I’m having trouble parsing but I think the first point is about the mutation rate in humans? I don’t expect that to be informative about flu virus except as a floor.
Ah yes, you’re right. I don’t know why but I made the mental shortcut that the mutation rate was about the DNA of cows / humans and not the flu virus.
The general point still holds : I am wary of the assumption of a constant mutation rate of the flu virus. It really facilitates the computation, but if the computation under this simplifying hypothesis leads to a consequence which contradict reality, I would interrogate this assumption. It’s surprising to have so few human cases considering the large number of cows infected if there is a human-compatible viron per cow.
Another cause of this discrepancy could also be that due to the large mutation rate, a non-negligible part of the virons are not viable / don’t replicate well / …
There are papers which show heterogeneity for influenza / RNA viruses but I don’t really know if it’s between the virus population (of the same kind of virus) or within the genome. And they are like a factor 4 or so in the papers I have seen. So maybe less relevant than expected.
Regarding the details, my lack of deep knowledge of the domain is limiting. But as a mathematician who had to modelize real phenomenon and adapt the model to handle the discrepancy between the model’s conclusion and reality, that’s the train of thought which comes naturally to mind.
I’m having trouble parsing but I think the first point is about the mutation rate in humans? I don’t expect that to be informative about flu virus except as a floor.
Ah yes, you’re right. I don’t know why but I made the mental shortcut that the mutation rate was about the DNA of cows / humans and not the flu virus.
The general point still holds : I am wary of the assumption of a constant mutation rate of the flu virus. It really facilitates the computation, but if the computation under this simplifying hypothesis leads to a consequence which contradict reality, I would interrogate this assumption.
It’s surprising to have so few human cases considering the large number of cows infected if there is a human-compatible viron per cow.
Another cause of this discrepancy could also be that due to the large mutation rate, a non-negligible part of the virons are not viable / don’t replicate well / …
There are papers which show heterogeneity for influenza / RNA viruses but I don’t really know if it’s between the virus population (of the same kind of virus) or within the genome. And they are like a factor 4 or so in the papers I have seen. So maybe less relevant than expected.
Regarding the details, my lack of deep knowledge of the domain is limiting. But as a mathematician who had to modelize real phenomenon and adapt the model to handle the discrepancy between the model’s conclusion and reality, that’s the train of thought which comes naturally to mind.