The suggestion that SARS-CoV-2 spreads faster than influenza because two studies on different populations at different times found R0 of 2.5 vs. 1.7 respectively is indeed false--that difference is obviously within the expected spread from different environments. I thought the top reply to that comment (quoting Wikipedia) clearly implied that, so I didn't think any further effort there was required. You posted other statements that were false in different ways, so I responded to those.
That said, SARS-CoV-2 really does spread faster than influenza; among other reasons, we know this because influenza cases went almost to zero during the pandemic, implying that the same behavior in the same population that clearly resulted in R0 > 1 for SARS-CoV-2 resulted in R0 < 1 for influenza. That's a relatively trivial and obvious claim, but it's falsifiable and it involves R0.
It's pretty common to reduce a time series to a single number. For example, in economics, it's common to look at a compound growth rate per year, averaged over the period of interest. Likewise, in epidemiology, it's common to look at a compound growth rate per estimated serial interval, averaged over the outbreak and corrected for immunity acquired during the outbreak. That's R0, with all the convenience and all the flaws of any other simple aggregate statistic.
> Therefore, my suggestion - meant constructively! - is to rebase the field on top of microbiological theory. Scrap the models for now. Delete "and everything else" from the R0 definition and come up with an algorithm to compute a measure of infectiousness from DNA/RNA or lab experiments only.
I hope you realize that biologists aren't all stupid? If they could somehow define "infectiousness of the pathogen alone, without environmental factors", then that would be incredibly useful, removing all the factors that complicate comparisons of R0. The fact that they've made no attempt to do so should be a clue that the concept that you're wishing for simply doesn't exist.
They do study growth rates in cell culture, or the amount of virus exhaled by a sick lab animal, or the amount of virus that a healthy lab animal must inhale to get infected with some probability. Those are well-defined and somewhat repeatable lab measurements, but they're not very predictive of spread in actual humans. Computational methods are even less predictive; the idea of calculating infectiousness in humans from a viral genome is mostly science fiction for now. They're trying, but this may be harder than you think.