Thank you for detailing your objections to Sanford’s thesis. Unfortunately, I do not have the time at the moment, and perhaps not enough expertise, to explore these issues further and answer you point by point.
However, I would like to leave the questions related to the origins of influenza and its evolution in its natural reservoirs and return to Sanford’s main thesis that the influenza virus is subject to the regime of genetic entropy during outbreaks in humans. In my literature searches over the last few days I have learned 2 things. 1) Plate-to-plate transfer experiments have shown that bottleneck events cause fitness loss. 2) Mutational load decreases the probability that a beneficial variant allele will emerge during the course of an infection. I think these two points give credit to Sanford’s thesis since it is clear that during a flu outbreak, bottlenecking is very strong and mutation load keeps increasing.
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