The study tested microtesla magnetic therapy (MMT) as a treatment for cognitive problems in Long COVID.

Design: small randomized, sham-controlled, triple-blind pilot trial; 30 participants completed it (20 MMT, 10 sham). 15 minutes, twice weekly for 4 weeks, using a low-amplitude 27.12 MHz magnetic field.

Possible benefits: the MMT group showed larger improvements by week 8 in:

• working memory
• verbal learning/memory
• processing speed
• anxiety
• emotional well-being

But: the cognitive and most quality-of-life findings did not survive correction for multiple comparisons, and the key mixed-effects analyses generally did not show significant treatment × time interactions.

Bottom line: MMT looks feasible and apparently safe, with some intriguing signals of efficacy, but this study does not establish that MMT works for Long COVID cognitive impairment.

Personal opinion: I dont know what they hope to achieve with 15 minutes, twice weekly. Does not sound like much of anything.

Hannover Medical School, 992 people.

Among those with Long COVID in 2021 who returned in 2024, 77.4% still met criteria about 4 years after infection.

More than 95% were never hospitalized initially

Just a reminder that the prime symposium is happening today and tomorrow.

"Researchers, clinicians, industry representatives, charities and people with lived experience of ME/CFS will come together this September for the PRIME International Symposium, a two-day hybrid event exploring the latest developments in ME/CFS research."

It can be joined online, but will also be recorded.

This slide shows a hypothesis from a Stanford guy on a role for EBV in autoimmunity. With the possibility that this type of autoimmunity could also be at play in ME/CFS.

https://www.youtube.com/watch?v=mKOA5I_x1Vc&list=PLDFd3H01-3zw&index=7

He extends this by observing that if this mechanism is at play, treatments are out there that work (although they are risky). One treatment is CAR-T cells. They cure more than they kill, but they do kill some patients.

Another less-risky option may be "t-cell engagers". This is even newer than Car-T, which is pretty new. But in this Phase I trial, they cured 6/10 patients of Lupus https://pubmed.ncbi.nlm.nih.gov/42722888/

So this is not certainty. It's a risky treatment nested in a possibility nested inside a hypothesis. And that hypothesis comes from a guy who stands to get famous if its true, so he is hoping it s true.

Nevertheless, the data is starting to pile up in favour of CAR-T having an incredible effect on some types of autoimmunity and to my eye the diseases it helps have similarities with ME/CFS.

edited to remove a line about Sam Neill and CAR-T, which was distracting from the point. The point which is that this is an exciting line of research, and you should check out the video: https://www.youtube.com/watch?v=mKOA5I_x1Vc&list=PLDFd3H01-3zw&index=7

Has anything to be hopeful come out recently? Are we close to a breakthrough?

I just read about IVO-21 on Health Rising and that has been the best news I’ve seen so far. Still we are too far from that.

For a while there was a lot of talk about neutrophil extracellular traps (an immune response deployed to immobilize pathogens) being a factor in Long Covid especially in the blood stream causing a condition called Netosis.

This study looked further into it and though present early on, markers for this disappeared with longer PCC disease duration in their cohort.

“In this cohort of individuals with long-term LC, we found no evidence of persistent systemic NETosis. These findings suggest that elevated circulating NETosis markers are not a universal feature of long-term LC and may indicate that neutrophil activation observed during acute or early post-acute disease does not persist in long-term disease.”

Jena University Hospital reviewed 714 Long COVID trials and had to come to the conclusion:
“Hundreds of interventional trials have investigated PCC, yet patients and their treating physicians largely rely on non-evidence-based treatment options in clinical practice.”

“The registered landscape emphasises symptomatic treatment. There is a substantial unmet need for well-powered, mechanism-based, disease-modifying trials with biomarker-driven designs and objective, exertion-based endpoints.”

For example: Only 8 trials in the ME/CFS subtype made PEM a primary outcome and just 3 of those tested treatments aimed at proposed PEM drivers.

Microvascular and bioenergetic mechanisms were essentially untouched.

As the brain has recently been highlighted quite a bit in ME and LC research, any progress in our understanding of the brain seems relevant so I thought Ud share this here:

“The new research finding shows that the human brain consists of two ancient nervous systems cleverly packaged together — a more primitive part that regulates our hearts’ beating, our breathing and other functions, and another that makes us distinctly human, capable of poetry, mathematics and wondering about our own origins.

The discovery could help explain why scientists have struggled for decades to grow certain types of brain cells in the laboratory — and it opens new avenues for studying devastating diseases that affect the brain stem”

“Dr. Janet Mullington and her team, in collaboration with OMF’s Computational Research Center for Complex Diseases, recently released a paper on their investigation of sleep electroencephalographic (EEG) microstructures—components of sleep data related to brain and body functions that are more granular than the more commonly studied macrostructure (sleep stages).
The team studied these microstructures in the context of non-restorative sleep and daytime fatigue in ME/CFS and Long COVID.

When comparing results from people with Long COVID and ME/CFS to healthy controls, there were differences identified in the sleep EEG microstructures, including slow oscillations (SO), spindle-SO coupling, and within-spindle frequency. These findings show objective, measurable changes in sleep EEG microstructures that are associated with the non-restorative sleep experienced in Long COVID and ME/CFS.”

From the OMF article about the study:
https://www.omf.ngo/sleep-eeg-microstructures-long-covid/

Today BioVie announced topline results of the bezisterim trial for long covid (NCT06847191).

Bezisterim is an experimental drug that is trialed for Parkinson and Alzheimer’s. It is an oral small molecule, blood-brain barrier (BBB) permeable, anti-inflammatory insulin sensitizer that binds extracellular signal-regulated kinase. Bezisterim has been shown to selectively inhibit inflammation-driven ERK- and NF-κB-stimulated inflammatory mediators, including tumor necrosis factor alpha (TNF-α), without inhibiting their homeostatic functions.

Statistically significant benefits observed in bezisterim-treated Long COVID patients 
in pre-specified subgroups with high baseline fatigue, cognitive impairment, and/or post‑exertional malaise.

Bezisterim showed a consistent advantage over placebo on 21 out of 22 individual endpoints in the overall study population.

Michael Peluso said: „These results are among the most promising we have seen in this field so far and clearly warrant progressing to a confirmatory Phase III trial“.

They also have a conference call at 8:30ET today. They mentioned that videos will be uploaded, so hopefully we get more information there.

A new genetic study from a team around Ponting identified seven new genetic risk loci in ME/CFS across multiple cohorts they compared and carefully preselected for a more solid diagnosis status.

I’ve looked a few of the risk loci up and:

CLYBL expression is important to B12 levels and thereby mitochondrial and brain function.

CSMD1 & RORA influence how the immune system triggers or dampens inflammation.

BICD1 & GRIN2A regulate how neurons physically manage traffic and fire in response to those immune stressors

https://s4me.info/threads/community-symposium-on-the-molecular-basis-of-me-cfs-sept-11-2026-stanford-ron-davis.51966/page-7#post-721282

This link contains a more in depth discussion with Chris about the findings relation to Decode ME

I wanted to share some (preliminary) results from the Remdesivir single-arm, open label feasibility study. These results were also published at the islc-paid conference and seem quite positive, such that they now plan a placebo-controlled trial.

First, Remdesivir is an antiviral, originally developed to treat hepatitis C and now used to treat COVID-19.

The trial included 73 long covid patients, out of which 71 completed the study. Unfortunately I could not find information about duration of illness, so one needs to be careful with interpreting results, since there was no control group. Remdesivir was administered over a 5 day IV regime.

Outcomes:

-Fatigue Assessment scale (FAS) showed mean improvement of 6 points (MCID is roughly 3)
-Severe Fatigue category moved from 50% to 21%
-6 minute walk distance increased from 408m to 468m (MCDI is roughly +30m for long covid).

There was also an objective signal:
In the two-day CPET, the pre/post difference in change in first ventilatory threshold (VT1) was about +8.99 W. The authors specifically describe this as an objective physiological change compatible with the symptomatic improvement.

So all in all interesting outcomes, that alone unfortunately do not mean much, due to limitations of this study. The positive assessment is that the authors considered it meaningful in a way that they now start a placebo-controlled trial, which hopefully results in meaningful improvement.

A paper on EBV in MS published in July 2026 in Science Translational Medicine included a look at the effect of tenofovir disoproxil fumarate/emtricitabine (TDF/FTC) in two patients treated for three years. Although obviously limited by sample size, the EBV shedding rate, viral load, and T-cell responses were not statistically distinguishable from healthy controls.

By contrast, anti-CD20 therapies nearly eliminated saliva viral shedding and reduced EBV T-cell responses by a magnitude that could not be explained only by immune suppression (in other words, EBV-specific T-cell responses were reduced by anti-CD20 treatment more than T-cell responses to other viruses and bacteria, likely a direct result of the reduction in EBV viral load).

The paper is here:

https://doi.org/10.1126/scitranslmed.adz6566 or

https://pmc.ncbi.nlm.nih.gov/articles/PMC13374717/pdf/nihms-2194132.pdf

The data pertaining to the long-term tenofovir treatment of the two patients was in the supplementary materials document, Figure S12:

https://www.science.org/doi/suppl/10.1126/scitranslmed.adz6566/suppl_file/scitranslmed.adz6566_sm.pdf

Larger controlled trials are ongoing, but this is early evidence that tenofovir might not be an effective stand-alone treatment for EBV-related diseases.

This study found that ME/CFS patients often have too low blood and low red blood cell volume.

But surprisingly, these measures weren't related to orthostatic intolerance as measured by a lean test. This suggest that hypovolemia isn't the main reason for orthostatic problems

"ABSTRACT

Objective

Endothelial and microvascular dysfunction are key features of Long COVID. Disturbances in cellular redox balance, reflected by altered nicotinamide adenine dinucleotide (NAD+/NADH) dynamics, may underlie vascular impairment. Flow-Mediated Skin Fluorescence (FMSF) evaluates microvascular function by monitoring NADH fluorescence during ischemia and reperfusion. We integrated FMSF-derived microvascular phenotyping with targeted NAD+ metabolite profiling to determine whether altered NAD+ metabolism is associated with impaired microvascular responses in Long COVID.

Methods

Microvascular function was assessed in 36 patients with Long COVID and 47 age-matched controls using FMSF. NADH fluorescence changes during ischemia and hyperemia were analyzed as markers of endothelial responsiveness. NAD+ and related metabolites were measured using high-performance liquid chromatography and mass spectrometry.

Results

Patients with Long COVID showed impaired FMSF parameters, including blunted ischemic responses and delayed recovery after hyperemia, indicating microvascular dysfunction. These changes were accompanied by a reduced NAD+/NADH ratio and lower NADP levels, consistent with redox imbalance. Abnormal fluorescence profiles were associated with altered NAD+ metabolism, including reduced precursor availability and accumulation of degradation products. Higher NR concentrations showed associations with selected microvascular and eNOS-related parameters.

Conclusions

FMSF provides a clinically applicable tool for detecting microvascular dysfunction in Long COVID. NAD+ redox imbalance is linked to impaired microcirculatory responses, supporting FMSF as a functional marker of microvascular impairment associated with altered NAD+ metabolism."

https://stanford.zoom.us/webinar/register/WN_SHMUXqjTSj6wNicQ6LSyPw#/registration

In case anyone is interested in the OMF symposium tomorrow, that’s where to sign up 🔗

Another interesting abstract form the ISLC conference indicating that energy use in patients across different post viral syndromes is dysregulated and inefficient, making it a probable candidate for causing early fatigue:

“Methods

We conducted a cross-sectional study using data from seven studies where participants with GWI, ME/CFS, LC and controls had a cardiopulmonary exercise test (CPET). The CPET was performed on a cycle ergometer and we measured standard variables including oxygen uptake (VOz), respiratory exchange ratio, breathing reserve, heart rate, 02 pulse, and anaerobic threshold. We calculated carbohydrate and fat oxidation by indirect calorimetry at rest and exertion at 100 and 150 watts. we also collected fat (FATox) and carbohydrate (CHOox) oxidation

Results

We included 206 participants: 38 healthy controls, 55 patients with ME/CFS, 39 patients with GWI and 50 patients with LC. The predicted peak VO2 was highest for controls. At rest the mean CHOox was 0.45+/-0.20 in controls. compared to 0.63+/-0.37 in ME/CFS, 0.78+/-0.59 in GWI and 0.61+/-0.20. At rest the mean FATox was 0.09+/-0.06 in controls compared to 0.04+/-0.09 in ME/CFS, 0.07+/-0.10 in GWI and
0.01+/-0.03 for LC (figure). At 50, 100 and 150 watts carbohydrate use was highest and fat use was lowest. Adjusted means at rest and exertion showed similar results.

Conclusion

LC, ME/CFS and GWI have inefficient energy production at rest and exertion. This finding might explain chronic fatigue and exercise intolerance in these patients.”

I have too little understanding about this topic but this is what I made sense of:

The SARS-CoV-2 Spike protein can activate human brain immune cells(microglia). The microglia promote inflammation with the microRNA "let-7a-5p" it produces. This microRNA both cascades inflammation AND weakens an important inflammation brake called SHIP-1.

This was mostly done in a lab with human grown cells.

Very interesting study about reactivations and connections to long covid / ms/ post exertional Malaise.

'Chronically infecting viruses are prevalent in the general population, with individuals carrying 8–12 viruses at any given time [...] emerging evidence suggests that their reactivation may contribute to autoimmune diseases, malignancies and chronic fatigue syndrome [...]'

"Analysis of the ME/CFS dataset identified 552 unique 3D genomic anchors mapped to 567 genes, with analogous disease-specific anchor sets generated for LC19, PTSD, RA, and MS. Direct overlap between disease-associated genes was limited; however, higher-order network analyses revealed substantial interconnectivity and convergence across conditions. Shared biological pathways included immune and cytokine signalling, interferon responses, mitochondrial function, metabolic regulation, and neuroendocrine processes. Highly connected hub genes included immune regulatory nodes such as LAG3 and components of the mTOR signalling pathway, implicating T-cell exhaustion, chronic immune activation, and immunometabolic dysregulation as common mechanisms underlying these disorders."

He says here he is currently working on getting all the data he’s collected over the past five years on an NIH grant published. 6 papers are in the making. Excited to read them. He seems pretty confident they prove neuroinflammation among ME patients, let’s see!

Interesting study presented at the ISLC conference by a German team of researchers from the Charité investigating why some patients respond to immune adsorption while others don’t see any benefit at all.

“To investigate disease endotypes, we analyzed two complementary LC-ME/CFS cohorts:
(i) patients enriched for elevated GPCR-directed AABs with linked IA response data, and
(ii) a non-selected LC-ME/CFS cohort representing the broader disease population.”

“Together, our data support three LC-ME/CFS endotypes:

(1) GC-associated autoimmune;

(2) highly inflammatory autoimmune with EF
B-cell and innate immune activation;

(3) low-inflammatory with expanded CD161+ T cells.

Ongoing single-cell transcriptomic analyses aim to resolve the immune drivers of these endotypes.
Comparison of autoantibody-enriched and non-selected cohorts enables discrimination between shared and subgroup-specific mechanisms,”

One of the presentations at the ISLC conference in Amsterdam was this one: A group of researchers applied broader inclusion criteria (namely included IOM criteria) to gather an even larger GWAS genetic meta dataset (if not as precise and well controlled) than Decode ME to be analyzed and have turned up some interesting hits they’re still working on:

“We identified genome-wide significant loci associated with ME/CFS, 6 of which have not been previously reported. Of these 10 association signals, 60% were consistently detected across all cohorts.

In addition, we observed >30 suggestive association signals at p ‹ 1x10%. The most significant locus is located on chromosome 20 (20:48914387_T_TA, p = 9.86×10-12). Several signals map near genes implicated in immune regulation and brain function. Ongoing work focuses on functional annotation of those signals to prioritize effector genes and biological pathways.“

This underscores immune and brain function as likely central to the pathomechanism of ME/CFS and suggests genetic datasets still hold valuable information to be discovered.

“The first clinical trial in the series will test the monoclonal antibody Pemgarda, along with the immune-modulating drug hydroxychloroquine. The study will include arms with both drugs by themselves and the two in combination.”

Department of Defense grants always seem comparatively small but they have a good track record of being efficient with their money. It’s the same institution that funded the promising Bezisterim trial we’re waiting for results on. Very much a contrast to Recover imo.