Norovirus for example creates a similar gastrointestinal illness to enterovirus, but even when there are these infectious outbreaks of norovirus on cruise ships for example, you never hear of ME/CFS as a sequela.
The Stanford research is definitely pointing to viral reactivation as NOT being the issue for us
In any case, chronic viral infection does not necessarily require reactivation. For enterovirus, this virus is not even capable of going into latency, and thus is not subject to the latency-reactivation cycle. The way enterovirus forms chronic infections is via a different mechanism to latency-reactivation, a mechanism which involves viral mutations transmuting enterovirus into an aberrant intracellular pathogen. See this article if interested.
By the way, given that eradication of SIBO (if present) has been shown to improve the symptoms of ME/CFS (see here), it's not really clear that your fecal transplant had any direct effect on the core pathophysiology of ME/CFS itself; it may have just eradicated the SIBO, which then as a knock-on effect improved the ME/CFS.
I used to have a chronic recurrent kidney infection, and when it flared up my ME/CFS symptoms were noticeably worse. So this is an example of how some secondary infections can amplify ME/CFS symptoms.