KaterinaRachelDelon

4 ,2 years with Longcovid, learning to live with it..go to hell LC..

[Michael Stingl @neurostingl]

Interessanter Preprint: Hinweise, dass Vorhandensein von Mastzellaktivierung die allgemeine Symptomlast bei hypermobilem EDS erhöht.

Das hat Therapierelevanz, weil es Behandlungsoptionen gibt und darf insofern in der Evaluation nicht übersehen werden.

https://t.co/feuJxZpVmr

[Zdenek Vrozina @ZdenekVrozina]

A multi-omics paper on long COVID in Frontiers in Immunology deserves more attention than it got. The through-line is uncomfortable - the cellular power supply stays switched off long after the acute phase is over.🧵

[Anil van der Zee © @AnilvanderZee]

1) This video shows a unique care unit in Norway called Røysumtunet for people with #severeME & very severe ME.

It is one of the only places where the sickest patients can receive specialised care.

We need this everywhere!!

#pwme #myalgicE #millionsmissing #severeME

[KaterinaRachelDelon @RachelDelon]

@MemorialME 😢

[Manuel Ruiz @manruipa]

If this topic matters to you, feel free to visit my profile. I write about Long COVID, ME/CFS, autoimmunity, dysautonomia and the immunology behind complex chronic diseases.

My goal is to make complex biology easier to understand, because patients deserve mechanisms, not stigma.

[Manuel Ruiz @manruipa]

If you are interested in immunology, autoimmunity, Long COVID, ME/CFS, chronic infections, and post-infectious diseases, you can find more posts like this on my account.

I’m just trying to explain complex biological mechanisms in a simple way, so more people can understand what may be happening behind these diseases.

Because understanding them better is the first step toward taking them seriously.

[Manuel Ruiz @manruipa]

(3/3)

So, if we summarize it simply, the therapeutic map would look something like this:

First, IVIG.
Then, FcRn inhibitors.
Then, immunoadsorption or plasmapheresis.
Later, anti-CD20 in very selected cases.
And in the long term, deep reset strategies such as CAR-T.

Obviously, this is not a fixed rule and would not apply equally to all patients. It would depend on the immunological subtype, biomarkers, severity, risks, and whether an autoimmune mechanism is truly confirmed in each case.

But as a general map, this would be a reasonable logic if the autoimmune model is confirmed.

Now, there is one idea that, for me, is inseparable from all of this:

If these diseases combine autoimmunity, antigenic persistence, and viral reactivations, then it would make no sense to treat only the autoimmune layer.

Because if you immunomodulate, reduce IgG, deplete B cells, or reset the immune system without controlling the infectious component, you could worsen the very component that keeps feeding the problem.

That is why, in my opinion, any therapy directed at autoimmunity in these patients should be accompanied by a well-designed antiviral strategy before, during, and after treatment.

Before, to reduce viral reactivations or active antigenic burden that may already be present.

During, to prevent immunomodulation, IgG reduction, B-cell depletion, or immune reset from facilitating new reactivations.

And after, to try to prevent the system from becoming reactivated against the same infectious stimulus that may have been maintaining the problem from the beginning.

This would be especially important in therapies such as IVIG, FcRn inhibitors, immunoadsorption, plasmapheresis, anti-CD20 therapies, or future CAR-T-like strategies, because all of them modify, in one way or another, the balance between autoimmunity, antibodies, B cells, and antiviral control.

So the answer to “what do we do now?” would be this:

In the short term, better stratify patients and use existing autoimmune therapies to reduce the disease burden.

In the medium term, incorporate more targeted therapies against pathogenic IgG.

In the long term, aim for a true immunological reset.

And throughout the whole process, never forget the infectious component and viral reactivations.

Because if Long COVID and part of ME/CFS truly are autoimmune/post-infectious diseases, then medicine will also have to stop treating them as if they were one single thing.

It will not be enough to switch off inflammation.
It will not be enough to suppress autoantibodies.
And it will not be enough to give an isolated antiviral.

We will need to treat the autoimmunity, yes.
But also the chronic stimulus that may be maintaining it.

[Manuel Ruiz @manruipa]

(2/3)

4. Plasmapheresis

Very close to this would be plasmapheresis, or plasma exchange.

The logic is similar, but more “brute force”: part of the patient’s plasma is removed and replaced, thereby reducing autoantibodies and other circulating mediators.

It can be useful in some autoimmune diseases, but it is more invasive, less selective, and usually has greater technical complexity than IVIG or immunoadsorption.

That is why I would not place it as a first option except in very specific and well-selected cases.

5. Anti-CD20 therapies, such as rituximab

Lower down, already in a more aggressive step, I would place anti-CD20 therapies, such as rituximab.

Here you are no longer only modulating existing autoantibodies, but depleting B cells in order to try to reduce the production of new autoantibodies.

This can be powerful, but it also involves more immunosuppression, a higher risk of infections, a higher risk of viral reactivations, and greater potential toxicity.

In addition, anti-CD20 therapies do not directly eliminate mature plasma cells, so they do not always reduce all autoantibodies immediately or completely.

That is why, although they could be useful in the right subgroup, I would not consider them a light option or an easy one to tolerate. They would be something for very well-selected, severe cases with clear biomarkers.

6. B-cell reset and CAR-T

And above all of this, in the most futuristic part, would be what could truly resemble a deep remission: B-cell reset, especially with CAR-T-like strategies.

Here, the goal would no longer be simply to reduce autoantibodies or dampen inflammation, but to restart the autoreactive B-cell compartment much more deeply.

This is already being explored in lupus and other severe autoimmune diseases, and conceptually it is one of the most interesting avenues.

But for Long COVID and ME/CFS, it is still far away. Not because the logic is bad, but because much more validation is needed, better subgroup selection, more safety data, and a very solid clinical justification before realistically considering its translation.

🔵Continued in the next post.👇🏻

[Manuel Ruiz @manruipa]

💊‼️Long COVID could be, at least in some patients, an autoimmune disease occurring alongside chronic infection, antigenic persistence, or viral reactivations.

Okay.
So now what?

Are there treatments?
Can autoantibodies be removed?
Can this autoimmunity be “switched off”?
Are we close to a cure?

The honest answer is this: we are not facing an immediate cure , although possibly a future one, but we are facing a huge shift in how we think about the disease.

Because if part of Long COVID, and possibly also ME/CFS, has an autoimmune basis, then it would no longer make sense to treat it as a diffuse syndrome with no therapeutic direction. We would need to do the same thing we do in other autoimmune diseases: classify patients properly, identify biomarkers, and design a stepwise treatment approach.

Not all patients would have the same mechanism.
Not all patients would respond in the same way.
And not all patients would need the same level of treatment.

But for the first time, a more logical therapeutic map is starting to emerge.

A clearer logic is beginning to appear: identify which patients have a real autoimmune component and, from there, think about which therapies could make sense.

At present, what is accessible would not be a cure, but treatments already known from other autoimmune diseases that could help reduce autoantibody activity, modulate the immune response, or decrease part of the immunological damage.

In the best-case scenario, these would be treatments to improve, stabilize, or reduce autoimmunity. Not to completely “erase” the disease.

If I had to rank the options in an orientative way, thinking about potential usefulness and safety profile, I would do it like this:

1. IVIG

The most reasonable short-term option would probably be IVIG, meaning intravenous immunoglobulin.

IVIG does not directly eliminate all autoantibodies as such, but it can modulate the immune system, compete with pathogenic autoantibodies, block part of the inflammation, and dampen the immunological attack without requiring such intense immunosuppression.

In many autoimmune diseases, it is used precisely because of this immunomodulatory effect. Among this type of therapy, it is probably one of the options with the best balance between potential usefulness and safety profile.

That said, it is not free of side effects, it is expensive, and access is limited.

2. FcRn inhibitors

Next, I would place FcRn inhibitors.

These drugs are very interesting because they reduce the total amount of circulating IgG and, with it, they can also reduce the burden of pathogenic autoantibodies.

The advantage is that they are quite targeted toward the humoral component of autoimmunity, meaning the antibody-mediated part.

The disadvantage is that they are not yet truly established for Long COVID or ME/CFS, and it would still be necessary to demonstrate very clearly which subgroup of patients would benefit the most.

Even so, conceptually, if we are talking about an autoantibody-mediated disease, this is one of the most promising strategies.

3. Immunoadsorption

At the next level, I would place immunoadsorption.

This technique consists of filtering the blood to remove immunoglobulins, especially those that may be participating in the autoimmune process.

It is a more targeted strategy than systemic immunosuppression and, in diseases mediated by autoantibodies, it can make a lot of sense.

Its main limitation is logistical: it is not a simple therapy, it requires specialized centers, and its effects may not last if the immune system continues producing the same autoantibodies afterwards.

(1/3)

🔵Continued in the next post.👇🏻

[Corinna Geiger @DrCorinnaGeiger]

Long COVID & ME/CFS teilen oft denselben autonomen Phänotyp – 92% reduzierter zerebrovaskulärer Blutfluss, 95% autonome Dysfunktion. Das sind KEINE psychischen Erkrankungen. Das sind messbare, neurologische Befunde. #MECFS #LongCovid #POTS
https://t.co/RlT0h7P4us

[Hugo Edgar Muñoz @HugoMuPe]

@Renacerpropiox Me quedo con lo que mencionas al final: nunca seamos parte de una estadística. Luchemos sin cesar, con fe, esperanza y pasión por la vida. Bendiciones.

[Renacer @Renacerpropiox]

Mi hijo tenía 16 años cuando lo atropelló un conductor ebrio. Estuvo en coma durante tres meses. El neurólogo nos hizo sentarnos en una sala de reuniones aséptica y nos mostró las imágenes. «El tronco cerebral está intacto», dijo con delicadeza. «Pero el resto... está oscuro. Si despierta, quedará en estado vegetativo. Nunca hablará, nunca os reconocerá, nunca podrá alimentarse por sí mismo. Tienen que plantearse un centro de cuidados a largo plazo».
Nos negamos. Lo trajimos a casa.
Montamos una cama de hospital en el salón. Le pusimos sus discos favoritos de Led Zeppelin. Le leímos cómics. Le hablamos durante 12 horas al día.
Seis meses después, le estaba afeitando la cara y contándole un chiste malo de papá.
No solo sonrió. Se rió. Una risa ronca y seca.
Entonces me miró y dijo: «Eso no tenía gracia, papá».
Hoy está terminando su carrera de ingeniería. Camina con un bastón, pero camina.

El médico lo llama una «anomalía». Yo lo llamo un luchador. Nunca dejes que una estadística determine tu destino.

[Covid Institute @Covid_institute]

Mast cells live in every tissue in your body.

They cluster at every place where outside meets inside.

That distribution is why MCAS in Long COVID looks like five different diseases at once.

[Zdenek Vrozina @ZdenekVrozina]

Omland at al., Impact of SARS-CoV-2 infection on subclinical myocardial injury in the general population:
the Trøndelag Health Study. https://t.co/JkSv8ThqdT

[Zdenek Vrozina @ZdenekVrozina]

The authors had an unusually valuable situation. People had their troponin I measured before the pandemic, and then again after a period during which some of them had SARS2 infection.

[Zdenek Vrozina @ZdenekVrozina]

This study is important because it captures a small, systematic shift in a marker of cardiac injury across the population after COVID-19.
And that is exactly the signal that can be easily missed in an individual, but may matter in public health🧵

[PolyBio @polybioRF]

We’re happy to share that PolyBio’s Spring 2026 symposium that took place last Friday is now available in a recording! Listen to PolyBio-supported project updates at your own pace, or share your favourite research with friends.

Presentations by researcher: https://t.co/59GBPdn5OJ
Full recording: https://t.co/6Sb6nctZgN

[Zdenek Vrozina @ZdenekVrozina]

This paper is interesting because it identifies a concrete neurochemical signal in the CNS that connects long COVID/PASC, PEM, fatigue, and reduced physical endurance - lower activity of the central noradrenergic pathway in cerebrospinal fluid🧵

[Manuel Ruiz @manruipa]

🔴⚠️This is exactly the pattern many of us have been pointing to for years.

HHV-6 appearing in Long COVID severity is not really surprising. In ME/CFS, higher salivary HHV-6/HHV-7 loads had already been associated with a worse clinical phenotype, and HHV-6 has been repeatedly reported across immune-mediated/autoimmune diseases such as multiple sclerosis, Hashimoto’s thyroiditis, systemic lupus erythematosus, autoimmune hepatitis and connective tissue diseases.

It seems the story is repeating itself… or perhaps it never really changed.

Another piece of the same pattern: persistent infection, immune exhaustion, loss of antiviral control, reactivation of latent herpesviruses and autoimmune/immunopathological contexts.

If a patient shows repeated reactivations of HHV-6 or other herpesviruses, this should be treated with antiviral therapy directed at the specific virus involved — not dismissed as incidental.

ME/CFS:
https://t.co/UqTBYOnjJh

Multiple sclerosis:
https://t.co/4Xkg0Qx4X8
https://t.co/UmU9fmWuBZ
https://t.co/L9WXkNDpNh
https://t.co/2163YLgtKK

Hashimoto’s thyroiditis / autoimmune thyroiditis:
https://t.co/87R5PKLPne

Systemic lupus erythematosus / lupus:
https://t.co/yDGbjiYQa1
https://t.co/spn501hd5W
https://t.co/7S8pw9E18h
https://t.co/Mypfv3y0uf

Autoimmune hepatitis:
https://t.co/0ssoU07M8H

HHV-6 / autoimmunity review:
https://t.co/l6S1ISSCoh

[Prof. Akiko Iwasaki @VirusesImmunity]

'STORM' is a short documentary about Scott Hugo. A story of Long COVID's impact on his life and family - a reminder of what is at stake in research on Long COVID.

His resilience humbles me.

Please watch and share 🙏🏼

https://t.co/tN7B5wcq2I