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ID and coronavirus conspiracy theories

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  • #46
    Originally posted by TheLurch View Post
    Behe's whole argument is bogus, because its based on there being no selective advantage to the mutations unless both are present, which we know to be wrong.
    Are you saying there's a selectable path to every structure? And beneficial mutations are by far the exception, and not the rule.

    But even if we grant him that premise for some hypothetical case, then he's got to show that the existence of neutral mutations in the population is rare, and there aren't many of them floating around.
    If they don't get fixed, then then it's in effect a low probability that a given mutation will be present.

    And, in any case, it's a huge side track from the topic under discussion, which is that the only analysis of the coronavirus genome has been done by biologists, and not the ID crowd, because after all these years, they've not developed any tools to analyze genomes.
    I'm not sure what you're insisting on, a lab procedure that would detect design?

    Blessings,
    Lee
    "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

    Comment


    • #47
      Originally posted by rogue06 View Post
      Lee, that is nothing but making up definitions to support a predetermined conclusion.
      I don't think so! Larry Moran concurred with Behe about low probabilities for independent mutations.

      Blessings,
      Lee
      "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

      Comment


      • #48
        Originally posted by lee_merrill View Post
        Are you saying there's a selectable path to every structure? And beneficial mutations are by far the exception, and not the rule.
        No, i'm saying Behe's lying to you. Or, as i conceded earlier, not lying because he's convinced himself of his own ideas despite the evidence.

        Originally posted by lee_merrill View Post
        If they don't get fixed, then then it's in effect a low probability that a given mutation will be present.
        Absolutely and utterly false. Many neutral mutations are present at high levels in populations without ever becoming fixed. All these genetic ancestry tests? THey're based on that reality.

        Originally posted by lee_merrill View Post
        I'm not sure what you're insisting on, a lab procedure that would detect design?
        No, i'm willing to let the ID guys benefit from all the hard work done by actual biologists in obtaining and sequencing genomes. Why haven't they developed an algorithm that scans the genomes and identifies indications of design?
        "Any sufficiently advanced stupidity is indistinguishable from trolling."

        Comment


        • #49
          Originally posted by TheLurch View Post
          No, i'm saying Behe's lying to you. Or, as i conceded earlier, not lying because he's convinced himself of his own ideas despite the evidence.
          But you said "Behe's whole argument is bogus, because its based on there being no selective advantage to the mutations unless both are present, which we know to be wrong." Which implies selective advantage for intermediaries.

          Absolutely and utterly false. Many neutral mutations are present at high levels in populations without ever becoming fixed. All these genetic ancestry tests? THey're based on that reality.
          So new protein-protein interactions should be easy to form. Only they're not, they occur about at the rate that Behe predicted.

          Source: The Edge of Evolution

          There have been no reports of new viral protein-protein interactions developing in an infected cell due to mutations in HIV proteins.21 No gene duplication has occurred leading to a new function. None of the fancy tricks that routinely figure in Darwinian speculations has apparently been of much use to HIV.

          © Copyright Original Source



          No, i'm willing to let the ID guys benefit from all the hard work done by actual biologists in obtaining and sequencing genomes. Why haven't they developed an algorithm that scans the genomes and identifies indications of design?
          Do you mean human design? Right now that can be indicated by the factors that Stoic outlined. Or as I mentioned, four or more non-selectable mutations that result in new function, a deduction from Behe's work.

          Blessings,
          Lee
          "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

          Comment


          • #50
            Originally posted by lee_merrill View Post
            But you said "Behe's whole argument is bogus, because its based on there being no selective advantage to the mutations unless both are present, which we know to be wrong." Which implies selective advantage for intermediaries.
            Behe's argument focused on the origins of drug resistance in malarial parasites - one case in particular that required two mutations. He based his argument on the claim that neither of those two mutations provided a selective advantage. That claim in specific is false.

            It's a separate flaw from the flaws related to the fact that he discounts the prevalence of neutral mutations, etc. In other words, his argument is stupid on so many levels that you seem to be getting confused about which level i'm focused on. If you're having trouble keeping track, ask.

            Originally posted by lee_merrill View Post
            So new protein-protein interactions should be easy to form. Only they're not, they occur about at the rate that Behe predicted.

            Source: The Edge of Evolution

            There have been no reports of new viral protein-protein interactions developing in an infected cell due to mutations in HIV proteins.21 No gene duplication has occurred leading to a new function. None of the fancy tricks that routinely figure in Darwinian speculations has apparently been of much use to HIV.

            © Copyright Original Source

            You do realize that here aren't many "viral protein-protein interactions" because most viral proteins interact with host proteins, right?

            Again, that's the specific flaw in this argument. There's two more general flaws to it. The first is that he's looking in the wrong place - the sort of evolution he's looking for would have occurred in the evolution of differences between SIV and HIV, which clearly have very different phenotypes (SIV is tolerated without significant consequence by our relatives), part of which is likely mediated by differences in the interactions between viral and host proteins. This is a subject i'm not very familiar with, though, so i can't go into details without time to do some reading here.

            The second more general flaw is that virus have extremely compact genomes, and don't provide a relevant example for the sorts of complex protein interaction networks that are needed to enable a cell to function. So, he's chosen an irrelevant example to make his argument. it's bogus in the same way that suggesting the evolution of resistance to a single drug is a good model for the whole genome evolution of a virus - the two have so little in common that it's hard to figure out how to even make the comparisons.

            These are all the ways that Behe is lying to you. Aren't you a little offended by that?

            Finally, i feel the need to point out that the reason this new coronavirus is more of a threat than previous ones is because it has evolved the ability to interact with a new human protein. So, using this as an argument given the current context is... what's the word...?

            Idiotic.

            Originally posted by lee_merrill View Post
            Do you mean human design? Right now that can be indicated by the factors that Stoic outlined. Or as I mentioned, four or more non-selectable mutations that result in new function, a deduction from Behe's work.
            For starters, you mentioned three. Plus it's important to remember that Behe has done no "work". He's made arguments using data produced by the work of actual biologists. These arguments are massive heaps of misinformation, as we keep pointing out, but they didn't involve work.

            That out of the way, you're misunderstanding my argument. Give me a few dozen coronavirus genomes and some time, and i can hunt down software tools that will allow me to identify which mutations are neutral, which are undergoing positive selection, which genes are experiencing purifying selection, etc. etc. I can identify the specific sites where two viruses underwent recombination, identify the ancestral viruses, etc. etc. All those tools exist because evolution is a well supported and well developed theory that is focused on real world behavior with significant consequences.

            There aren't any intelligent design tools. At all. Give an ID advocate a dozen viral genomes, and all they can do is stare blankly at them.

            What does that tell us?
            "Any sufficiently advanced stupidity is indistinguishable from trolling."

            Comment


            • #51
              Originally posted by TheLurch View Post
              Behe's argument focused on the origins of drug resistance in malarial parasites - one case in particular that required two mutations. He based his argument on the claim that neither of those two mutations provided a selective advantage. That claim in specific is false.
              That would push the edge of evolution back even further, then, for Behe's calculations are based on the actual rate of the development of resistance.

              It's a separate flaw from the flaws related to the fact that he discounts the prevalence of neutral mutations, etc.
              Well, again, he uses rates derived from what evolution actually did, so the prevalence of neutral mutations was taken into account.

              You do realize that here aren't many "viral protein-protein interactions" because most viral proteins interact with host proteins, right?
              I would expect his statement would include new viral-protein with host-protein interactions.

              ... the sort of evolution he's looking for would have occurred in the evolution of differences between SIV and HIV, which clearly have very different phenotypes (SIV is tolerated without significant consequence by our relatives), part of which is likely mediated by differences in the interactions between viral and host proteins.
              I'm not sure what you mean by evolution of differences, Behe examines evolution of HIV itself.

              The second more general flaw is that virus have extremely compact genomes, and don't provide a relevant example for the sorts of complex protein interaction networks that are needed to enable a cell to function.
              But Behe also examines the malaria parasite, which is considerably more complex than a virus.

              Finally, i feel the need to point out that the reason this new coronavirus is more of a threat than previous ones is because it has evolved the ability to interact with a new human protein.
              Which may be why Behe puts the edge of evolution at the level of a double-CCC. How many mutations were required to generate the new capability of this coronavirus, I wonder?

              Give me a few dozen coronavirus genomes and some time, and i can hunt down software tools that will allow me to identify which mutations are neutral, which are undergoing positive selection, which genes are experiencing purifying selection, etc. etc. I can identify the specific sites where two viruses underwent recombination, identify the ancestral viruses, etc. etc. All those tools exist because evolution is a well supported and well developed theory that is focused on real world behavior with significant consequences.

              There aren't any intelligent design tools. At all. Give an ID advocate a dozen viral genomes, and all they can do is stare blankly at them.

              What does that tell us?
              No, they can see if there are double-CCC events in them, or even more complex events, which would indicate design.

              Blessings,
              Lee
              "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

              Comment


              • #52
                Originally posted by lee_merrill View Post
                That would push the edge of evolution back even further, then, for Behe's calculations are based on the actual rate of the development of resistance.
                Behe does nothing of the sort.


                Well, again, he uses rates derived from what evolution actually did, so the prevalence of neutral mutations was taken into account.
                No you all do not.


                I'm not sure what you mean by evolution of differences, Behe examines evolution of HIV itself.
                But Behe also examines the malaria parasite, which is considerably more complex than a virus.
                Not based on the unbisaed scientific perspective.
                Glendower: I can call spirits from the vasty deep.
                Hotspur: Why, so can I, or so can any man;
                But will they come when you do call for them? Shakespeare’s Henry IV, Part 1, Act III:

                go with the flow the river knows . . .

                Frank

                I do not know, therefore everything is in pencil.

                Comment


                • #53
                  Originally posted by shunyadragon View Post
                  Behe does nothing of the sort.

                  No you all do not.

                  Not based on the unbisaed scientific perspective.
                  Substantial points are appreciated, instead of these denials.

                  Blessings,
                  Lee
                  "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

                  Comment


                  • #54
                    Originally posted by lee_merrill View Post
                    Substantial points are appreciated, instead of these denials.
                    Why? You don't offer anything much beyond "These ID guys i like said the following, and i believe them always."
                    "Any sufficiently advanced stupidity is indistinguishable from trolling."

                    Comment


                    • #55
                      Originally posted by lee_merrill View Post
                      That would push the edge of evolution back even further, then, for Behe's calculations are based on the actual rate of the development of resistance.
                      They're actually not. They're based on the appearance of one very specific pathway to resistance. We don't know if other pathways are possible, or even that they've evolved and we've not detected them. We also don't know how often this particular pathway might have evolved independently.

                      Basically, he's using our lack of information to produce the answer he wants to see.

                      Originally posted by lee_merrill View Post
                      I'm not sure what you mean by evolution of differences, Behe examines evolution of HIV itself.
                      What about HIV indicates it should be under selection to evolve new protein-protein interactions? It's a highly successful virus that seems to be doing just fine as it is.

                      In contest, the evolution of HIV from SIV opened up an enormous new reservoir of potential hosts. If you want to look at interesting evolutionary events, you look there.

                      Behe hasn't. What does that tell us?

                      Originally posted by lee_merrill View Post
                      But Behe also examines the malaria parasite, which is considerably more complex than a virus.
                      No, he doesn't look at the malarial parasite. He looks at a single gene where mutations enable drug resistance. That's it.

                      Originally posted by lee_merrill View Post
                      Which may be why Behe puts the edge of evolution at the level of a double-CCC. How many mutations were required to generate the new capability of this coronavirus, I wonder?
                      I have no idea what "double-CCC" means. it's not a scientific terms, so you probably need to define it.

                      Which capability? The ability to infect human cells? The enhanced infectivity? The secondary enhancement of infectivity? Other stuff in the virus? Evolution has solved multiple "problems" (from the virus' perspective - created problems from ours), both in parallel and in series. That's what it does.

                      Originally posted by lee_merrill View Post
                      No, they can see if there are double-CCC events in them, or even more complex events, which would indicate design.
                      Then why haven't they done so? And how would they identify them? Where are the tools that i can download that would identify them? Since i don't know what "double-CCC" means, here's your chance to provide a rigorous definition that can be implemented as an algorithm, as opposed to just relying on Behe to say "looks designed to me." If you can't - and i'm guessing you can't - then that should also tell you something.

                      Are you ever going to listen to all these things that should be telling you something?


                      (also, you should probably use "that have been claimed to indicate design", since there's absolutely no evidence they do).
                      "Any sufficiently advanced stupidity is indistinguishable from trolling."

                      Comment


                      • #56
                        Originally posted by lee_merrill View Post
                        Substantial points are appreciated, instead of these denials.

                        Blessings,
                        Lee
                        No problem . . . you ignore the 'substantieted posts; from The Lurch and I over th emillennia. The Lurch has done a better job than I to mop the floor with Behe.

                        Over the millennia The Lurch has shot Behe through so many holes, and your assertions have been responded to before with peer reviewed science.
                        Glendower: I can call spirits from the vasty deep.
                        Hotspur: Why, so can I, or so can any man;
                        But will they come when you do call for them? Shakespeare’s Henry IV, Part 1, Act III:

                        go with the flow the river knows . . .

                        Frank

                        I do not know, therefore everything is in pencil.

                        Comment


                        • #57
                          Originally posted by lee_merrill View Post
                          I don't think so! Larry Moran concurred with Behe about low probabilities for independent mutations.

                          Blessings,
                          Lee
                          And that has absolutely nothing to do with your assertion that

                          mutations have to be simultaneously present


                          is what is meant when evolution deniers pretend that all the mutations must take place simultaneously

                          I'm always still in trouble again

                          "You're by far the worst poster on TWeb" and "TWeb's biggest liar" --starlight (the guy who says Stalin was a right-winger)
                          "Overall I would rate the withdrawal from Afghanistan as by far the best thing Biden's done" --Starlight
                          "Of course, human life begins at fertilization that’s not the argument." --Tassman

                          Comment


                          • #58
                            Originally posted by TheLurch View Post
                            They're actually not. They're based on the appearance of one very specific pathway to resistance. We don't know if other pathways are possible, or even that they've evolved and we've not detected them. We also don't know how often this particular pathway might have evolved independently.

                            Basically, he's using our lack of information to produce the answer he wants to see.


                            What about HIV indicates it should be under selection to evolve new protein-protein interactions? It's a highly successful virus that seems to be doing just fine as it is.

                            In contest, the evolution of HIV from SIV opened up an enormous new reservoir of potential hosts. If you want to look at interesting evolutionary events, you look there.

                            Behe hasn't. What does that tell us?


                            No, he doesn't look at the malarial parasite. He looks at a single gene where mutations enable drug resistance. That's it.


                            I have no idea what "double-CCC" means. it's not a scientific terms, so you probably need to define it.

                            Which capability? The ability to infect human cells? The enhanced infectivity? The secondary enhancement of infectivity? Other stuff in the virus? Evolution has solved multiple "problems" (from the virus' perspective - created problems from ours), both in parallel and in series. That's what it does.


                            Then why haven't they done so? And how would they identify them? Where are the tools that i can download that would identify them? Since i don't know what "double-CCC" means, here's your chance to provide a rigorous definition that can be implemented as an algorithm, as opposed to just relying on Behe to say "looks designed to me." If you can't - and i'm guessing you can't - then that should also tell you something.

                            Are you ever going to listen to all these things that should be telling you something?


                            (also, you should probably use "that have been claimed to indicate design", since there's absolutely no evidence they do).
                            CCC is "chloroquine complexity cluster"

                            I'm always still in trouble again

                            "You're by far the worst poster on TWeb" and "TWeb's biggest liar" --starlight (the guy who says Stalin was a right-winger)
                            "Overall I would rate the withdrawal from Afghanistan as by far the best thing Biden's done" --Starlight
                            "Of course, human life begins at fertilization that’s not the argument." --Tassman

                            Comment


                            • #59
                              Originally posted by rogue06 View Post
                              CCC is "chloroquine complexity cluster"
                              That leaves me about as informed as i was before hand.
                              "Any sufficiently advanced stupidity is indistinguishable from trolling."

                              Comment


                              • #60
                                Incidentally, a small bit of searching has indicated that chloroquine resistance seems to have evolved at least three times independently:
                                "Here, we provide conclusive evidence that mutant haplotypes of the pfcrt gene product of Asian, African, or South American origin confer chloroquine resistance with characteristic verapamil reversibility and reduced chloroquine accumulation."
                                https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2954758/

                                There might be a fourth, per CDC documents. Obviously, that says something about the probability of these mutations arising that, from what i've seen of Behe's arguments, isn't considered by him.
                                "Any sufficiently advanced stupidity is indistinguishable from trolling."

                                Comment

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