You might want to pay considerably more attention to the data in the paper than to the text.
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[“as far as I know” is implied in all my comments]
Traditionally, I think they are serotypes and serotyping is still used to the best of my knowledge. Serotypes may have been established before sequencing was widely used or available.
Additionally, since influenza viruses recombine you can’t use one or two genes to label a strain or lineage. There can be separate strains and lineages with the H1 and N1 serotypes and genotypes.
No, the formal term is subtype. IIRC, they were at least initially described serologically, but they may be defined by sequencing now.
Here is a good description:
I think you mean “reassort,” not “recombine.” I’ve made that error too.
Put another way, H and N only account for two of the genomic segments. Two H1N1 isolates can have their remaining six segments from disparate sources through reassortment. In terms of bases, H and N only account for ~3000 bases of the ~13500-base genome.
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The 1918 version of H1N1 genome presents a duck like CUB (Codon Usage Bias) that is evolving toward randomness over time. IOW, the initial H1N1 CUB did erode other time. I really don’t see why you are complaining about the language of « erode », which perfectly captures what is going on regarding CUB in H1N1. Is reality « loaded »?
Thanks for the correction. That does make more sense when looking at a segmented genome.
Erosion means a removal of material which isn’t happening in this case. It is better described as a shift.
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No. Your definition of erosion doesn’t capture all the meaning of the word, not at all!
From your link, with my emphasis:
the fact of soil, stone, etc. being gradually damaged and removed by the waves, rain, or wind
the fact of a good quality or situation being gradually lost or destroyed
the weakening or damage done to something by a series of gradual losses of parts of it
the gradual reduction or destruction of something
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Yes in this case the only sensible descriptive word is replacement. One set of codons is being replaced with another. You might say the previous distribution is being “eroded”, but another one is taking it’s place, which is then simultaneously being constructed. Hence replacement is the correct word, not erosion.
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No, erosion is the correct word, for we observe a gradual reduction over time of the initial CUB present in the 1918 version of H1N1. And the gradual reduction or destruction of something (here CUB) is precisely one of the meaning of erosion.
So if, say, poverty is reduced, it is eroded? I bought some new batteries to erode the ones in my flashlight? That is an odd way of speaking, but in any event, realities do not follow our diction. The codons present in the 1918 virus were themselves the result of the same upstream process of synonymous and non-synonymous mutation as unfolded downstream. Preceding centuries of single point nucleotide mutation, re-assortment, and possible recombination, passing back and forth between host species, crafted the 1918 strain. Prologue is past as well.
Can you explain why this matters, at all? Recall that C and S are making a very specific claim: the change in codon bias is deleterious, i.e. has a fitness cost, and they provided precisely zero evidence even implying that this is the case.
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It matters because in the case where CUBs cannot be explained by genomic base compositions, then they very likely have function. So the erosion of these CUBs over time is also very likely to affect their functions.
…So it just…doesn’t matter that about half the changes they documented are, in the context of humans, unquestionably beneficial, given how the human immune system detects CpG dinucleotides? You can’t just assert a set of changes are harmful 1) with no evidence and 2) outside of the context in which they occur.
And, just to tie this up neatly:
where CUBs cannot be explained by genomic base compositions, then they very likely have function.
This is absolutely, 100% not true. There are a ton of other explanations for codon bias beyond base composition and translational selection. That’s the point of that paper I referenced earlier. Biased mutation rates. Host-specific selection other than translational selection. Biased DNA repair and/or gene conversion. Enzymatic degradation. All cause codon bias. None “have a function” in the virus.
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This focus on the “decay” rhetoric is diagnostic of creationism, and prototypical for a movement in direct conflict with observational reality.
That’s why they obsess so much about terms like “entropy”, “devolution”, “rust”, and “erosion” and various analogies that appeal to such processes. It’s all they have.
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No, that would be a very awkward use of the word. But note that it would be perfectly correct to say that if wealth is gradually reduced, it is eroded.
This is completely wrong, for C and S used the 2009 pandemic strain as a reference genome ONLY for assessing mutation accumulation in this very lineage, not the human lineage. IOW, contrary to what you say, they are not guilty of lumping these two lineages, not at all. For interested readers, I invite them to have a look at point 6 of the piece below where Carter responds to @dsterncardinale’s critics regarding C and S’s research on H1N1.
I’ve responded to that piece at length. Short version: I’m right and they’re wrong. One of the parts of the H1N1 paper I quoted above, which I will repeat below, bears out my criticism:
Emphasis mine. They’re counting it as a single lineage.
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A duck like viral genome managed to “randomly” evolve to infect humans and facilitate human to human transmission. In what way is that erosion?
The hemagglutinin head evolves faster than the stalk. There is more variation in the hemagglutinin stalk than transcription DNA. That is not loss of function, that is the virus adapting the function under immunological pressure and other host defenses, variation of the target sialic acid receptors, body temperature and serum pH across species, vaccination in human and food production, co-evolution of neuraminidase, and the progression of epidemics. There is positive selection. Mutation is random, but viral isolates do not display some overall trend of erosion.
Descendants of the 1918 strain, which is itself the product of mutation, continue to infect tens of millions of people and animals each year, despite immunologically resistant populations and vaccination programs. That is by definition a successful, adaptive virus.
Influenza is pervasive throughout the animal kingdom, and in keeping with this the virus exhibits both extensive genetic diversity and mixing by re-assortment. It has been around a very long time.
it is notable that Wenling hagfish virus, from a jawless vertebrate (a hagfish), occupies the basal position in all of the vertebrate influenza virus, again suggesting that these viruses have been in existence for hundreds of millions of years.
Divergent Influenza-Like Viruses of Amphibians and Fish Support an Ancient Evolutionary Association
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If it is the case that Influenza has been around a very long time, then you probably have a problem because long time is not what molecular clock estimates tell us about RNA virus origins. Interestingly, in the paper below, Holmes suggests that a way to reconcile deep time and molecular clock data is « if RNA viruses differ dramatically in replication rate or have experienced periods when replication was either latent or extremely slow, then this would reduce substitution rates in the long run and would correspondingly extend divergence times ». We have here a possible explanation of why genetic entropy of RNA viruses may be much slower in some of their natural reservoirs than during outbreaks in other host species. Here is another quote from the same paper still more explicit: « Although synonymous substitution rates in influenza A viruses from aquatic birds, horses, pigs, and humans vary no more than is usual among RNA viruses, the nonsynonymous rate is greatly reduced for the avian viruses compared to that seen for human viruses. This supports a model in which there has been a substantial rate acceleration coinciding with the species jump from birds, in which influenza A virus persistently replicates in the gastrointestinal tract and is asymptomatic, to humans, in which it replicates in the respiratory tract, causes regular epidemics, and is subject to strong immune selection pressure »
https://jvi.asm.org/content/77/7/3893