Seibert et al. found elevated levels of GPCR auto-antibodies correlated to “intensity of neurological disorders including psychomotor speed, visual search, attention, and fatigue”.
The literature on auto-antibodies in Long COVID (and post vac) has been conflicting. Here are the papers which cast some doubt on the auto-antibody theory:
The Yale teams using the REAP auto-antibody panel did not find abnormal levels of auto-antibodies in Long COVID or post-vax myocarditis patients. (Twitter thread; links to 2 papers in the Long Haul Wiki link below)
See Etiology - Long Haul Wiki for links to the papers. I didn’t have time to dig up information on a Long COVID auto-antibody study where the researchers didn’t publish their results.
And for the other side of the debate… there are also studies which suggest that auto-antibodies are involved.
The Wallukat et al. study. Wallukat’s company Berlin Cures offered testing services for GPCR auto-antibodies. See Functional autoantibodies against G-protein coupled receptors in patients with persistent Long-COVID-19 symptomshttps://doi.org/10.1016/j.jtauto.2021.100100
For both Long COVID and post vaccination syndrome, new-onset autoimmune diagnoses are surprisingly high.
Treatments for auto-immunity
The auto-immunity theories would predict that certain treatments work well. Here is some data on many of those treatments.
Review post on how people have recovered from autoimmune disease
People have recovered from autoimmune disease! However, response rates are often low. Some of those treatments (e.g. carnivore diet) don’t work as well in long haulers.
BC007
Wallukat’s company Berlin Cures is working on this. Some patients got this drug custom-made for them because they’re a little crazy. Anecdotes from them suggest that BC007 is not the answer for Long COVID, though I haven’t spent much time looking into it.
IVIG
Doesn’t seem to work, but the sample size could be bigger. There’s also a smidge of data on PLEX.
Corticosteroids
Data in the middle of this post. Corticosteroids were popular and not a single person seems to have recovered on them.
The Siebert et al. paper
Severity of neurological long-COVID symptoms correlates with increased level of autoantibodies targeting vasoregulatory and autonomic nervous system receptors
Results : In this group, serological tests showed that, in addition to positivity for anti-spike protein antibodies, a high percentage of subjects were positive for antibodies against G protein-coupled receptors and molecules involved in the response to SARS-CoV-2. In a panel of 16 autoantibodies tested, a few were positively associated with some of the symptoms reported by patients:
anti-ATR1 with lymphadenopathy and/or tonsillitis;
anti-ACE2 with skin symptoms such as ecchymosis, skin oedema, and rash;
anti-MAS1 with widespread burning sensation;
and anti-STAB1 with skin oedema and rash.
Anti-ADRA2A were negatively associated with memory loss and/or mental fog. ACE2 correlated with the serum levels of anti-S antibodies, supporting the hypothesis of an anti-idiotype mechanism in the immunopathogenesis of PACVS. Conclusions : This exploratory analysis suggests that the levels of autoantibodies directed against ACE2, and probably also MAS1 and STAB1, may serve as biomarkers for PACVS.
From a paper on immunoadsorption at Charité – Universitätsmedizin Berlin, Germany (Carmen Scheibenbogen). ME/CFS patients were treated, they got sick before COVID. No control group so… I have a feeling that the results aren’t reliable at all because the SF36 questionnaire may be measuring reporting biases (how empathetic and charismatic the doctors are, how much the patients want IA to work, etc.).
Here’s a snippet from the abstract anyways:
Discussion
There is increasing evidence that autoantibodies, including those targeting β-adrenergic and muscarinic acetylcholine receptors, may contribute to the pathophysiology of PCS and ME/CFS. We here provide evidence from an observational study that depletion of autoantibodies by IA can lead to improvement in overall physical functioning, as well as the severity of several key symptoms, including PEM, fatigue, pain, immunological, cognitive, and autonomic symptoms in a subset of post-COVID ME/CFS patients.
The clinical improvements observed after autoantibody removal via IA support the hypothesized involvement of these autoantibodies in the pathophysiology of ME/CFS and PCS in the responders. Meanwhile, a smaller group of patients did not show a response to the treatment. This highlights the potential diverse mechanisms underlying this condition, and indicates that autoantibodies may play a role only in a subgroup of patients.
Conclusion
In conclusion, our study suggests that IA treatment may result in rapid clinical improvement in a subset of patients. Further trials with both more patients and clinical outcomes reported are needed to confirm our findings. Our study serves as proof of concept for the initiation of clinical trials using drugs specifically designed to target autoantibodies. Targeting B cells may offer a promising approach to long-term symptom relief by addressing the underlying mechanisms driving autoantibody generation.