Specific patterns are difficult to find in Long Covid

Lack of pattern in Long Covid research is the clue to the disease. In my view, it confirms that the anatomical location is in deep structures, rather than superficial.

The featured study infers that the autoantibodies potentially associated with fatigue in Long Covid are likely to have been present prior to the infection.

Some patients with substantially elevated neurotransmitter antibodies and only mild inflammation were showing severe symptoms. Similarly, patients with normal autoantibodies but significantly elevated lipids, inflammatory markers, and signs of oxidative stress also suffered from severe forms of chronic fatigue.

It seems the immune perturbations are exacerbated after a COVID-19 infection in a subset of the population, creating the symptoms of Long Covid.

Note in the image below, the dotted line represents the normal cut off range. In effect, all the patients had elevated levels of these adrenergic autoantibodies.

Antibodies against the β1 and β2 adrenergic receptors (AdR) and the M3 and M4 acetylcholine receptors (AChR) were measured in the blood of Long-Covid patients (n = 27) pre- and post-apheresis. Reference values are marked with a dotted line. RAA: receptor autoantibodies. ***P < 0.001 (paired two-sided t-test).

Read full paper here:
Achleitner, M., Steenblock, C., Dänhardt, J. et al. Clinical improvement of Long-COVID is associated with reduction in autoantibodies, lipids, and inflammation following therapeutic apheresis. Mol Psychiatry (2023). https://doi.org/10.1038/s41380-023-02084-1