O-Glycosylation patterns in Post-viral Fatigue Syndrome: Sialic Acid-preserving Chemical Release, 2025, de Otazo Hernández

[DHagen]

The matter is particularly confusing when there are a huge number of papers that continue to be published that either purport to document neuroinflammation or that take it as a given (to say nothing of the patient community that has, quite understandably, largely accepted the idea) - it's just that most of the members of this forum, notably including dedicated researchers, are unconvinced by or disagree with these findings.

But that could change. See, for example, the initial reaction to this paper, shared today.

Some time ago, completely baffled by the contradictory information, I started this thread, which might help to understand some of the issue (then again, it might not...).

It's all really quite a mess.

 

[Jonathan Edwards]

It would be a pity if @Violeta really did disappear.

I can understand the confusion for someone new to these things. The problem is a bit more than the hang-over of atom for things that can be divided. There is not only a word hang-over but a concept hang-over. A considerable number of 'ME expert physicians', advocacy groups, charities, researchers and so on, including the ICC committee, who still think that the ME letters refer to what people had in bed in the Royal Free in 1955.

 

[forestglip]

Several posts, starting from the following post, were moved to the thread: An Introduction to Common Misunderstandings and Controversies for Newcomers

Some time ago, completely baffled by the contradictory information, I started this thread, which might help to understand some of the issue

Yeah, I almost wonder if we could have some kind of mini explainer for new people giving them a heads up on things like this. Not to enforce any view, but just so they aren't blindsided when they post something that'd be completely accepted everywhere else ("ME/CFS is neuroinflammatory" etc.) and get like 3 people asking them to clarify what they mean.

 

[Hutan]

I don't think we ever saw a paper get published on this work? So, it's just that abstract in the first post?
That concludes

O-glycosylation profiles with intact sialylation of ME/CFS patients and healthy controls reveal an altered O-Glycan pattern which may contribute to the chronic inflammatory state observed in ME/CFS.

As @Snow Leopard pointed out, the abstract does not tell us how the O-Glycan pattern is altered. And as @arnoble pointed out, they have stated that the alteration might explain 'the chronic inflammatory state in ME/CFS', when in fact we don't have good evidence that that exists.

 

[Chandelier]

I don't think we ever saw a paper get published on this work?

There seems to be another paper in the pipeline funded by

Sponsors:
WE&ME Foundation, Vienna Science and Technology Fund (WWTF)

Life Sciences - Wiener Wissenschafts-, Forschungs- und Technologiefonds

Life Sciences

www.wwtf.at

Exploring the Glycome: Identifying Glycosylation-Related Biomarkers for severity stratification in Chronic Fatigue Syndrome

Post-infectious Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a systemic inflammatory condition characterized by severe fatigue, sleep disturbances, intestinal problems and post-exertional malaise (PEM).
The cause of the pathology remains elusive and for this reason, treating ME/CSF symptoms remains difficult.
In this project, we will test the hypothesis that changes in glycosylation in the peripheral blood of ME/CFS patients is a useful novel biomarker for severity stratification of ME/CFS patients during episodes of PEM and general fatigue.
Proper glycosylation helps maintain immune tolerance, while improper glycosylation can lead to inflammation and autoimmunity.
The enhanced pro-inflammatory state in post-infectious ME/CFS might lead to a hypo-glycosylated state in the body, which might result in inflammatory immune responses.

We will use advanced mass spectrometry to detect changes in sialic acid, O- , N- glycosylation and antibody N-glycosylation as surrogate markers for the damage at the glycocalyx in the peripheral blood of post-infectious ME/CFS patients.
Furthermore, we will assess the inflammatory capacity of aberrantly glycosylated antibodies in vitro. Combining our complementary, interdisciplinary expertise of analytical /synthetic chemistry/autoimmunity (Davide Ret) and immunology in the field of rheumatology and autoimmune diseases (Selina Keppler) will enable us to address the biochemical changes as well as the biological implications of aberrant glycosylation during post-infectious ME/CFS.

Depending on our results, we will work on approaches how to mitigate and restore aberrant glycosylation using interventions such as sugar supplements or enzyme inhibitors in future follow-up studies.
A better understanding of the biological triggers and markers for severity stratification is an important step towards better treatment options.

 

[Hutan]

That was an announcement of a plan to do work in the 2025 year, using EUR100,000 give or take for the work. Was the 2025 abstract part of the work? It sounds like it.

What I can't understand is why they keep going on about

The enhanced pro-inflammatory state in post-infectious ME/CFS

when some of these authors did a 2024 study looking at inflammatory cytokines in people with ME/CFS, and failed to find any differences from healthy controls. That 2024 paper is one of two papers cited on the abstract with its talk about the inflammatory ME/CFS state, and the other paper has nothing to do with ME/CFS. Where are they getting this idea about the inflammatory state?