It’s a bit more complicated than this, since in his treatment of “neo-Darwinian theory”, Sanford makes a host of extremely dubious assumptions about the DFE of mutations. He arrives only at his conclusion by assuming the near-constancy of an extremely deleterious-skewed distribution, which has never been verified by measurement in any experimental or wild population of organisms.
So the conclusion here should be stated more like this:
Rather, his thesis is that given only his personally imagined constant DFE of mutation/selection (given only neo-Darwinian theory plus Sanford’s very idiosyncratic, empirically unverified and constant DFE of mutations), all species must go extinct. The corollary being that if life on earth is old, then Sanford’s personal, synthetic caricature of neo-Darwinian theory is false.
What lifestyle removes the necessity of replication for transmission?
How is the idea supported by the data, now or ever?
As Michael posted, per the studies, far from stasis, there were appreciable mutations, so this data conflicts with Sanford’s idea. That is not a scoff.
If you truly believed that, you would be directly citing evidence, not arguments. Do you not understand this distinction? You appear to be strenuously avoiding the evidence, which all but screams that you either don’t find it to be convincing, or that you predict it won’t be convincing if you looked at it, or most likely some combination of the two.
I think that’s a serious ethical accusation. Is there any evidence to support it?
The earliest Ebola outbreak was reported in 1976 (there might have been earlier, unreported ones), 45 years later (enough time to have accrued a huge mutational load leading to GE considering the nature of RNA virus genomes) we are still seeing new outbreaks. Of course, the virus has circulated in bats and other wildlife reservoirs for even longer, latently and actively. I wonder when GE will extinguish the virus.
The idea I was referring to is not GE but the idea that the Ebola virus can adopt a lifestyle within an host that reduces its sensitivity to GE. Obviously, the data on the recent Ebola outbreak support this idea.
For genetic entropy in hep B to happen by “deleterious mutations invisible to selection”, the deleterious effect must be smaller than 1/N.
Hepatitis B has a very short genome, 3.2kb in length.
So to have sufficient deleterious-but-invisible-to-selection mutations for an individual in say a population of 1 million hep B virii, there would have to be 100000 mutations of deleterious effect 0.000001 to achieve an effect of size 0.1.
But their genome only has 3200 base pairs!
So. Did each of these base pairs mutate 30 odd times gradually over time to do this? No, obviously this cannot happen, as there are only 4 possibilities per nucleotide.
Conclusion:
GE is impossible for Hepatitis B.
You can do a similar calculation for Ebola, which is 19kb and again similarly prove GE cannot occur for Ebola, and similarly for influenza A, which is 14kb, and H1N1 which is 13.5kb.
So for Hep B, Ebola, influenza A, H1N1, there MUST be a limit to how much degradation via mutation invisible to selection.
If anyone can find a flaw in the above math and logic, I am very happy to be corrected.
What is obvious from the 2021 EBOV outbreak data is that latent EBOV genomes experienced a significantly low mutation and evolutionary rate. That’s it. The only way latent virus genomes could evade GE (which hasn’t been shown to exist) is to cease mutating, which is unrealistic in biological organisms. Latent or not, viral genomes replicate, and as they replicate, mutations happen.
You also seem to be ignoring the HIV data, which shows that a huge chunk of its proviruses (latent virus genomes) are defective upon reactivation years after infection, partly due to mutations experienced while integrated within host genomes. As much as 90% of latent HIV genomes become defective with time.
You seem to have treated the total number of possible hep-B genomes as merely being 4 \times genome length = 12800.
It’s actually 43200\simeq 3.9 \times 101926. Way more than enough to contain 100000 mutations of very small deleterious effects.
Put another way, every mutant at one position in the genome can be seen in the context of one or more mutations elsewhere in the genome. So even though every position only has 4 different states (sticking to substitutions only), there are many more possible combinations among sites.
Illuminating link, where the theological, almost devotional, impetus for GE is on display.
The line from this interview which jumped out at me was
All this is consistent with a miraculous beginning, a young earth, and a perishing earth—which “will wear out like a garment” (Hebrews 1:11). Only the touch of the Creator can make all things new.
This encapsulates the popularity of GE to many the church. At the start is a perfect and purposeful creation. The day of the fall pronounced death, but why did Adam and Eve not physically die that day? Well internally they did, the process of corruption unleashed in their genes. It has only become worse over the past six thousand years as decay has accumulated, with death on the individual level cascading to the looming threat of the inexorable extinction of mankind. So you have the entire sweep of history, from the paradise of Genesis to the apocalyptic eschatology of Revelation, engraved on the tableau of our very genes. This is preaching to the choir.
Like the old version of the creationist argument from the 2nd law of thermodynamics, GE is held to refute evolutionary adaptation. As a bonus, if the objection be raised that GE is incompatible with the fossil record of the ancient extent of life, well, there you have it - life is young. Unfortunately, for the lay congregation, this illusionary message which seems to integrate science and gospel will have tremendous appeal.
That’s an apt comparison. Just as the 2LoT argument ignores the input of energy into the system, the GE argument ignores the input of beneficial mutations into the system, among other problems.
They don’t so much ignore it as they argue they are too few and of too little magnitude of effect to matter in the long term. They’re wrong when they argue this, but it’s too simplistic to say they really ignore beneficial mutations.
Look. Sanford has predicted the possibility of a quiescent viral state of RNA viruses within some of their reservoirs whose effect would be to slow down their evolutionary rate compared to the rate observed during outbreaks. Now, the data from the recent Ebola outbreak precisely document a nearly 10 times slower evolutionary rate of the virus in a survivor compared to the evolutionary rate expected during sustained human-to-human transmission. So contrary to what you think, Sanford’s conjecture is all the more serious because it has been confirmed by the facts.
Look. We’ve measured the rates in different hosts. Influenza doesn’t have such a state. Period. “Dormant in the survivors of previous outbreaks” doesn’t mean “not replicating except for during outbreaks”. Sanford is wrong about this and pretending otherwise is unserious.
Note that several opponents to GE on this site have scoffed at this idea of latent viral infection for RNA viruses, thinking that it was impossible. The data of the recent Ebola outbreak prove them to be wrong. A good example of what Behe called « The Pretence of Knowledge »!