers explain how drug resistance evolves.
For a single selection pressure:
The basic science and mathematics of random mutation and natural selection
And for multiple simultaneous selection pressures:
The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance
This math fits the experimental and empirical data of biological evolutionary descent with modification and adaptation. It explains why it takes a billion replications for each adaptive mutation in the Kishony and Lenski biological evolutionary experiments. You won't accept this mathematical and physical fact of life because it doesn't fit your belief system.

It is worth summarizing this discussion on ERVs since Taq has been playing an ongoing April Fool joke on everyone.The reader should recall that Taq is using the existence of ERVs in humans and chimpanzees as proof that the two species are related. In Message 772 we had the following exchange:

Kleinman:

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203,000 retroviral infections to a germ cell line and the lineage does just fine is part of your belief system.

Taq:

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It's an observed fact as detailed in the 2001 human genome paper.

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A few posts later, Message 787, I asked Taq the following:

Kleinman:

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Tell us what the genetic structure of a virus is, for example, HIV and tell us if multicellular replicators have any similar types of genetic structures.

Taq:

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A generic retroviral genome looks like this:

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Multicellular replicators have insertions of these retroviral genomes in their genome. They are easily recognizable as retroviral genomes and LTRs from retroviruses. The 4-6 bases of host DNA at either end of the viral genome for full length insertions is also a dead give away because those are created during insertion of the retroviral genome.

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Taq has said something different from his initial claim. He now says, "They are easily recognizable as retroviral genomes and LTRs from retroviruses." He is now shifting his argument from ERVs to LTRs. Note that his figure shows that an exogenous retrovirus has a gag, pol, and env region where the genome is coding for proteins unique to the virus. For those not familiar with what an LTR is, you can read the following Wikipedia link where you can find a discussion on Repeated Sequence DNA:
Repeated sequence (DNA) - Wikipedia(DNA) and slightly further down in this link: Taq's argument has made a shift from talking about ERVs now to talking about LTRs. Then in Message 794, I asked Taq the following and he gave this response:

Kleinman:

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You haven't fully answered the question, do multicellular replicators have any genetic structures like viruses?

Taq:

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Vertebrates do have DNA sequences in their genome that are like viruses because they came from viruses.

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Here is a short discussion of Repeated sequence (DNA):
Repeated sequence (DNA) - Wikipedia(DNA) And further done in that post, I asked the following:

Kleinman:

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And have the unique viral proteins been identified in the claimed 203,000 viral infections you claim our ancestors have had and been passed to us?

Taq:

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About 90% of human ERV's are solo LTR's due to homologous recombination, as mentioned earlier. Again, these LTR's are specific to viruses, and we know where they come from. The other 10% still have parts of the coding regions from the original provirus.

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Miraculously, 90% of the ERVs have lost their protein coding regions and only LTRs remain and the other 10% have only parts remaining, no intact viral genomes in that 203,000 ERVs that relate humans and chimpanzees. But Taq says that he is absolutely sure these LTRs are from retroviruses and he gives his proof in Message 802:

Taq:

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There's little doubt that this is a truck. In the same way, there is little doubt that we are looking at insertions from retroviruses even if a few of the parts are missing. In case you aren't aware, DNA deletions happen. It's a normal type of occurrence. Homologous recombination is also a very natural process that will delete everything in the protein-coding regions and only leave one LTR.

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The correct picture he should use for his argument looks like this: Taq can look at this picture and tell us what vehicle these tires came off simply by the brand of tire. If the tire name is Goodyear, it came from a Ford, and if the tire name says Bridgestone, it came from a Dodge, and if the tire brand says Michelin, obviously that came from a Mercedes.It is no surprise that Taq would rather argue about what he thinks atheism and agnosticism mean, or post a bunch of references that he claims explain how drug resistance evolves and then gets angry because I point out that he doesn't quote from any of them.What Taq calls evidence is his biased interpretation of his observations. He may think that humans and chimpanzees are related but he does this based on his incorrect understanding of the physics and mathematics of biological evolution.

AZPaul3:

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Bogus.
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An intransigent Kleinman pushing his religious agenda.

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The following two papers that give the mathematics for descent with modification (and adaptation) are what AZPaul3 is calling bogus.
For a single selection pressure:
The basic science and mathematics of random mutation and natural selection
And for multiple simultaneous selection pressures:
The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance
He seems to think that the peer reviewers at Statistics in Medicine did an inadequate job peer reviewing these papers. The following video explains what is happening in scientific publishing:
https://www.youtube.com/watch?v=5-K3obvnKYQ&ab_channel=Bu...
Here is the website where they are monitoring retracted papers:
Retraction Watch – Tracking retractions as a window into the scientific process
Here is AZPaul3's big chance to get these "bogus" papers pulled. Is AZPaul3 all talk and no action?

Kleinman:

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None of Taq's references explain how drug resistance occurs and why it takes a billion replications for each adaptive mutation for a single selection pressure in the Kishony and Lenski experiments.

Taq:

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All of them do. Read the papers you fucking moron.

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None of your references explain how drug resistance evolves and why it takes a billion replications for each adaptive mutation in the Kishony and Lenski biological evolutionary experiments. You are wrong and you know it. That's why you can't post a single quote.

Kleinman:

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Did they identify 203,000 retroviruses in these genomes?

Taq:

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They weren't only trying to detect the presence of ERV's, and they were widespread amongst vertebrates.

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So, now you claim an LTR is an ERV?

Kleinman:

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What happens if a germ cell has more than one retrovirus active in the cell at a time?

Taq:

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Apparently, nothing. There are koalas with over 50 recently inserted ERVs and they are having offspring without a hitch.

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That's a relief for those with HIV, they don't have to worry about herpes simplex, herpes zoster, or cytomegalovirus,... affecting them.

Kleinman:

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Is your claim that the LTRs remain but the protein-coding region has disappeared? Do the LTRs ever get a mutation when they are replicated?

Taq:

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Already answered multiple times.

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Sure, we got your nonsensical answer that LTRs are the same as ERVs, LTRs would be ERVs if they had viral protein-coding regions. But you claim you can identify proteins even when they don't exist. So the 10% of LTRs that have some remaining protein-coding regions associated with them, why isn't the LTR altered as well?

Kleinman:

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Are all LTRs associated with retroviruses?

Taq:

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LTRs are by definition from retroviral insertions.

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Is that definition like your definition of an atheist? Are all LTRs identical?

Kleinman:

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If you don't have the viral protein-coding genes in the genetic sequence, and the LTRs have evolved, how can you be sure this genetic sequence is from a retrovirus?

Taq:

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The same way you can identify a partial fingerprint.

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You can tell the genetic structure of a protein-coding region from DNA repeats? Tell us what the genetic structure of the protein-coding region is in the 90% of LTRs that have no protein-coding regions. And do fingerprints evolve as genetic sequences do?

Kleinman:

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How do you determine that this piece of genetic material is the remnant of a retrovirus rather than host DNA when the viral protein-coding DNA is gone?

Taq:

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The same way we know a partial fingerprint is from a finger.

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Is your claim now that the genetic sequences for LTRs never evolve? Explain to us why LTRs don't evolve.

Kleinman:

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Can the host vertebrate genome have its own LTRs that are not from a virus?

Taq:

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Can a murder weapon have its own fingerprints?
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All you are trying to do is used the Omphalos argument. Arguing that the human genome was created with genetic scars from retroviral insertion is nonsense. It's like saying the universe was created last Thursday, complete with a false history and false memories.

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Perhaps this will help you with your confusion:
Long terminal repeat - Wikipedia Do vertebrates have retrotransposons that are not ERVs?

Kleinman:

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He is now shifting his argument from ERVs to LTRs.

Taq:

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LTRs are ERVs, you fucking moron.

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Do you have to be so obnoxious when you can't explain yourself. Here is the image that you posted showing a simplified representation of a retroviral genome:

LTRs represent only a small part of that genetic sequence. Now you say it represents the entire genetic sequence. Can't you get your story straight?

Kleinman:

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The correct picture he should use for his argument looks like this:

Taq:

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You would deny that those are tires. Instead, they are round pieces of rubber that were created with the Earth 6,000 years ago. They never came from a tire factory, nor did they ever reside on a car.

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You make very silly claims when your illogical argument collapses. You are the one claiming that you can identify the genetic structure of proteins based on LTRs. And your claims become much stranger when you claim that LTRs are ERVs when LTRs are only a very small portion of the genetic structure. Try to stay on point, if you can.

Kleinman:

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Taq can look at this picture and tell us what vehicle these tires came off simply by the brand of tire.

Taq:

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I can tell you they are tires. In the same way, LTRs are the tires of the ERV vehicle. Your argument seems to be that the Earth was created with those tires already in place.

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Now you are claiming that host genetic structures don't have any DNA repeats. Why would you want to make this claim?

Kleinman:

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It is no surprise that Taq would rather argue about what he thinks atheism and agnosticism mean, or post a bunch of references that he claims explain how drug resistance evolves and then gets angry because I point out that he doesn't quote from any of them.

Taq:

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You fucking moron. You don't even understand the papers you claim to reference. You don't even understand that modeling asexual reproduction does not accurately model the evolution of sexual species. You can't even understand that the mutation rate is different in humans and in bacteria.

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Taq, do you think that crossing over or recombination has a marked effect on descent with modification and adaptation? Tell us how an allele can accumulate 5 adaptive mutations using crossing over or recombination. Because that's what it takes to get the high-efficiency beta-lactamase allele to penicillin-type antibiotics.