All these questions by @Rumraket are legitimate and important ones, but I am not sure anyone gets the answers yet. But the important point regarding GE in influenza is that the mere possibility for this frozen evolution phenomenon prohibits Sanford’s detractors from asserting that his thesis is impossible on the sole basis that influenza has been around for a long time.
Very interesting indeed! Thanks a lot for these tremendous resources that undoubtedly would deserve a new thread.
Of course we still have the thousands of other scientific facts which kill Sanford’s YEC based GE claim deader than fried chicken. 
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You have the thousands minus 1. And I am confident that you will have soon the thousands minus 2, then minus 3 etc…, until the resurrection of the chicken😉
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OTOH, I should reference this paper by Worobey who comes out guns blazing against the idea of stasis as concerning influenza.
Worobey [2014] also analyzes the 1918 strain in this 2014 paper:
We infer that the virus arose via reassortment between a preexisting human H1 IAV lineage and an avian virus…
Our results suggest that the 1918 pandemic virus originated shortly before 1918 when a human H1 virus, which we infer emerged before ∼1907, acquired avian N1 neuraminidase and internal protein genes.
Genesis and pathogenesis of the 1918 pandemic H1N1 influenza A virus
In other words, rather that being parachuted in from some frozen state, swine flu H1N1 had an etiology which is very familiar and in keeping with the conventional “arm’s race” influenza model involving a cycle of virus shift and drift, epidemic, and host adaptation.
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Only if you use many fallacies of equivocation. Persistent viral infections involve replication. You’re trying to claim that persistence is synonymous with latency, which is patently false.
I do know a bit about the difference between persistence and latency. Here’s my last paper from my PhD work. It is still being cited 32 years later:
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Sure if you had actual evidence that there was a significant and recurrent contribution to influenza persistence from these sorts of re-emergence from long periods of frozen dormancy. As I said, mere possibility doesn’t tell us anything.
There’s another, related problem here that has to do with the ability of GE to make quantifiable predictions. We need to know how fast Influenza should be going extinct due to GE, if there was no contribution from these periods of dormancy(but there is no such prediction). And then we need to know the mean contribution to influenza persistence for these putative long periods of dormancy.
If you can’t tell us how quickly Influenza should be going extinct, nor how often and for how long it goes into a frozen state, then the hypothesis is effectively untestable, because no amount of time that Influenza has existed could then be taken to contradict the GE hypothesis. You’ll just be able to concoct some ad-hoc history of frozen dormancy if you never give us any concrete numbers.
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Did you mean the galliformes order kind, according to AiG?
Btw, here is the Galliformes order which AiG believes is all one kind
It is rather absurd how much evolution they believe has occurred in a short time since Noah’s Flood, yet deny “macroevolution”.
Yeah sure, the number of collected fossils and shared derived DNA sequence is going down all the time. Wait… 
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Do you see the irony of this remark from an evolutionist whose proposed mechanisms for the history of life is nearly entirely based on mere possibility!
I am confident that progresses will be made on these issues in the near future. But meanwhile, an interesting thing to see here is the predictive value of the theory of genetic entropy applied to influenza. Indeed, in order to be true, this theory need to posit that some states of viral dormancy exists for influenza. And guess what, such states have been found!
It seems that you don’t understand what GE is all about. Indeed, GE doesn’t claim that everything is going extinct (although Sanford hold that view), but that given only strict neo-Darwinian theory, most life forms are doomed to extinction (I say most rather than all life forms for it may be the case that some life forms such as bacteria be particularly immune to GE). IOW, GE is compatible with deep time and common descent, but not with strict neo-Darwinian theory.
Diseases caused by RNA viruses
Ebola
Polio
Measles
Rabies
Hepatitis
West Nile
Zika Fever, Yellow Fever
Common Cold, SARS, MERS, and latest but not least: COVID-19
While representing very diverse ecologies, all of these are characterized by high rates of mutation typical of RNA viruses, and all are still very much with us. This adaptability is responsible for the propensity of RNA viruses to successfully jump species to begin with. Outside of smallpox, RNA viruses have been responsible for the principal epidemic events of recent history. Nor is there any evidence that these viruses were less attenuated or more virulent in ancient times. This observation fits well with the established arms race model of epidemiology where viral mutability is essential to crossing species barriers and escape from host defenses, and poorly with Sanford’s mutational accumulation model.
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I would if that statement was true. The proposed mechanisms for the history of life have all been observed.
Unfortunately it’s not really clear what the timescales of extinction for anything is on GE, which makes it difficult to see how GE predicts that any period of such dormancy is really necessary. It all seems to basically just work at some vague “things should be running down yo” kind of level.
No, and that highlights a problem with the idea. It’s not at all clear what should be going extinct, and much more importantly, how fast. All we’re ever really told is fitness should be going down.
And a collection of unsubstantiated and physically dubious assumptions regarding the DFE of mutations, plus it’s (unquantified) relation to things like organismal complexity, then given these assumptions “most life forms are doomed to extinction” on timescales nobody seem able to say.
But you’re not sure why, or what the range of values are. Just that because fitness can be observed going up for bacteria, it’s been judged to be most rhetorically pertinent to change the tune and start saying maybe sorta kinda bacteria are immune to GE. But (maybe) everything else isn’t, who knows?
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@Giltil Following up on my placeholder above…
Sanford’s conception of Genetic Entropy in regards to influenza is beset by massive internal contradictions which are obvious even before getting into the weeds of genetic analysis. Along with the inconsistency that GE results in H1N1 extinction within a human lifespan even though the virus was preserved in some natural reservoir with full potency over millennia, there is the question as to why loss of genetic integrity is correlated with virulence attenuation in human hosts, but not in reservoir populations where, as Sanford states, “there are usually no clinical symptoms” [ note - that is not quite true ].
Another discrepancy Sanford ignores is the question of how his purported reservoirs of unmutated and attenuated influenza viruses aligns with the actual observation of variation in reservoir population. In most of the antigenic subtypes of influenza, there are at least hundreds or thousands of genetic variants, and where there is any degree of geographic or temporal separation, it is rare to obtain isolates which are actually identical. It would be expected that the variation on record is just the tip of the iceberg, given that resources for surveillance are limited. There is constant, ongoing churn in all reservoir genomes. But do see for yourself.
The National Center for Biotechnology Information hosts a database at their Influenza Virus Resource site, and there is no registration required to use it. With a minimal understanding of influenza, the drop down parameters to construct a query are intuitive, and result in a sweet listing of nucleotide sequences for any of the eight segments you selected, complete with reference to the source submission, author list, and host species. For H16, I netted a couple of hundred records; for H1 there were over 25 thousand. The database here: NCBI Influenza Virus Resource
So Sanford is positing natural reservoirs are special snowflake viruses when in fact there is a blizzard. To use YEC taxonomy, which of the myriad of viruses are supposed to represent baramins? Are all influenza strains from H1N1 to H18N* descended from one created kind? - that would entail that mutation has run rampant from long before 1918. Were all the subtypes created as their own baramin? How did influenza go from benign and benevolent, to virulent, without mutation? How does influenza “jump” to new species without mutation? How does all this adaptive mutation occur all the while without accumulating deleterious mutation, especially as Sanford is insistent that beneficial mutation is comparatively exceedingly rare? Sanford’s model of preserved genomes from creation just skates past such questions arising from his own paradigm.
What is really observed comports well with the conventional, evolutionary, model of infectious pathogens, so Sanford is attempting to solve a problem which already enjoys a well supported explanation. It is not surprising that, in working backwards from his set of pseudoscientific presuppositions, he winds up with a flawed model which is both a self-conflicted morass and contradicted by observation.
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Thank you for detailing your objections to Sanford’s thesis. Unfortunately, I do not have the time at the moment, and perhaps not enough expertise, to explore these issues further and answer you point by point.
However, I would like to leave the questions related to the origins of influenza and its evolution in its natural reservoirs and return to Sanford’s main thesis that the influenza virus is subject to the regime of genetic entropy during outbreaks in humans. In my literature searches over the last few days I have learned 2 things. 1) Plate-to-plate transfer experiments have shown that bottleneck events cause fitness loss. 2) Mutational load decreases the probability that a beneficial variant allele will emerge during the course of an infection. I think these two points give credit to Sanford’s thesis since it is clear that during a flu outbreak, bottlenecking is very strong and mutation load keeps increasing.
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Since you have neither the time nor expertise to explore further, what you think is irrelevant.
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