Bases on theoretical analyses and experimental data, Sanford claims that RNA viruses such as Influenza or Ebola tend to degenerate through genetic entropy during outbeaks. Critics of this thesis
often argue that such a thing is impossible because RNA viruses have existed in their natural reservoir for too long. However, this objection only works if the genetic entropy of RNA viruses occurs at the same rate in all hosts and in the various environments in which the viruses exist. But as we have seen in a previous thread (Influenza may be in evolutionary stasis in its natural reservoir after all), there are evidences that influenza viruses may be subjected to less genetic entropy in their natural biotic or abiotic reservoirs than during outbeaks in humans. Now, new very surprising data from the recent Ebola outbreak in Guinea indicate that the virus may lay dormant in survivors of previous outbreaks, offering a new mechanism by which RNA viruses can resist GE.
Guinea_2021_EBOV_Virological.pdf
https://www.sciencemag.org/news/2021/03/new-ebola-outbreak-likely-sparked-person-infected-5-years-ago
Sanford claims that GE is inevitable in all conditions. If this isn’t the case then Sanford’s argument falls flat. Remember, Sanford is claiming that the Earth can’t be old because life could not exist for more than a few thousand years due to GE.
Where is the same evidence for influenza?
IOW, we have confirmed instances in which GE definitely does not happen.
Therefore, GE happens.
Seriously?
I read this the other day, and thought then that you would be interested 
For sure this is a very intriguing case.
Not really. The rate of mutation vary up or down, and the objection is still valid. Sanford proposed that H1N1 was attenuated in the course of a couple of years, and went extinct in the course of decades. Putting aside geology, even the YEC timeline of 6 thousand years is orders of magnitude more. So you need a rescuing device(s) that 1) confers stasis over millennia, and 2) works for ALL pathogens, including each and every one infecting humans, animals, plants, bacteria, and so forth.
Host responses to infection vary from all the way from quickly dying to incorporating the microbe into its biome in a symbiotic relationship, and coexistence in one reservoir can be virulent in another host. As part of that varying host relation, that the rate of replication can vary is granted. But for GE the challenge is that all hosts eventually die, from other causes if not from the infection. To avoid sharing the fate of the host, the virus must infect, to infect the virus must shed, to shed the virus must replicate, and in replicating all RNA viruses are exposed to mutation. Furthermore, as host defenses adapt, it is imperative that pathogens mutate.
The genetic phylogenic tree of Ebola is defined by branching from gazillions of mutations, so right there is a plain picture that Ebola has not enjoyed exemption from mutation.
So GE remains fraught with a self contradiction from which it needs rescue. Just how badly one wants GE to be true is correlated with the special pleading to find an avenue of exception from the very conclusion of GE.
This is silly.
The argument now is that these viruses just…didn’t mutate…for the entire time they existed before crossing into humans?
Putting aside how laughable that idea is, it’s self-defeating for GE proponents because it makes GE context-dependent rather than universal and inevitable. If we’re going with “well it depends on the environment” then…yup! That’s how fitness works! Thanks for agreeing with what the critics have been saying.
It is pertinent to note that the two, 2021 Ebola virus variants identified did not enter any evolutionary stasis. They only experienced a slower evolutionary rate consistent with latent or persistent viral infection:
Reports from the remaining two teams on the recent Ebola virus strains.
These findings don’t support GE at all. Even at a lower substitution rate due to latency most of these ancient viruses which gave rise to strains responsible for current disease outbreaks should have gone extinct, well, because thousands of years is a long time.
Latent viral genomes may exist as episomes or proviruses within host cells. Proviruses appear to be more vulnerable to mutational degradation, due to their ability to integrate into host genomes, which subjects them to a wide range of mutational events. This indicates that latency wouldn’t save proviruses from GE. In the studies below, we see that even dormant HIV is not spared from mutation accumulation which may or may not deleterious:
Overall, the GE hypothesis doesn’t stand up to scrutiny.
Not true.
That’s why in the past I tried emphasizing my understanding that half (or more than half) of the argument about GE is about how selection works on the human genotype and phenotype. The entire book is spent on humans only except for a few paragraphs. So yes, it does depend on the environment and replication process and replication ability (no idea if those are the correct scientific terms) of the ORGANISM in question.
The arguments against GE need to be better. Don’t make it easy.
Then he can’t argue that the Earth has to be young.
Sanford and allies also claimed that influenza strains went extinct because of GE. When the evidence started stacking up on the other side of the argument they changed their tune. These ad hoc rescues don’t portend well for GE.
Then we agree that the earth is not 6000 years old?
Why are you using the frame of “argument” but not evidence?
We don’t need arguments. We only need to point to the evidence that is being ignored and/or misrepresented.
I’ve learned through experience that I’m largely wasting my time with this, but for anyone else who is interested, here’s what Sanford says about GE (this is from the 2nd edition):
it can very reasonably be argued that random mutations are never good.
Yet I am still not convinced there is a single, crystal clear example of a known mutation which unambiguously created information.
So what does the real distribution of all mutations really look like? […] BENEFICIAL MUTATIONS ARE SO RARE THAT THEY ARE TYPICALLY NEVER EVEN SHOWN IN SUCH GRAPHS. Figure 3b shows a more realistic view of the distribution of mutations, ranging from lethal (Â1) to neutral (0).
(Caps in original.)
Therefore, I cannot draw a small enough curve to the right of zero to accurately represent how rare such beneficial mutations really are. Instead, I have just placed an easily visible triangle there (Figure 3d). Figure 3d is the most honest and true representation of the natural distribution of mutations (except that it is vastly too generous in terms of beneficial mutations).
It is becoming increasingly clear that most, or all, of the genome is functional. Therefore, most, or all, mutations in the genome must be deleterious.
(Bold in original.) I include this one because for many viruses, and to a lesser extent prokaryotes, the genomes are extremely dense with few non-coding, non-regulatory regions. So what Sanford is erroneously claiming about the human genome (that it is almost entirely functional) is actually true in many cases. And if he is correct about the distribution of fitness effects (he isn’t), then those small, super-dense, high-functionality genomes would be susceptible to GE.
Sanford is not hedging, and he’s not describing context-specific effects. He’s very clear. All mutations bad. So all mutations to functional regions bad. So higher functional fraction → higher % of mutations are bad in an absolute sense.
Of course, we don’t have to wonder of Sanford thinks GE applies to viruses, because he claimed it caused H1N1 to go extinct. And please, but all means, let’s litigate that one again. Make my day.
Because GE is about interpretation of the evidence.
He doesn’t use GE to argue that. Only that humans could not have evolved.
- I’m not aware of more than 1?
I remembered one reason why I stopped discussing this with you last night after I made my post You contradicted yourself in your post when discussing what Sanford says. You are misleading when you present what he says and IMO you don’t understand the natural selection part of his argument or don’t address it.
No, a better description of the argument is that RNA viruses may adopt more than one lifestyle either in their natural reservoirs or in humans, for example a lifestyle prone to GE during outbreaks and a lifestyle that allows them to better resist GE such as the one infered from the recent Guinea outbreak.
You can scoff all you want, but the fact is that this idea is now supported by the data of the new Ebola outbreak.
What’s the problem? Can you see that a car is more exposed to wear and tear when it is running than when it is left in the garage.
Careful now. You’re treating the hypothesis of GE as if it is quantifiably falsifiable. Nobody knows the supposed magnitude of effect that GE should have. Nobody has been able to predict when anything should be going extinct due to GE.
That I am aware, not even a range of times-to-extinction have been put forward. All we ever really get from GE proponents is some nebulous claim that fitness should be declining, and then a lot of ad-hoc interpretation of various real-world events as being consistent with GE, yet also terminally indistinguishable from effects consistent with canonical understandings of population genetics (such as strong and repeated population bottlenecking).
In response to observations that fitness is increasing in evolving laboratory populations of bacteria, GE proponents have sought to redefine what GE is all about, shifting the definition away from reproductive fitness and insisting it’s somehow about some “integrity of information in the genome” idea that they can’t quantify, while also (out of the other side of their mouthes) suggesting that maybe sorta bacteria don’t suffer from GE at all because of their simplicity(which they also can’t quantify, nor show how relates to the supposed rate of fitness decline).
The whole thing is at bottom smoke and mirrors carried mostly by a host of analogies to “rust”, and vacuous rhetorical devices such as “there are many more ways to break than to improve a machine”.
And H1N1 subtypes are still being targeted in every year’s influenza vaccine since then!
False. For example, here is what Sanford says in his H1N1 paper: in light of the strong tendency toward natural genetic attenuation which we document here, we suggest that the natural reservoir most likely involves a very quiescent viral state, as might occur within a host where there is very little viral replication, and hence much lower mutations rates.
Note that his suggestion is now supported by the real data gained from the recent Ebola outbreak.
It is Sanford who chose to build his case on H1N1. He refers to that paper with tiresome constancy. His inept treatment of that relatively simple instance does not bode well for his understanding of more complex organisms and ecologies.
I do not recall your replying to discussion of the distribution of fitness effects, which is really at the heart of the matter. I suggest that the genetic arguments against GE are in themselves very sound. In the broader context of science where it is well established that life on earth is ancient, GE is rubbish from the get go. The arguments against GE do not need to be better because 1) in science, a hypothesis is not considered true until proven otherwise, 2) the data already easily falsifies the hypothesis, and 3) convincing yourself is not the bar for science.
That’s true. But the fact of the matter is that Sanford doesn’t think that GE proves that the Earth is young. Rather, his thesis is that given only mutation/selection (given only neo-Darwinian theory), all species must go extinct. The corollary being that if life on earth is old, then the neo-Darwinian theory is false.
I see your point and entirely agree.
They documented no such thing.
This is just not a serious argument. We have measured the rates.
It’s misleading to quote Sanford making his own argument? Perhaps you could point me to the part where he explains the context specificity of GE.
This natural selection part?
As we will be seeing, there is no selection scheme that can reverse the damage that has been done during our own generation  even if further mutations could be stopped. No amount of selection can prevent a significant number of these mutations from drifting deeper into the population and consequently causing permanent genetic damage to the population.
Or the part where he says…the opposite of that? Where might I find that part?
Now obviously Sanford, you, and everyone else in this conversation know that “neo-Darwinism” refers to evolutionary theory circa 1940, and isn’t representative of evolutionary theory in the 21st century. Right? But that would make the bait-and-switch deliberate, either by Sanford or by you in the post I quoted. So either there is a serious knowledge gap regarding evolutionary theory somewhere in the chain, or a bait-and-switch. I would love to know which, and from whom.