I wouldn't say so. They did find high statistical significance (p=0.0004) in the first test, and then it's very legitimate to explore subsets to find out what drives this. (But in general there appears to be plenty of p-hacking here)
[IgG] Complexes from infectious ME/CFS, including post-COVID ME/CFS Disrupt Cellular Energetics and Alter Inflammatory Marker Secretion, 2026, Prusty+
- Thread starter Nightsong
- Start date
Utsikt
Senior Member (Voting Rights)
Edit: I thought I was in another thread. Ignore this!
Last edited:
I'm pretty sure the comments are about the Prusty study.
Utsikt
Senior Member (Voting Rights)
Oops, I thought I was in another thread! Thanks!
ChronicallyOverIt
Senior Member (Voting Rights)
Watching the OMF Symposium right now Robert Naviaux just presented on this as fact…. What the hell is OMF doing…
This guys presentation is a mix mash of mitochondrial buzz words
This guys presentation is a mix mash of mitochondrial buzz words
Paul Watton
Established Member (Voting Rights)
The paper has now been accepted for publication in the journal "Brain Behaviour Immunity - Health"
Chandelier
Senior Member (Voting Rights)
Full title:
Immunoglobulin G Complexes from Post-infectious ME/CFS, including post-COVID ME/CFS Disrupt Cellular Energetics and Alter Inflammatory Marker Secretion
Zheng Liu 1 , Claudia Hollmann 1 , Sharada Kalanidhi 2 , Stephanie Lamer 3 , Andreas Schlosser 3 , Emils Edgars Basens 4 , Georgy Nikolayshvili 4 , Liba Sokolovska 4 , Gabriela Riemekasten 5 , Rebekka Rust 6 7 , Judith Bellmann-Strobel 6 7 , Friedemann Paul 6 7 , Robert K. Naviaux 8 , Zaiga Nora-Krukle 4 , Franziska Sotzny 9 , Carmen Scheibenbogen 9 , Bhupesh K. Prusty 1 4
Highlights:
- This study addresses a critical gap in understanding the role of autoimmunity in ME/CFS and PASC, two debilitating conditions with overlapping features and few effective treatments.
- By demonstrating that IgG antibodies from ME/CFS patients can directly alter mitochondrial structure and function in human endothelial cells, specifically inducing mitochondrial fragmentation and metabolic reprogramming, this study provides a mechanistic link between autoantibodies and endothelial cell dysfunction.
- Furthermore, proteomic analyses reveal unique immune complex signatures in ME/CFS and PASC, highlighting disease-specific IgG activity and supporting the idea of antibody-mediated metabolic dysregulation.
- These insights are especially important because they establish a foundation for novel, targeted therapies that modulate antibody activity or protect mitochondrial function.
Abstract
Background
Autoimmunity is a key clinical feature in both post-infectious Myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) and Post-Acute Sequelae of COVID (PASC).Passive transfer of immunoglobulins from patients' sera into mice induces some clinical features of PASC.
However, the physiological effects of immunoglobulins on cellular alterations remain elusive.
In this study, we tested the potential effects of immunoglobulins from ME/CFS patients on endothelial cell dysfunction.
Methods
We have isolated immunoglobulins from 106 individuals, including ME/CFS (n=39), PCS-CFS (n=15), MS (n=20) patients, and healthy controls (n=41).Protein composition of the isolated immune complexes was studied using mass spectrometry.
The effect of isolated immune complexes on mitochondria was evaluated using confocal microscopy and a Seahorse XFe96 Extracellular Flux Analyzer, and the impact on inflammatory cytokine secretion was studied using a multiplex bead-based assay.
Results
Here, we demonstrate that IgG isolated from post-infectious ME/CFS patients selectively induces mitochondrial fragmentation in human endothelial cells and alters cellular energetics.This effect is lost upon cleavage of IgG into its Fab and Fc fragments.
The digested Fab fragment from ME/CFS alone was able to alter the cellular energetics, resembling the effect of intact IgG.
IgG from post-infectious ME/CFS, including post-COVID ME/CFS patients, induced distinct but separate cytokine secretion profiles in healthy PBMCs.
Proteomics analysis of IgG-bound immune complexes revealed significant changes in immune complexes from ME/CFS patients, affecting extracellular matrix organization, whereas those from post-COVID ME/CFS patients pointed to alterations in hemostasis and blood clot regulation.
Conclusions
We demonstrate that IgGs from ME/CFS patients carry a chronic protective stress response that promotes mitochondrial adaptation via fragmentation, without altering mitochondrial ATP generation capacity in endothelial cells.Together, these results highlight a potential pathogenic role of IgG in post-infectious ME/CFS and point to novel therapeutic strategies targeting antibody-mediated metabolic dysregulation.
Graphical abstract
https://doi.org/10.1016/j.bbih.2026.101187
