Indeed may be to early to anoint St Bruce:)
On the other hand, I was struck by two aspects of Patterson's approach to the long hauler problem.
First, Patterson collects a ton of data. He has modified the analytic equipment so that he gets tons of stuff from a single 4 milliliter blood draw. I am certainly clueless as to the ins and outs of blood measuring equipment but I nevertheless took away the conclusion that Patterson's equipment is different from the norm because he measures many more cytokines and many more features of single cell expression.
Second, Patterson elects to perform signal processing analysis on his data set, and the data set may be substantially larger and different from what everyone else is working with, including Recknor and Seethamraju.
Patterson's claim is that the signal processing analysis yields not only distinctions between long haulers and everyone else, but also that the day 3 signal vector is predictive of a day 14 severe patient and the day 14 sever patient's severe signal vector.
Patterson's claim that his signal processing analysis separates long haulers speaks directly to Cytodyn's problems on CD10, which missed its endpoint in no small part due to patient inclusion/exclusion.
It is certainly possible that Patterson's LHI is premature and not usable.
On the other hand, I cannot think of any other diagnosis for any other medical disease that is made by signal processing analysis. Is Patterson the first to employ signal processing analysis as a diagnostic tool?
Possibly yes as covid may be more multifactorial than other diseases and Patterson's experimental observations are more multifactorial than other observers.
Whatever it is that Patterson is doing, others should be able to reproduce very quickly once its published so we should see pretty quickly how Patterson's LHI holds up.