Yes. That's clear now. The UK has an organized program to figure out what's going on with long COVID.[1] It's been known for a year or two now, from MRI scans, that long COVID is associated with brain and lung inflammation. But the underlying mechanism is not yet known.
This UK longitudinal study [2] is especially useful. "Three in five people with long COVID have impairment in at least one organ (seen in MRI scans) and one in four have impairment in two or more organs, in some cases without symptoms." This has been going on long enough now that the longitudinal studies, where the same patients are re-tested, are starting to produce results.
[1] https://www.gov.uk/government/news/new-research-into-treatme...
[2] https://journals.sagepub.com/doi/10.1177/01410768231154703
Were the antibodies detected, or was their activity detected? Because if it's just about the presence of autoantibodies, the simple explanation may be that aab quantities may not significantly differ, but their activity/activation might.
1) Clear molecular signals of pathology mean that minimizers' claims that longcovid is just psychosomatic or malingering are unsupported.
2) Seeing high antibody titers against COVID & EBV adds weight to the viral persistence and reactivation hypothesis: longcovid may be due, in part, to ongoing low-level infection elsewhere in the body along with reactivation of other viruses like EBV or HPV.
3) Autoantibodies were found again, but not significantly different than those seen in non-longcovid control groups, which is interesting because it had been suggested that longcovid may induce immune quality control dysfunction and increase overall autoimmune reactivity.
Hopefully these results can help guide better study design and management for longcovid trials.