Ulrika Essner

Nytt från Dr den Dunnen! Fortfarande två år senare ger antikroppar från samma longcovidpatienter liknande symptom hos möss. Tre olika forskargrupper har gjort samma fynd - det här verkar vara något substantiellt. Nästa steg är behandlingsstudier - Heja! 🔥

Arbetet med VIPER rullar på! Det här har jag själv donerat en summa till och hoppas mycket på!

@AndraEklund1 @horizontalviews Ljudböcker är mitt livselixir! Lyssnar massor och läser lite. Intressanta intervju poddar som t ex Bildningskomplexet hjälper också till att hålla huvudet igång och humöret uppe. Rekommenderas varmt!

@horizontalviews Exakt. Jag har inte gett upp hoppet om att kunna läsa igen. Om jag lyssnar på en riktigt, riktigt bra bok brukar jag köpa den för att stoppa in den i bokhyllan och kunna läsa den någon gång framöver.

Jag klarar inte av att läsa en längre text längre, 3,5 år efter covid. Varit en bokmal hela mitt liv och har 5 års universitetsutbildning (speciallärare).

@atranscendedman The difference between what’s difficult and what’s impossible is that’s what is difficult you can start doing right away, the impossible just takes a little more time…

It feels like we’re living in the year where the impossible starts quietly becoming possible.

I’ve spent the past weeks talking to #ME patients and carers in Wales. There is a spectrum of severity, but there are thousands in dark rooms across the country, unable to walk or talk. Tomos is one of them. Watch/listen/read on BBC Wales news today ⬇️ bbc.co.uk/news/articles/…

An interesting new review proposes that Long COVID is not just about what keeps the immune system on, but also about what fails to turn it off🧵

⚠️Saying viral persistence would require a “mysterious invisible virus” assumes we fully understand how these viruses behave. We don’t. There is evidence of viral reactivation, especially with EBV, even when standard tests look negative: • Blood PCR often negative • Saliva PCR positive in some studies • IgG against early antigen (EA) positive → a known marker of reactivation So the issue is not “no virus”, it’s: ➡️ where you look ➡️ when you look ➡️ how you look Herpesviruses don’t behave like acute infections. They are: • latent • tissue-resident • intermittently reactivated A negative blood test does NOT rule out activity in: • mucosa • lymphoid tissue • local reservoirs There’s also a pattern in science we keep repeating: One negative study → “See? There’s no virus behind this disease.” But we’ve been wrong before. For years, people said there was no viral involvement in: • multiple sclerosis • lupus Because detection was inconsistent. Now? EBV is strongly linked to both. So no, this doesn’t require a “special invisible virus”. It requires accepting that: • known viruses (like EBV) have complex latency biology • detection is compartment-dependent • and current methods are limited Sometimes the smartest move is not to dismiss a hypothesis… …but to look at diseases where we said the same thing before, and ended up being wrong.

Have there ever been ME/CFS studies that looked for pathogens (viral/bacterial/ fungal) in tissues ?

Our new placebo-controlled rapamycin trial is based on 4 publications of our own work on the mechanisms & biomarkers disrupting autophagy in a subset of #MECFS & #Longcovid patients. Phase 1 of our rapamycin treatment and biomarker trial was published in the selective Jnl of Translational Medicine: link.springer.com/article/10.118…. 1/4 🧵

Long COVID may not begin only after the acute infection has passed. In at least some patients, the immune system appears to go off track from the very start. A breakthrough study.🧵

@pausedByLC Interesting! Please keep us up dated. What could be an indication for IVIG?

Recently, I also had some immunological blood work done to check if there is an indication for IVIG. Findings: - IgG3 < IgG4, - No influenza antibodies are detectable; I got vaccinated in October 2025. More tests are scheduled for next week.

@atranscendedman Please remember the very severe group! We are so many quite young, previously perfectly healthy people now trapped in our beds and homes. We need treatment trials and off-label help NOW!

I’m talking to the NIH next week about what it’s like to live with Long COVID. What’s the one thing people still don’t understand and the part that really needs to be seen and said out loud?

@internetuserf12 Do you keep an eye on Amatica Health in the UK? Patients together collecting a lot of data that will likely lead forward to more precise knowledge…

We don’t yet know the primary lesion in ME/CFS. We do consistently observe multi-system dysfunction - mitochondrial, immune, autonomic, and metabolic. Until an upstream node is identified, most treatments target downstream effects - essentially a game of whack-a-mole. One emerging hypothesis is that antigen-presenting cell (APC) injury may represent a central regulatory node.

@atranscendedman @liamsLCjourney Do you have something good published on biomarker based subgroups of LC and/or ME in your library? Really interesting subject! 🤩

@liamsLCjourney there are very clear phenotypes that are being published in the literature. more papers to be published this year about where virus is being found and hypotheses around what cluster of symptoms it causes.

Recently, I've gradually come to the realization that I need to admit a hard truth: I have "Myalgic encephalomyelitis (exacerbated by COVID)", not "Long COVID". In 2016, I developed a strange series of symptoms, now all-too-familiar to me: sleep maintenance insomnia, waking up feeling "hungover", unrefreshing sleep, heavy fatigue. There was no known trigger. I worked with a primary care doctor and we ran some basic tests, but never figured it out, and it gradually faded away in two months. In 2022, I lifted heavy weights to failure after a COVID infection and developed severe PEM. I went to the doctor and he told me they had been seeing this often in young people who had recently had COVID. (I never associated what happened in 2016 with my current symptoms until recently). I immediately assigned the label "Long COVID", and for years, I have been describing my symptoms as such, hanging out in Long COVID groups, observing the discourse and trying to apply it to my case. But I never felt that I fit in. Most people with Long COVID have a long, complicated journey with dozens of different symptoms, and take dozens more supplements and interventions to treat each one. But eventually, they do seem to chip away at their dysfunctions and get better. I've only ever had two symptoms: fatigue and PEM. And nothing really worked to treat them. Then I started hanging out in ME spaces. I kept meeting more people like me: they may have had many bodily systems affected, but they were fatigue- and PEM-dominant, and they first started to notice after COVID. And like me, they were having a much harder time recovering, even though others had even more complicated symptoms than them! There are many in my position. Depending on which figures you look at, 25-50% of those with Long COVID have ME as their primary subtype. I think it's hard for someone to admit they have ME for a few reasons, among them that the recovery rates are much lower and it's harder to explain to others. Of course, The Categories Were Made For Man, Not Man For The Categories: these are just labels. Our conditions have far more to do with each other than they don't. It's important to stick together, to educate each other, and to support each other. So I'm going to remain in both communities, trying to contribute and spread knowledge wherever I can. But as far as my medical journey, I will be primarily treating ME going forward, rather than Long COVID.

@liamsLCjourney As long as there’s no biomarkers, bio-markerbased subgroups and treatments for ME I think it’s hard to know if it is ONE disease. Probably not. For sure ME symptoms can be triggered by covid alone. I am one ex.

@seanstidston @NurseGoodhart @NBoydGibbins No point in subgrouping the symptoms- but great to subgroup Big hard data on immun-, neuro-, and vascular systems. Just what Amatica Health are doing! The more patients and data, the better chans of understanding

@NurseGoodhart @NBoydGibbins Yeah most definitely but I guess the predisposing factors are they truly a subgroup of the illness post. I just think subgrouping so many symptoms isn’t going to help progress things. But what do I know.

Long COVID and ME/CFS can be treated A 20+ year patient I know yesterday told me they had gone from tolerance for only 2 hours of phone per day in a dark room to 12+ hours of function, talking and going outside after a successful treatment. They are cooking for the first time in half a decade Less than 1% of the possible therapeutic space has been explored, and the patient population may be defined 100 subgroups. Meaning if a patient tries 10 drugs at random they may have only a 1 in 1000 chance of response Matching treatments to diverse mechanisms, developing precision combinatorial therapies, and temporal therapeutic resolution may all be needed. But the problem is tractable with enough data scale

@surf4children Do you make diagnostics regarding immunsystem abnormalities for your LC-ME patients? Curious about what can be relevant to look for and how to interprit…

GM all, what do we talk about? I think I’m publishing a new case this weekend again highlighting the vascular perspective. Or you have other interests ?

@horizontalviews @dn Suck! Så förljuget att endast ”sköra individer” skulle kunna drabbas hårt av postcovid. Alla jag är bekant med insjuknat var, liksom jag själv, fullt friska, sportiga och aktiva före covid-19 infektionen som ändrade allt.

@DN försöker rapportera om postcovid. Fullkomligt vidrigt. Lyfter fram den vinkeln som är mest "skyll dig själ" av alla tiotusentals forskningsrapporter. Denna vinkel är endast till för att spela ner problemet. Vidrigt.

@horizontalviews Yes! But don’t you think it’s the immunsystem that’s the main culprit, that start the avalanche of sympoms? I think the delayed process points to the immunsystem.

Sounds about right from a patient perspective

@surf4children Could it be if there is a hidden strong driver of the immun-reaction, like massive viral persistens? Or do you think it is more due to individual immunsystem function? (If its not working with IVIG)

@EssnerUlrika correct. IVIG are strong immune regulator of the immune system, it is indeed used in several immune mediated conditions characterized by hyper active immune system. may not work for all anyway

do you understand why i use IVIG for both #longcovid and #mecfs? nowadays IVIG are the best and safest option for generilized idiopathic inflammation, and the most used since decades in countless diseases. challenge me if you can, or ask me further if you’re curious