Before I respond to this, do you agree you were in error about a higher evolutionary rate speeding up descent into GE?
No, I donât. Under GE, higher mutation rate leads to fastest genetic decay. Since there is a positive correlation between mutation rate and evolutionary rate, it means that under GE, higher evolutionary rate is associated to fastest genetic decay.
HIV having the highest known mutation rate, but showing no signs of fitness decline provides a powerful data-based refutation of this claim.
HIVâs insane evolutionary rate allows it to maintain a huge amount of genetic diversity, providing plenty opportunities for natural selection and drift to act. HIVâs mutation rate is high, but it is below the error threshold for RNA viruses.
HIV has an evolutionary rate that mops the floor with the rate of your species, why hasnât it gone extinct?
Given that species jumps are generally associated with mutation to adapt tropism to the new host, that would mean that the virus has experienced higher evolutionary rate and been exposed to faster genetic decay. So you need yet another special pleading to permit transmission while allowing for virulence as a proxy for fitness.
Speaking of special pleading, what of those bacteriophages - where do they hang out for shelter from GE?
GE is degraded by special pleadings, each exception granted yet another deleterious piece of information which aggregates to the eventual extinction of the entire argument.
Please provide your sources. I had tried to look this up within the last year, and all I found seemed to indicate that rates in different hosts for influenza were not well known. Iâd genuinely be interested in the papers.
Just so weâre straight on the relationships here, SARS-CoV-2 is an RNA virus, H1N1 is a subtype of an RNA virus, but HIV is a retrovirus. There is zero reason to lump them together.
Telling us what allegedly happens âunder GEâ is absurd when you have yet to show that it exists.
If they are provided, would you engage with the evidence (not the words) they convey, or would you ignore them if they donât support what you wish to be true?
Directly refuted by Springman et al. 2010: âEvolution at a High Imposed Mutation Rate: Adaptation Obscures the Load in Phage T7â.
yes, the evidence would be the influenza mutation rate in non-human hosts. I donât ignore evidence anyway - Iâm interested in how itâs interpreted.
Do bacteriophages have a genome that is smaller than other viruses? IIRC again, Sanford explains organisms with small genomes and high mutation rates may not be affected by GE because this makes natural selection more effective with these types of organisms. Seems to be exactly what the title of that paper suggests.
Dan, I was listening to just the intro of a recent interview of yours - I donât remember which one, and you had said you just learned that Sanford had said bacteria may not subject to GE. I was surprised by that because I felt like it had been discussed at length on the forum since Iâve been here and you contribute frequently.
Sanford in his H1N1 papers seemed to characterize our understanding of reservoirs as an unexplored territory that could accommodate unknown mechanisms of stasis from which epidemics emerge. As in many other of his assertions, this is not an defensible portrayal. While there is much room for further study, antigenic variation in the wild is far from some complete mystery. The US Wildlife Health Center, just for one, does surveillance of thousands of fowl every year, out of concern for the poultry industry.
I would not even call it evidence, that there is significant mutation in all hosts for influenza is an routine established fact. Rates may vary, but there is nothing remotely close to stasis. Here are some papers, they do not give neat mutation rates, but phylogenic evidence is clear that drift is constant.
âŚHigh rates of nucleotide substitution obtained for the H13 HA genetic lineages were consistent with those previously reported for H4, H6, and H7 subtypes circulating in wild ducksâŚ
Phylogeography and Antigenic Diversity of Low-Pathogenic Avian Influenza H13 and H16 Viruses
Sixty-three HA-NA subtypes were found in a sampling of 13,466 North American ducks over 26 years and seventy-one subtypes were found in 4,266 North American shorebirds over 16 yearsâŚ
Ecology of avian influenza viruses in a changing world
The rates observed were extremely high, at >10â3 substitutions per site, per year, with little difference among wild and domestic host species or viral subtypes and were similar to those seen in mammalian influenza A viruses.
Avian Influenza Virus Exhibits Rapid Evolutionary Dynamics
the viral surface glycoprotein HA (the major viral antigen), has evolved through point mutations, leading to a number of genetically and antigenically distinct clades and subclades. Currently, ten major clades (i.e., clades 0â9) are recognized, many of which have multiple second, third and fourth tier subclades.
H5N1 influenza virulence, pathogenicity and transmissibility: what do we know?
BTW, if you really want to track viral phylogenies for yourself, it is worthwhile to access Trevor Bradfordâs site called Nextstrain.
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Influenza genome (eg the H1N1 Sanford claims went extinct due to GE) has a genome of about 13k bp. T7 phage is about 40k.
Also, according to Sanfordâs model, if we can call it that, faster mutations just mean faster death, since mutations are virtually all harmful. In other words, according to Sanford, there is no combination of mutations that can be selected to save a population. The study I referenced is a direct refutation of his model by showing that this isnât the case, and by imposing a high mutation rate (ie by forcing the population to experience every possible mutation many times over) you do actually find higher fitness states. Thatâs impossible, according to Sanford.
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Bingo.
For all the twisting and turning, no GE proponent can point to an example of GE actually occurring in any normal wild population. Robert Carter, one such proponent of GE, tried to use viruses as an example of how GE is actually occurring, but as these discussions on viruses show, that backfired in a massive way. Now we see GE proponents inventing ad hoc excuses for why viruses have not gone extinct.
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You do ignore evidence, because you have no idea whether the interpretations you tout are based on evidence.
No. They are larger than some, smaller than others. They all vary. Thatâs very basic evidence that you are ignoring to preserve the notion of GE.
Another example of no evidence. If you disagree, please provide the evidentiary basis for Sanfordâs explanation.
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This is false. I invite you to reread Sanfordâs H1N1 paper for you would see that several times in that piece he acknowledges that adaptive mutations commonly occur within H1N1.
Two things here.
Firstly, the work you referenced has assessed fitness after only 200 generations. During this quite small time scale, it is reasonable to think that the set of possible adaptive mutations would spread rapidly in the population and would overcome the effect of deleterious ones. It would have been interesting to assess fitness on a longer time scale, say 1000 generations. I am willing to bet that in this case, a decrease in fitness would be observed.
Secondly, the authors of study you referenced did not use bottlenecks. But if they had used strong bottlenecks, which is the situation that prevails during most epidemics, no doubt that a decline in fitness would have been observed.
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If repeated and strong bottlenecking is a requirement to observe the effect of GE, then GE doesnât appear to predict something that deviates from conventional population genetics.
Also, do you have any reference to substantiate the claim that strong bottleneck is a prevailing situation during most epidemics?
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So it is a nice sunny day, 4004 BC, and a freshly created bacteriophage is comfortably nestled within its brand new host. It could be any RNA or DNA phage, but we will settle on the ancestral baramin to which T7âs belong. So please, how do the children of T7 baramin make it to Springmanâs lab to begin with? Then, after all these years, the robust little beggar still had enough tricks up its sleeve to pull off adaptive mutations which overcome the effect of deleterious ones over the course of a further couple of hundred generations. The 1000 generations you ask for has been exponentially exceeded before the experiment even began.
I have asked on a couple of occasions now, where might bacteriophages hide out from the effects of GE? Given their hosts, replication is an inherent need for parasitic survival. I would suppose that the ever inventive Sanford would devise some special means, and that is great. With enough exception clauses and special pleadings, we can all carry exception cards, and we can set our anxieties of deleterious extinction aside.
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Problem 1: The phage populations were saturated. More generations wouldnât change the math. I would appreciate if you could address the contradiction between these findings and Sanfordâs claims.
Problem 2: They very specifically characterized what beneficial genotypes appeared and what was going on in the population. What they describe is called a âquasispeciesâ; the beneficial mutations were not becoming more frequent (due of the high mutation rates constantly changing them), but those same mutation rates kept generating the highly beneficial genotypes. We donât have to wonder what the dynamics looked like or what âwould have happenedâ if they had kept going. We know what was going on, how, and why. It directly refutes Sanfordâs claims.
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Thatâs an odd use of âgenerations,â Gil. How many replications did that involve? Wouldnât replications be the more relevant metric?
You couldnât have put it better
Sure. Regarding Influenza, this one for example, according to which between 1 to 13 particules are transmitted in most cases.
It is the word used by the authors all along their article. See by yourself :
https://www.genetics.org/content/184/1/221
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