Severity of neurological long-COVID symptoms correlates with increased level of autoantibodies targeting vasoregulatory and autonomic.., 2023, Seibert

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Severity of neurological long-COVID symptoms correlates with increased level of autoantibodies targeting vasoregulatory and autonomic nervous system receptors

Abstract
Background
The Long-COVID syndrome constitutes a plethora of persisting symptoms with neurological disorders being the most disabling ones. The pathogenesis of Long-COVID is currently under heavy scrutiny and existing data on the role of auto-immune reaction to G-protein coupled receptors (GPCR) are conflicting.

Methods
This monocentric, cross-sectional study included patients who suffered a mild to moderate SARS-CoV-2 infection up to 12 months prior to enrollment with (n = 72) or without (n = 58) Long-COVID diagnosis according to the German S1 guideline or with no known history of SARS-CoV-2 infection (n = 70). While autoantibodies towards the vasoregulation associated Adrenergic Receptor (ADR) B1 and B2 and the CNS and vasoregulation associated muscarinic acetylcholine receptor (CHR) M3 and M4 were measured by ELISA, neurological disorders were quantified by internationally standardized questionnaires.

Results
The prevalence and concentrations of evaluated autoantibodes were significantly higher in Long-COVID compared to the 2 other groups (p = 2.1*10−9) with a significantly higher number of patients with simultaneous detection of more than one autoantibody in Long-COVID group (p = 0.0419). Importantly, the overall inflammatory state was low in all 3 groups. ARB1 and ARB2 correlated negatively CERAD Trail Marking A and B (R ≤ −0.26, p ≤ 0.043), while CHRM3 correlated positively with Chadler Fatigue Scale (R = 0.37, p = 0.0087).

Conclusions
Concentrations of autoantibodies correlates to intensity of neurological disorders including psychomotor speed, visual search, attention, and fatigue.

https://www.sciencedirect.com/science/article/abs/pii/S1568997223001799
 
A German team: Hölkeskampring

From the introduction:
Some very recent studies analyzing AAb in Long-COVID reveal conflicting data with respect to the lower level of AAb, which might be explained by the upregulated inflammatory response following COVID-19, that lead to the binding of AAb to their targets in tissue [13]. However, the interrelation between AAb targeting GPCR and inflammation in context of COVID-19 has not been addressed so far.
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So, they are hypothesising that the lack of good evidence for autoantibodies in Long covid so far might be because the auto antibodies are being bound in tissue, rather than floating around in the blood. They suggest that inflammatory state might make this happen.

Unfortunately the paper is not open access, so I haven't read the paper. But it doesn't sound as though they found evidence of an inflammatory state. And yet it does sound as though they found evidence for higher levels of autoantibodies, in blood.

It sounds to me as though more work needs to be done at the tissue level to prove or disprove this hypothesis about autoantibodies in Long covid.
 
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