Over the past few years, I’ve spoken with countless people living with Long COVID—individuals still struggling with exhaustion, brain fog, and inflammation long after the initial infection.
At our recent Vejon Health Conference on Apheresis Therapy (sponsored by Molecusan UK), I had the privilege of hearing from international experts who are seeing promising results by filtering inflammatory molecules and spike protein fragments from the blood.
What struck me most was how their real-world findings align perfectly with what my own research has been uncovering: macrophage overactivation lies at the core of Long COVID.
The immune system that won’t stand down
Macrophages are the body’s cleanup crew—cells that clear debris and coordinate healing. But when exposed to the spike protein, they can become stuck in an activated state.
Dr Bruce Patterson’s work first showed that fragments of the spike persist inside CD16⁺ monocytes for more than a year. Even without active virus, these cells continue to release inflammatory cytokines like IL-6 and TNF-α.
Then, a new study by Simonis et al. revealed something even more important: exposure to mRNA spike can reprogram macrophages through epigenetic changes—essentially locking them in a pro-inflammatory mode for months.
That explains why the immune system seems to “remember” the infection even when it’s gone.
Why apheresis therapy matters
At the conference, Markus Klotz shared results from patients treated with H.E.L.P. Apheresis and Inuspheresis®. These procedures physically remove inflammatory proteins, microclots, and autoantibodies from the blood—and many patients show real improvement in fatigue, circulation, and brain clarity.
Dr Yannick Kok presented lab evidence confirming this: microclot complexes, measurable through his FibriScore® test, drop significantly after apheresis.
And Prof. Brigitte König explained how persistent spike protein damages mitochondria—the energy powerhouses of our cells—further linking inflammation with fatigue.
Presentation 1 – Markus Klotz: Subtractive vs Modulating vs Additive Therapies (00:07:30 – 00:40:30)
Theme: Therapeutic Apheresis and Multimodal Combination Therapy for Long COVID, Post-Vaccine Syndrome, and Chronic Illnesses.
Mr. Klotz opened with a deeply personal account of his own long COVID journey — from severe illness and functional disability to full recovery through apheresis and combined therapy. His clinic in Cyprus and Switzerland has now treated over 1,200 patients with chronic post-viral or post-vaccine conditions.
He described a framework of subtractive, modulating, and additive therapies:
Subtractive: Removing pathological substances such as spike protein, cytokines, autoantibodies, and microclots through H.E.L.P. apheresis or Inuspheresis®.
Modulating: Adjusting immune responses via hyperthermia therapy, improving receptor function, and aiding detoxification.
Additive: Supporting recovery with nutraceuticals, peptides, IV infusions, and immune therapies.
Mr. Klotz emphasized that apheresis alone benefits around 60% of patients but combining it with multimodal interventions—such as fever-range therapy, peptide therapy, IVIG, and Molecusan nutraceutical protocols—can greatly enhance outcomes.
He also introduced an upcoming AI-driven register study in Zurich, designed to correlate treatment combinations with patient-reported outcomes and biomarker trends. This initiative aims to develop predictive, personalized treatment plans based on data from thousands of apheresis patients.
Presentation 2 – Dr. Yannick P. Kok: Fibrinaloid Microclot Complexes as a Marker for Chronic Inflammatory Disease (00:40:30 – 01:05:00)
Theme: Understanding and Measuring Microclots in Long COVID and Chronic Illness.
Dr. Kok presented new findings from Ayus Laboratories AG on Fibrinaloid Microclot Complexes (FMCs) — abnormal protein aggregates resistant to breakdown that form in various inflammatory diseases, including long COVID, Parkinson’s, diabetes, rheumatoid arthritis, and Alzheimer’s.
He explained how SARS-CoV-2 spike protein binds to fibrinogen, promoting dense, amyloid-like microclots that resist fibrinolysis and impair oxygen delivery.
Using advanced imaging flow cytometry with Thioflavin T (ThT) fluorescence, his team can visualize and quantify these microclots, comparing patients’ samples to healthy controls.
Key innovations included:
FibriScore® – A quantitative biomarker system to monitor treatment response and inflammation.
Inuspheresis® filter studies showing significant reduction of FMCs after therapy, followed by gradual normalization over time.
Evidence that FMCs increase with disease severity and correlate with fatigue and vascular symptoms.
Dr. Kok concluded that microclots are a unifying biomarker of chronic inflammation and that apheresis may serve both as a diagnostic insight and a therapeutic intervention to clear these pathogenic structures from circulation.
Presentation 3 – Prof. Brigitte König: Spike Persistence, DAMPs, and Mitochondrial Damage (01:05:00 – 01:34:00)
Theme: New Advances in Spike Testing and Insights into Mitochondrial Dysfunction in Long COVID.
Prof. König presented the latest laboratory data from MMD Magdeburg, focusing on how persistent spike proteins and danger-associated molecular patterns (DAMPs) disrupt immune balance and cellular energy.
Her talk emphasized three interlinked drivers:
Spike Protein Persistence – Detection of circulating spike and viral mRNA in monocytes, exosomes, and tissues, with ongoing immune activation.
Mitochondrial Dysfunction – SARS-CoV-2 spike protein interferes with mitochondrial respiration, leading to energy deficits, oxidative stress, and chronic fatigue.
Inflammatory Markers and DAMPs – Molecules like HMGB1, HSP70, uric acid crystals, and mitochondrial DNA act as “danger signals,” sustaining inflammation and autoimmunity.
She highlighted novel laboratory markers—Zonulin, CD14, LBP, MPO, and Properdin—to assess gut permeability, complement activation, and innate immune dysregulation in post-COVID syndromes.
Her conclusion underscored mitochondria as “the powerhouses of immunity” and a central target for restoring metabolic and immune resilience in long COVID.
Roundtable Discussion and Key Takeaways (01:34:00 – 01:50:00)
The closing roundtable, moderated by Dr. Philip McMillan, integrated the science and clinical experience shared across the presentations. Several unifying themes emerged:
Spike persistence and microclot formation appear to be fundamental in sustaining post-COVID inflammation.
Apheresis therapy provides measurable removal of spike proteins, autoantibodies, and microclots—showing tangible biochemical and clinical improvement.
Mitochondrial restoration may be the next major therapeutic goal, as cellular energy failure underpins fatigue, immune exhaustion, and neuroinflammation.
Multimodal integration—combining subtractive (apheresis), modulating (hyperthermia), and additive (nutraceutical) therapies—offers the most promising results.
Data-driven personalization through AI, FibriScore®, and biomarker tracking will be crucial to refining patient care and identifying who benefits most from therapy.
A new way of seeing Long COVID
What unites all these insights is simple but profound: Long COVID is an immune system stuck in “fight mode.”
By clearing what fuels that inflammation—spike fragments, microclots, and cytokines—apheresis may give the immune system a chance to reset.
Pairing that with approaches that restore mitochondrial health and retrain macrophages could finally help the body remember how to heal.
For me, this conference was more than scientific discussion—it was a glimpse of hope that, through collaboration between clinicians and researchers, we may soon cool the fire at the heart of Long COVID.
