No one mutation makes the [corona]virus spread better. A general reduction in function from an accumulation of many mutations may temporarily help prevent the [corona]virus from going extinct by helping it propagate to more people; but this will not save it in the end, because that accumulation of mutations is damaging and it keeps getting worse with each added mistake.
These predictions based on genetic entropy have been falsified by the recent course of events. Consider:
An early mutation in China, D614G, rapidly spawned a variant that overtook the original virus there and became the version of novel coronavirus that spread across the globe. Laboratory testing shows that it is far more transmissible and infectious than its ancestor.
The P.1 variant in Brazil is more transmissible and even seems to have some ability to evade antibodies for the early D614G strain. It accounts for 42% of the cases in Manaus and has spread to Japan and the U.S.
All of these variants contradict the predictions made by genetic entropy proponents.
If you take a look at the paper I cited, it refers to D614G, so that’s point #1. It’s in dispute.
No, I do not believe that has been shown yet and you may not be parsing @PDPrice quote correctly. I have been reading everything that comes across my news feed and websites I check about these variants. Almost every day. There’s also one in CA now that’s independent of the others.
The 70% is based on modeling and is an estimate.
But let’s look at the actual quote from Price more carefully:
As far as I’ve seen, this is correct. Most current I’ve seen is that scientists think these mutations together increase transmissibility.
I’m not going to argue a reduction in function, except that the function changes seem to help transmission, so I’d prefer we pick different terms because I find the arguments about what function means to be extremely annoying. But - “accumulation of many mutations” as far as I’ve seen is correct. These variants have more mutations than others.
As far as I’ve seen, likely. But at l least, not disproven so far. Too early to say it has been.
So I’ve been looking for a paper that is similar to the one I’ve cited in the thread you quoted me on, on any of these variants. I’ve seen nothing yet. I know the CDC is watching it carefully. I’m just reading a lot of hype. Now there are popular articles that say these same variants may be more deadly. That doesn’t seem to jibe with more transmissible.
So I can find sources on what I wrote above anyone wants any, but since I feel like and I don’t know if anyone cares, I don’t feel like it unless you let me know.
This is not exclusively true, but there are indeed instances of synergistic mutation. That multiple mutations can work together to enhance viral fitness runs even more counter to GE, which asserts that beneficial mutations are comparatively very rare and are never coordinated positively with other mutations to benefit the organism, but are swamped out by the preponderance of deleterious mutation.
No one mutation makes the [corona]virus spread better. A general reduction in function from an accumulation of many mutations may temporarily help prevent the [corona]virus from going extinct by helping it propagate to more people; but this will not save it in the end, because that accumulation of mutations is damaging and it keeps getting worse with each added mistake.
The @PDPrice quote here is a contorted sin against reason and observation, but I would not hold my breath waiting for a retraction. A “general reduction in function” does not yield an improvement in propagation. The function of the spike antigenic coronavirus protein is gaining entry to tissue cells. That is it, the reason for being. How can improving that function be a general reduction in function? - that is just gibberish.
Genetic Entropy is inconsistent with the epidemiology of the 1918 influenza epidemic, in that the second wave was more virulent than the first. In COVID-19 however, we have a much more detailed, real time, picture of the timing and geography of genetic variation; what we see looks like the evolutionary arms race and nothing like GE.
Thanks for the favor of a response that lives up to your name.
I have read all your posts in the previous thread, but found none that seem to cite a paper on Sars-Cov-2, and in your post I quoted, the assertion about Sars-Cov-2 seems bereft of any references. That said, you might be thinking of another thread that I missed, or I might have suffered blindness. If you could provide a link, I’d be grateful. Thanks.
The case is not iron-clad, but it seems like a couple of individual mutations (D614G and N501Y) have a selectable positive effect. For the virus, not for us.
Whether it takes one mutation or 23, the fact is that several variants have arisen that defy the prediction of genetic entropy. By focusing on a tree (the number of mutations involved), you seem to have missed the forest of evidence that strongly contradicts genetic entropy.
Take a look at the rest of Price’s prediction that I quoted in the original post:
A general reduction in function from an accumulation of many mutations may temporarily help prevent the [corona]virus from going extinct by helping it propagate to more people; but this will not save it in the end, because that accumulation of mutations is damaging and it keeps getting worse with each added mistake.
The variants that have gained ground in the past few months have literally dozens of mutations. B.1.1.7 has 23, but I am unable to find definitive mutation counts on the others. Now consider Paul’s prediction:
(more mutations) = (less capability)
But these variants, which have literally dozens of mutations, are more capable. From the perspective of the virus, that is.
I’ll have to go search out some references for your other comments tomorrow.
But I think this is a misunderstanding of GE and not a prediction Sanford makes really. Hehe, sometimes I feel weird trying to correct the scientists on a hypothesis when I’m not a scientist but I try my best. How I see it: The predictions of GE are 1. that mutations do not add new information (information can be unlocked, but not added through mutation). 2. That eventually mutations will lead to an organism’s extinction. 3. Natural selection can’t stop slightly deleterious mutations from accumulating except in bacteria.
That’s it. I believe what I wrote there fits in with what Price wrote. I don’t think there are other specific predictions that Sanford makes, but I often see people inferring all kinds of others. Ok, but then give me the quote please. The book itself focuses on humanity and barely touches viral evolution.
Thank you. If my replies ever don’t, then take me to task!
Additionally, has GE provided a rigorous definition of “information” (ideally one that provides actual examples of the measurement of information under it for actual biological systems)? Otherwise, this is not a “prediction”, but rather an unverifiable assertion.
There is no definition of information in Genetic Entropy. No way to quantify or measure it is specified anywhere, and it’s relation to fitness is never specified in any measurable way. GE predicts absolutely nothing regarding information content. The whole information thing is just a rhetorical device. You will not find information in any models, equations, or simulations of genetic entropy anywhere, including Sanford’s Mendel’s Accountant program. It’s pure bluster.
But Sanford can’t even show why it would not do so in bacteria. When Price, Carter, and Sanford says that maybe fitness shouldn’t decline in bacteria, they’re just making up an ad-hoc excuse because real-world data conflicts with their previous assertions. Sanford wrote an entire article detailing reasons why he thinks, for example, that the E coli bacteria in Lenski’s long-term evolution experiment are going extinct to genetic entropy.
Well we know that much is not true. The N501Y.V2 variant is an asparagine to tyrosine substitution at amino acid position 501 in the S protein. How do you characterize the amino acid asparagine as information all locked up, and somehow the amino acid tyrosine is information liberated; free, free at last? The result is a protein novel in respects of shape, polarity, and affinity to human ACE2 receptors. Novel, as in new.
This mutation, which has been favored at least twice in independent lineages, looks a lot like garden variety evolution does it not? We have a random mutation which yields an adaptation of a key antigenic protein which appears to competitively advantageous, as was the prior D614G mutation. And this is after the virus already underwent essential mutations to efficiently spread from bats to civets to exploit the new host population of humans. So we have an extended chain of positive mutations, and precious little of the deleterious sort.
Asn479 and Arg479 are viral adaptations to human ACE2, whereas Lys479 is incompatible with human ACE2; Arg479 is a viral adaptation to civet ACE2, whereas Asn479 and Lys479 are also compatible with civet ACE2.
Oh by the way, that statement is physically impossible. If a human being or some designer can add information, then so can mutation. There is no change in the sequence of DNA that a designer can make, which some combination of mutations can’t also make. If a designer changing GCCTA into AGCTA is adding information, then it is adding information if mutation results in that change too. This is logically unassailable.
So you are saying information that was needed by hCoV-19 to make the jump from its animal reservoirs to humans was stored in the virus’s genome and got unlocked via some genome-modifying process? If yes, who stored that information?
Sanford is so ignorant regarding Biological information that he co-organizes in 2011 at Cornell university a symposium called « Biological Information: new perspectives » and co-edited its proceedings. https://www.worldscientific.com/worldscibooks/10.1142/8818
I’m not sure what you’re saying is in dispute. D614G is more transmissible. The set of mutations in the UK strain make it more transmissible. The South African and Brazilian strains are very likely more transmissible, at least in populations with existing immunity.
I assume you mean the increased transmissibility of the UK strain. It’s an estimate based on data, and on multiple types of data in fact.
and I don’t know if anyone cares, I don’t feel like it unless you let me know. 
