@Giltil can you post the graph in question here?
I wish we’d known that when we were assessing codon bias in different lineages of Lassa virus in 2013.
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Inter-host competition is acting even within this scenario, at least once there are reasonable number of infected people. If there are a lot of susceptible hosts available, then inter-host competition also favors making a lot of offspring as fast as possible, so as to be the first virus to arrive in those susceptible hosts, beating out slower-replicating competitors arriving from other hosts. Same effect, multiple causes.
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Yes! Absolutely.
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They know this how?
H1N1 is not extinct. Is (H1N1) pdm09 a different created kind? A baramin? Does every influenza variant come to us by special creation?
Nor is the 1918 variant some sort of H1N1 archetype, it very likely was derived from an avian source via swine, having acquired a good deal of mutation along the way.
It is not generally appreciated that descendents of the H1N1 influenza A virus that caused the catastrophic and historic pandemic of 1918-1919 have persisted in humans for more than 90 years and have continued to contribute their genes to new viruses, causing new pandemics, epidemics, and epizootics…
It is remarkable not only that direct “all-eight-gene” descendants of the 1918 virus still circulate in humans as epidemic H1N1 viruses and in swine as epizootic H1N1 viruses, but also that for the past 50 years the original virus and its progeny have continually donated genes to new viruses to cause new pandemics, epidemics, and epizootics. The novel H1N1 virus associated with the ongoing 2009 pandemic is a fourth-generation descendant of the 1918 virus.
Morens, Taubenbeuger, Fauci - The Persistent Legacy of the 1918 Influenza Virus
If that were true of RNA viruses in general, 2020 would not have been the miserable year we experienced. In the light of the past year, Sanford’s ideas should be an embarrassment.
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Now add another 4 billion of those to fully appreciate the magnitude absurdity GE implies.
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All of this is objectively false.
H1N1 is a subtype, not a strain. It is not extinct and has never been through extinction, apparent or otherwise.
Here is an accurate graphical summary of influenza reassortments through 2009. Note that it has zero resemblance to S&C’s plot, except that it shows how they are misrepresenting reassortment as mutation:
https://www.nature.com/articles/nature08182/figures/1
[@moderator: edited]
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Even to the point of attenuating replication by producing and packaging defective genomes.
The function of the H (hemagglutinin) and N (neuraminidase) are also important for binding to cells and releasing viral particles from cells, respectively. These genes have been continually evolving in one influenza strain or another for thousands or millions of years, and yet they have kept those functions. How is this possible if genetic entropy is a real thing? No influenza viruses should exist right now if GE is true.
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My favorite thing about that figure, as astute readers will note, is that human H1N1 is nowhere to be found. C and S tally up mutations across multiple lineages as though they’re a single lineage. Everyone will also note that nowhere in that paper nor its supplementals are data on mutation accumulation with pre-2009 H3N2, swine H1N1, or avian H1N1. Which are important for the mutation accumulation side of things because it’s those lineages, not the human 1918 H1N1 lineage, that contributed genome segments to the 2009 pandemic strain. But…nope. Just gonna treat the 1918 and 2009 pandemics as the same lineage.
I think I’ve said it before, but in case it wasn’t clear: There is practically nothing correct about this paper. Nothing.
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I think you’re being too easy on it. 
@T_aquaticus and @Timothy_Horton, please note: this is a peer-reviewed paper published in a lower-tier, but not trash, journal, yet it does not contain any actual science.
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I don’t see why?
I went back and looked at the H1N1 paper - not remembering seeing a reference to fitness and I only saw only one reference to H1N1 virulence regarding whether the strain could ever reach its original strength, if I’m explaining that right.
And then I quickly looked at another paper where they use MA to model RNA mutation and fitness but they modeled a generic RNA virus.
So I think it would be helpful and more fair for everyone to be clear about which paper they’re criticizing. As I see it, they’re getting lumped together causing confusion.
This is a very fair point.
I’ve specifically been talking about the H1N1 paper, “A New Look at an Old Virus”. They talk about “mortality” rather than “virulence”, which is actually another error because mortality is only one component of virulence but they mean severity of the illness caused; the argument is that the decline in mortality is evidence that the virus is suffering attenuation due to the accumulation of deleterious mutations.
Edit: Here is a link to that paper.
In their abstract, C and S write:
While there have been numerous adaptations within the H1N1 genome, most of the genetic changes we document here appear to be non-adaptive, and much of the change appears to be degenerative. We suggest H1N1 has been undergoing natural genetic attenuation, and that significant attenuation may even occur during a single pandemic.
Later, they write:
It is therefore reasonable to ask if the striking reduction in H1N1 mortality might be due, in part, to natural attenuation resulting from deleterious mutation accumulation.
And, to provide one more of many examples:
Regardless, general attenuation due to genome-wide mutation accumulation might best explain the very low mortality [54-56] associated with the 2009 pandemic. The earliest 2009 outbreak strain had already accumulated 1,889 mutations compared to the 1918 strain.
That last one is notable because, again, two separate lineages, so what C and S say there is nonsensical.
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I can find instances where drug companies falsified data and/or ran imperfect clinical trials. That doesn’t mean we throw out clinical trials or cite clinical trials as a largely reliable process. The same goes for peer review. Perhaps it would be better to say that peer review is the first hurdle any conclusion needs to overcome, and can serve as a first order filter on nonsense.
You’re not, because they are not.
H1N1 is not a strain. H1N1 is not a lineage, as they falsely claim.
The Y axis in Figure 2 has a false label. The figure misrepresents reassortments as mutations.
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[quote=“dsterncardinale, post:41, topic:12939”]
Thanks for the reference.
I have two comments.
- your abstract ends with the following 2 sentences : Our results suggest that analyzing codon bias as either due to base composition or translational selection is a false dichotomy that obscures the role of other factors. Constraints such as genomic architecture and secondary structure can and do influence codon usage in plant viruses, and likely in viruses of other hosts
So if we imagine a similar situation for H1N1, it would mean that the CUB observed in the 1918 version of H1N1 was due to constraints such as genomic architecture and secondary structure, right ? But in that case, the erosion of H1N1 codon specificity with time documented by C and S (see fig 6 of their paper) would likely be detrimental for it would likely affect these factors (genomic architecture and secondary structure). IOW, to appeal to some other constraints beside translational selection is of no help for dismissing C and S’s claim that the erosion of CUB is maladaptive.
2) in the discussion section of your paper, we read the following : Dicot-infecting potyviruses and geminivirus CP CUB were moderately correlated with their host CUB, but we did not find as high a correlation as in phage or human RNA viruses.
I see a contradiction here. On the one hand, you have stated in this thread that translation selection is basically non-existent in RNA viruses and on the other hand, the quote above indicates a high correlation between human RNA viruses CUB and their host CUB, which is a signature of translational selection!
No one has agreed to the loaded language of “eroded”. It was likely DRIFT, which is not maladaptive.
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It’s a seriotype?