I can’t say that I find that paper persuasive, nor do I really understand the proposed mechanism. In any case, that’s not relevant to the current thread. As far as the first claim goes, 1) there is some experimental and theoretical evidence to support the truth of the claim, and 2) I never made that claim, and in fact doubt that it’s true.
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Done.
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I disagree. A mutation that reduces absolute fitness from 1.0 to 0.999999, say, is not selectable in a species like (historical) humans, nor is the one reducing it to 0.999998, nor the ones after that – but the species is on the way to extinction.
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The relevant question is not the number of mutations, but the effects. For GE to work, every member of a population must suffer approximately equal fitness declines simultaneously. The differences must be small enough that selection cannot distinguish between the different genotypes present. That’s an unrealistic assumption, to put it mildly.
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Yes, this is definitionally true. “Negatively impacts fitness” is synonymous with “is selected against”. To say it’s impossible to hurt fitness without being selected against is to understate the problem. They are literally the same thing. Sanford is disputing a tautology.
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I just did a search on the response article and there is not a word on natural reservoirs.
Apart from the inept scientific errors, the H1N1 paper fatally flawed by incoherence. Even if YEC is right, Sanford is wrong. There is no means of preserving a viral strain for millennia so that some genetic arch type is inferred by virulence, while maintaining that an essential and general principle of deleterious mutation then brought it to extinction. This is a dishonest claim.
For a competent perspective on the history of H1N1, this presentation by Michael Worobey, Professor, Ecology and Evolutionary Biology, The University of Arizona, is informative and personable, directly from a researcher who has published several papers specifically on H1N1, influenza in general, and more broadly diseases due to RNA viruses.
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This is a rejection of basic mathematics.
This is an admission that none of the listed authors understand basic mathematics. Since GE is inherently a mathematical argument, its authors not understanding how math works is something of a problem.
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It’s very disturbing that you’re still repeating this extremely false statement, which fails to square with anything in the field of population genetics. And worse still that it falls to me, and me alone, to correct you.
Putting aside that I have a Ph.D. in genetics and am an evolutionary biologist, would any of the population geneticists here like to weigh in on this?
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To make such a claim in good faith, you’d have to be familiar with everything in the field of population genetics. Is that true?
I see no reason for that to be the case. It’s not like Sanford and Carter are busy doing research.
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In the response, Carter repeats their misunderstanding of the history of H1N1 here
… the human H1N1 disappearing in 1957. It was reintroduced in 1976 and circulated until 2009, when it went extinct again.
which first appears in the Carter Sanford H1N1 paper…
Human H1N1, the remnant of the 1918 lineage, appears to have gone extinct a second time.
And @PDPrice has confidently asserted that the 1918 strain is extinct, just like dinosaurs.
Apparently, Paul’s memo did not reach the influenza research community…
It is not generally appreciated that descendents of the H1N1 influenza A virus that caused the catastrophic and historic pandemic of 1918-1919 have persisted in humans for more than 90 years and have continued to contribute their genes to new viruses, causing new pandemics, epidemics, and epizootics…
It is remarkable not only that direct “all-eight-gene” descendants of the 1918 virus still circulate in humans as epidemic H1N1 viruses and in swine as epizootic H1N1 viruses, but also that for the past 50 years the original virus and its progeny have continually donated genes to new viruses to cause new pandemics, epidemics, and epizootics. The novel H1N1 virus associated with the ongoing 2009 pandemic is a fourth-generation descendant of the 1918 virus.
Morens, Taubenbeuger, Fauci - The Persistent Legacy of the 1918 Influenza Virus
Here is how is actually went down.
The influenza virus, by mutation, has successfully plagued human and animals for millenia. Are there strains, clades and sub-clades that come and go? No kidding, thousands and more, but the genes live on and on. Influenza is always mutating, incessantly by drift and occasionally conspiring via shift. That is essential to its persistence. To suggest this is an exhibit of a universal, deleterious decline of genetic fitness is so daft, so opposite the reality, it is flabbergasting that the idea was even concocted.
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Yeah, the “1918 influenza went extinct” argument is complicated by the persistent existence of descendants of the 1918 lineage.
Also, note the Fauci cameo.
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It seems to me like it’s a semantic quibble all around. If the fitness is not exactly 1.0 – and it’s never exactly 1.0 – then the allele is under selection. But if it’s close to 1.0, then the effect of that selection may be smaller than the effect of drift. The probability of fixation is still changed by the fitness, though.
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They already have, and they’ve said you’re wrong. Even here in this relatively small thread it’s already been said. You just don’t care.
Why don’t you correct him yourself, if you know your stuff? His statements are hilariously bad.
If so, that’s a ridiculous model.
I wouldn’t. What are you on about?
Is it? It seems perfectly realistic for nearly neutral mutations. What’s wrong with it?
I’d say it’s false, whether definitionally or otherwise. This notion of threshold selection just doesn’t seem at all realistic. I think you’re equivocating between relative fitness (which selection operates on) and absolute fitness (which it doesn’t).
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I’m not talking about a real threshold, I’m talking about the definition of fitness. If something reduces reproductive output (as Sanford claims is an inevitable result of GE), it is necessarily selected against. Sanford’s model has a cliff, if you will, where this starts to happen. But that doesn’t matter. That doesn’t reflect reality, and let me be perfectly clear: I’m not defending his model in the slightest. The relevant thing is that it’s the “thing hurts reproductive output → selected against” that matters. That’s just the definition of the terms.
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Not true if the entire population is affected evenly. Selection is differential reproductive success. No variance, no selection.
I don’t believe it does. Can you point to this cliff?
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In other words, it’s deleterious but not selectable. It’s below the threshold of selection. Just like Kimura said in his paper. I would say you may be the only scientist here at the moment who (evidently) grasps this concept. Most of the others keep parroting “if it’s deleterious, that means by definition that its selectable” over and over.