Can this study really be expected to provide data on the viral load of the point of infection, and at the time of infection? (I would guess that measurements of the distribution of the viral load, after the infection has progressed for some time, would be dependent on how the person's imune system is responding, and conseqently not good evidence for this proposition.)

If not, then is this a well-established feature of respiratory virus infections?

In other words, to what extent is this claim backed by evidence? And is it evidence from studying C19 specifically?