but I've always leaned more toward immune function rather than pure viral persistence - but I'm really just going by (compromised) gut feeling.
Yes, me too.
If you look at the results of interferon therapy for ME/CFS, this often leads to dramatic improvements for enterovirus ME/CFS patients. And as they improve, their enterovirus viral titres drop, suggesting enterovirus is the cause of their ME/CFS symptoms.
But several months later, they usually relapse back into ME/CFS, and their viral titres go up again.
If ME/CFS were purely a viral persistence issue, you might expect that interferon would make permanent improvements, and that once interferon reduced viral load, that load would remain low, kept in check by a robust immune response. Much in the same way as antibiotics will bring a bacterial infection under control, and thereafter the immune system stops the bacterial infection from flaring up again.
But the fact that the virus returns some months after interferon therapy suggests to me that the is some immune weakness or issue that prevents the immune response from keeping these viral infections in check.
If we could figure out what causes this immune weakness is, and if we could rectify it, then think the viral infections of ME/CFS would be cleared automatically as the immune response returns to normal.
I think this immune weakness pertains only to low-level intracellular infections, such as the low-levels of enterovirus RNA found in the cells of ME/CFS patients. In general I don't think there is any immune dysfunction when it comes to responding to acute viral infections, such as colds.
Indeed, many ME/CFS patients appear to have hyper-immunity when it comes to colds, as they report rarely catching any colds (although there is a small subset of patients who are the opposite, and catch everything going).