Of course there is some amount of positive selection in H1N1 history. Nobody deny that, even C&S. But the evenly distributed, gradual and linear accumulation of mutations over time observed in H1N1 is not what would be expected if only positive selection was at play. Rather, it is the sign that something else is happening, most probably the continuous erosion of genetic information.
Of course something more than only positive selection is at play. Be it purifying selection, genetic drift, reassortment, zoonotic events, all occurring under an arms-race between an ever-changing host and the parasite, and so on. It is ridiculous to think that just because this can’t all be reduced to continuous positive selection, then this means we have to jump to some phraseology emotionally tolerable to creationists about erosion, decay, rust, and entropy.
How do you quantify the genetic information in a genome to tell if it eroded, increased, or remained the same over time?
They can’t assess genetic entropy if they are conflating mutation with reassortment.
Evidence, Nigel. The quote refers to mutation rates. C&S aren’t looking at them. They are completely incompetent.
Reassortment, which you are ignoring.
Genetic entropy is not real. Just want to make sure we’re clear about that.
Very strongly recommend you read Holmes’ book on RNA viruses to clear up the misunderstanding here. The problem with small genomes and fast mutation rates is saturation; nobody thinks RNA viruses are young, but it is true that because of their rapid substitution rates, phylogenetic signals are lost more rapidly, which gives the illustion of recent emergence.
Holme’s subsequent 2014 paper regarding molecular clock calibration…
According to our analysis, rates of evolution almost inevitably appear to decline over time because of the combined effects of natural selection and saturation. Consequently, and critically, estimates of rates are only applicable to the timeframe used to obtain them and cannot readily be extrapolated to other scales of analysis. In particular, short-term rate estimates will lead to underestimates of the timing of ancient divergence events, whereas using long-term rate estimates will cause the timing of recent events to be overestimated. These effects are particularly problematic in viruses, where the ages of many ssRNA virus families are probably orders of magnitude older than suggested by current estimates.
Analyses of evolutionary dynamics in viruses are hindered by a time-dependent bias in rate estimates
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