[TTPrograms]

The sample distribution of viruses is incredibly important for this sort of analysis, and much of the argument here only makes sense through the lens of uniform virus sequencing. If you have imbalanced sequencing and imbalanced transmission you can also explain these differences.

The important thing is that mutations occur at a certain rate per virus per unit time. If you have an isolated population that's sequenced infrequently then (1) that strain will appear to evolve more slowly as there's a smaller population capable of mutating, and (2) once that strain is sequenced it's going to look far from what you've seen already since you haven't been tracking the intermediate mutations in this population.

The S/N ratio can be analyzed in terms of a random walk in high dimension. Variance in these walks grows over time (in terms of distance from origin, i.e. number of mutations), so the discrepancy doesn't seem super far from what's plausible under the null hypothesis. Perhaps someone can do the math on that.

The hypothesis merits further investigation, but the strength of the evidence presented here really requires some complex statistical analysis to determine if innocuous explanations fit. The analysis is far more complex than I would expect an epidemiologist or virologist to apply in the course of their work.