Effect of immunoadsorption on clinical presentation and immune alterations in COVID-19-induced and/or aggravated ME/CFS.
Anft, Moritz, Wiemers, Lea, Rosiewicz, Kamil S et al. · Molecular therapy : the journal of the American Society of Gene Therapy · 2025 · DOI
Quick Summary
This small study tested whether a blood-cleaning treatment called immunoadsorption could help people with ME/CFS symptoms that developed or worsened after COVID-19. The treatment removed harmful antibodies (immune proteins) from patients' blood, and researchers found it temporarily reduced inflammation markers and improved some brain function tests. However, patients' main ME/CFS symptoms and fatigue scores did not significantly improve, and the harmful antibodies came back within a month.
Why It Matters
This study provides preliminary evidence that autoantibodies may play a role in post-COVID ME/CFS, offering a potential mechanistic target for treatment. The findings could inform future research into immune-based interventions, though larger controlled trials are needed to determine whether immunoadsorption could become a viable therapeutic option for this patient population.
Observed Findings
Immunoadsorption nearly eliminated ANSR autoantibodies from patients' blood
Neuropsychological function improved significantly at 30 days post-treatment
Hand grip strength showed modest but statistically significant improvement
Removed proteins rebounded within one month; ME/CFS questionnaire scores did not significantly improve
Inferred Conclusions
ANSR autoantibodies may contribute to neurological symptoms in post-COVID ME/CFS, at least in spike protein-positive patients
Immunoadsorption can acutely reduce circulating autoantibodies and inflammatory mediators but requires repeated treatments to maintain effects
Autoantibody removal may improve certain measurable functions (grip strength, cognition) without substantially alleviating core ME/CFS fatigue and symptom burden
Remaining Questions
Why does symptom improvement not correlate with autoantibody and cytokine reduction, and what mechanisms drive ME/CFS symptoms if not these immune factors?
Would repeated or maintenance immunoadsorption treatments produce sustained clinical benefits, and what is the optimal treatment frequency?
What This Study Does Not Prove
This study does not establish that autoantibodies cause ME/CFS, only that their removal correlates with some improvements in specific measures. The small sample size (n=12), observational design, and lack of a control group mean results cannot prove efficacy or determine whether benefits were due to the treatment itself. The rapid rebound of removed proteins and lack of sustained symptom improvement raise questions about the treatment's clinical utility.
How do spike protein-positive and spike protein-negative post-COVID ME/CFS patients differ mechanistically, and should treatment approaches differ between groups?
Would a larger, randomized controlled trial with longer follow-up confirm these preliminary findings and determine whether immunoadsorption offers clinically meaningful benefits?