There isn’t a single genome. There never has been.
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I think FI might be the relevant framework here. I mean, the H1N1 genome is composed of a set of functional elements. These FE accumulate mutations linearly with time. At a certain point of time, these FE will not exhibit the level of FI necessary to implement their function at the level required to maintain fitness.
Sure, that’s possible. I already whiffed once; I can do it again. But I figure a wider variety of responses will help more quickly narrow down what counts and what doesn’t. And if it turns out nothing counts, that’s a result too.
I’ll admit, it is difficult for me to understand how the matter of evolutionary processes generating information is still a question in light of such examples, but here we are. Of course, any given person could be unfamiliar with the process of affinity maturation. But it’s such a pervasive question that I don’t think such unfamiliarity can be the full explanation in all cases.
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I does seem unlikely I will get the specific answer I am looking for, but it does hurt to ask.
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FI it is. FI describes the proportion of sequences (in a genome) with a level of function greater than or equal to a given level (I should review that paper again).
What function should we consider?
A note aside: I am not sure FI is the right measure to consider. For Sanford to make his case would require showing that FI of some function in the entire extant genome has dropped below some reference threshold.
Back on task - Is “Functional Elements” defined anywhere?
… these FE will not exhibit the level of FI necessary to implement their function at the level required to maintain fitness.
That’s rather vague. Are you asserting that H1N1 is going extinct? (Surely not)
If so, has some other variety of virus evolved to replace it?
We have the whole H1N1 genome to work with here, or *multiple genomes" as @Mercer notes. If we broaden the question to include multiple functions and “Functional Elements”, whatever those are, then it seems highly unlikely the entirety of the H1N1 virus has lost fitness.
I acknowledge that the definition I’ve asked for is difficult, but if the information Sanford refers to is measurable, then we ought to be able to break the problem down into smaller, simpler pieces until we have something to measure. I think complicating the question by considering multiple functions and FE is the wrong way to go.
It *could be" that Sanford has no definition for information at all. This is how it appears to me. If this is the case then I can stop pestering you for an answer that doesn’t exist.
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And it would appear that, with this, @Giltil actually thinks he has answered the question of how creationists define Functional Information.
How odd.
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Wow. I hadn’t paused to consider that. Great point.
Another great point.
Much like the appearance-of-age argument, these “Creator-as-prankster/deceiver” scenarios keep popping up.
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This!
Simple demonstration to show functional information is intrinsically tied to the environment: Many of the enzymes encoded in our genome are also shared with deep-sea hyperthemophilic prokaryotes that live in superheated hydrothermal vents. However, none of our enzymes would work in these organisms. All of them would break down almost immediately. Most proteins in the human body irrecoverably denature even before the temperature reaches 65 degrees C and completely stop functioning.
Those bacteria have many of those same enzymes, yet they are adapted to extremely high temperatures. They can function at 120 degrees C or even beyond for some strains.
That means the FI for a human-encoded enzyme must be specific to the environmental context of human beings and their body temperature. They work best around 37 degrees C. If the temperature increases too much, the function stops, and if the function stops then there is no function, and if there’s no function there’s no FI. So FI must be intrinsically tied to a specific physical environment with parameters within a certain range where the function can happen.
Same goes for those hyperthermophiles and their genetically encoded proteins. They work best at the conditions in which they live, and if temperature gets too high or too low, these too will break down or stop functioning.
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This statement blithely ignores the arms race model of viral evolution. Function and fitness are both contextual to host population response. The corollary is that a virus that does not mutate at all will lose function and fitness.
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I wholeheartedly agree with all what you say here, except that I ignore the arms race model of viral evolution. But this arms race model doesn’t affect Sanford thesis, not at all.
What happened to “I avoid nothing”?
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I do not see how the two are compatible.
The arms race model (aka the Red Queen Hypothesis"it takes all the running you can do, to keep in the same place") applied to viruses is that the only constant is change, and that selected mutations are adaptive. There never is or was some static zenith of fitness. Playing the tape backwards on Genetic Entropy arrives at unmutated and optimal genomes encoding uncompromised function, for which virulence is a proxy in the case of H1N1.
It makes little sense that viruses can be adaptive even while undergoing a more generalized decay. They do little beyond hijacking host processes to churn out more copies of themselves, and it is a matter of the record that they are capable of adapting and optimizing those functions to that end. If this adaptation has positive effect, it cannot simultaneously be deleterious. By way of selection, information of the host population is conferred to information encoded in the viral genome.
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I disagree. Take the example of a standard car. It is easy to envision how some small changes can be introduced to make the car more fit to a particular environment. But such adaptations won’t protect the car from a more generalized decay, starting with the accumulation of rust, that will eventually lead to a malfunctioning car.
The same phenomenon applies to a given virus lineage. Absent some sort of rejuvenated event, this lineage can indeed adapt to new environments but in the long run, it cannot escape genetic entropy.
The car analogy probably isn’t the best choice given the obvious flaws that have been discussed on this forum at great length. Accumulation of rust is a whole new flawed analogy though, as rust generally isn’t something that is designed into a vehicle. 
You might salvage the analogy with a highly specialized design, where the car becomes useful for only one sort of road but not for others.
Here the existence of environmental information should be obvious.
However, an analogy to cars, or maybe some simpler mechanical object, might be helpful in pinning down a definition of information - or maybe functional information - which we still do not have.
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Not if you keep removing the rusty parts and modifying the remaining parts so that the car remains functional, or even improves its function.
This is an analogy to natural selection, which somehow does not figure in your analogy.
But, right, you “ignore nothing.” Tell us again about that.
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The problem with that analogy is it is only a tool meant to explain what you think, it doesn’t show that the same thing must happen to viruses. Viruses aren’t made of steel that can literally rust.
The genes in viruses add fitness to the virus through their functions. Replication, receptor binding, capsid proteins that contain the genome, etc. They can only degrade through reducing the effects on which their functions depend, such as catalysis, binding, stability, etc. They don’t actually rust, and mutations can only be neutral, or increase or decrease those functions, and through that fitness.
Taking the effect of stability on protein function (which contribute at least up to some range), assuming that mutations pile up that slightly reduce stability of a protein (and through that small reductions in fitness), it takes a single strongly stabilizing mutation to reverse a lot of slightly destabilizing mutations. And those just aren’t that rare. Reviews on the distribution of the stability effects of mutations indicate something around 15-30% of mutations are stabilizing on protein structure.
The same would be true for binding, catalysis, etc. The simple fact is that, despite all the clever analogies about sand in backpacks or rusting cars, biochemistry just doesn’t function like that.
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Let’s not take this “example”, as it is entirely disanalogous.
You are conflating the design of a car (analogous to the genetic makeup of a virus, or other living organism), with the fact that cars wear out and eventually cease to function (analogous to a living organism aging and dying).
Any “small changes” to the design of a (new model) of a car would not entail that the new car would ‘inherit’ the existing rust on previous models.
This confusion appears likely to a failure to remember that evolution occurs in populations, not individuals (so what happens to an individual car, in terms of rust, and even any after-market modifications, is not relevant to analogising cars to evolution).
But this is not a generalisable phenomenon – just a bad analogy. And even a good analogy isn’t evidence. So we have no reason to believe that this “applies to a given virus lineage.”
Likewise, they do not need to “escape genetic entropy”, because we likewise appear to have no evidence that genetic entropy exists (outside of John Sanford’s fevered imagination).
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Remind me - how is it that any viruses exist? They reproduce so quickly that genetic entropy surely should have banished them to the trash bin of history.
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To carry the analogy further, what if the rusty car could reproduce, and some of its offspring inherited more of the rust and others less of the rust, and the less rusty cars were more successful in producing greater numbers of less rusty cars? Well that was cringe. Maybe the rusty car analogy does not shed much light.
It is obvious that every extent virus has escaped genetic entropy, or else they would not have continued to exist. Sanford’s puerile response to this objection departs from the world of the rational.
Given a viral strain with an adaptive trait, there may well be variations in replication, many intact, some mutations which may be deleterious, a few of which may be beneficial, a few reverse, and occasionally a mutation that combines with a prior deleterious mutation for an overall positive effect. It may be expected that adapted traits in concert with overall positive fitness will enjoy the advantage. All of this has been witnessed with SARS-CoV-2.
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And what is the biochemical equivalent to this analogy?
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