What's new is a second independent patient cohort, functional testing of the antibodies, data on nerve fibers and brain activity. Still not peer-reviewed.

82 people with LC, 30 convalescent (had COVID, recovered clean), 35 healthy controls. Samples 416 days after, 80% of infections from the 2020. Anyone with an autoimmune diagnosis was excluded. Autoantibodies were hunted with four independent methods.

That hunt largely came up empty. They found no striking difference in the number of autoantibodies between LC and convalescent controls. A screen across 21,000 human proteins separated the two groups with an area under the curve of 0.53. So essentially a coin flip. People who recovered are autoreactive too.

Tissue staining = same way. Reactivity against the locus coeruleus (brainstem nucleus, noradrenaline source) and the thalamus looks elevated but once you adjust for age and sex, the only thing left standing in the whole panel is mouse meninges.

Agreement between the four methods was mostly at chance level. Of 147 people, 6 counted as high-burden on all four assays.

What does hold - it's in composition and function. On one model target (MED20), LC patients show a shift toward a more aggressive antibody profile. Less IgG4, stronger binding to activating immune cell receptors relative to inhibitory, greater ability to trigger phagocytosis - immune cells eating the tagged target. Same amount, different charge.

Sorted by which receptors their antibodies hit, patients split into two clusters, and one of them is defined by antibodies against β1 and β2 adrenergic receptors, endothelin rec A, and muscarinic M4. That's the receptor-targeting axis that runs through the POTS and dysautonomia literature.

Then the core experiment. Mice got a single injection of total IgG, each mouse receiving antibodies from one specific human donor. Mice given IgG from LC patients had a lower threshold for heat pain by day three, tired out faster on a treadmill, trended toward weaker grip.

The tissue data. Those mice lost small nerve fibers in the skin - the diagnostic criterion for small fiber neuropathy, and their blood levels of NfL - marker of nerve fiber damage - went up. Human IgG was visible stuck around the surviving fibers. All scored blind. Whole-brain activity mapping, done with no stimulation at all, lit up regions tied to pain, fatigue, and arousal.

What didn't happen. Blood pressure and heart rate were unchanged, so no POTS like picture. No anxiety, no change in movement, normal blood counts, normal plasma cytokines, clean histology. And after that single injection the pain effect was gone by day six.

What was transferred was total IgG, not specific autoantibodies. No depletion, no reconstitution with a single antibody.

Yes, the antibody fraction from LC patients is enough to produce part of their picture in a mouse. Which antibodies inside that fraction do it isn't shown.

The search for a single diagnostic marker has failed so far, but the functional test says there is something in that antibody fraction. That's movement.