Isn't this expected based on the work of @BhupeshPrusty and Bob Naviaux? "In this study, we found that none of 25 patients with ME/CFS had peripheral blood evidence of a fully reactivated HHV-6 or HHV-7 infection, and only 8 of 20 (40%; 95% CI = 0.19–0.64) had evidence of partial reactivation measured by FISH analysis of HHV-6 small noncoding RNA U14 in whole blood. However, using an in vitro reporter cell assay, we showed that serum from ME/CFS patients contained an activity that produced mitochondrial fragmentation, decreased mitochondrial ATP production, and induced a powerful antiviral state." naviauxlab.ucsd.edu/wp-conte…

Very interesting preprint from @Ronaldw_Davis's Stanford group! It backs up Lipkin's (aka The Virus Hunter) study concerning viruses present in #MECFS patients. Ron said several years ago he didn't think antivirals were going to be the answer. Looks like he was right...again. 🧩

Next up: @DrRebeccaRyan! Immediately talking about autonomic dysfunction, POTS, and MCAS, in the context of “functional” GI disorders - which she points out are NOT psychologically driven. So excited for this one. #ICanCME2025

This clip from 2018 perfectly captures just how passionate @davidtuller1 is and how shocked he was by the way the PACE trial was defended. His crowd funding has just 1 day to go and he’s ~$10k from his target. I’ve just donated again so he can carry on doing his important work

ME/CFS is not going back in the box. That shit is over. We are at the beginning of something new. Families & friends are starting to get the right information. Once most of them forgive themselves, anger will come. Some of that energy will find its way into redemption and grace.

Excellent live tweeting again from @SpichakSimon covering the #ICanCME2025 conference today! #MECFS

It’s strange that, as far as I know, smooth muscle has never (?) been studied in ME/CFS. Given its major role in blood vessels, the gut, and autonomic regulation, all affected in ME/CFS, this seems like a major blind spot. Am I missing something? What's going on there?

Excited to have you back, Simon. #ICanCME2025

I trust the @OpenMedF team because the core researchers/key members of the organization have loved ones who have #MECFS. They are motivated and have first-hand knowledge. OMF has several centers around the globe with one goal: find answers/treatment(s)/cure. 🧩💙🧩 Donate! Share!

1) 🇦🇺 Interesting interview with molecular biologist Dr Daniel Missailidis. He has been conducting ME/CFS research since 2016 at at La Trobe University, focusing on the intersection of energy metabolism and immune dysfunction.

Something depressing about novel findings from excited researchers that does not concord at all with my own l results… either there’s a clear subgroup problem, or the heart of the matter isn’t being hit. I’d say we need a massive injection of funding to look at all possibilities

Ok...getting ready for Day 3 of @ICanCMEResearch Conference! I misspoke yesterday...follow THIS guy if you want/need to read about what's going on at the conference. I've managed to attend, but can't concentrate, so will read back through Simon's posts to fill in the gaps. 🙏🫶

We’re so lucky to have @RobWust researching LC and ME. He’s passionate about his work and listens to people living with these illnesses to learn. A real example to follow. #ICanCME2025 💙

​Following up on Naviaux’s excellent work around extracellular ATP (eATP) / “Cell Danger Response”, which can act as an “alarm signal” relay and/or loop that bridges nervous system cells and other tissues. This extracellular ATP signalling has been observed in ME/CFS, ASD, ADHD, PTSD and various other disorders / syndromes. pubmed.ncbi.nlm.nih.gov/3867… The pathway also works in both directions, allowing a systemic cascade / loop to be created from any source, where sufficient eATP signalling exists to overcome CD39/73/ADA purine salvage metabolism, which also provides the corresponding “alarm dampening signal” - adenosine and inosine. Interestingly enough, the main de novo “dampening signal” synthesis pathway is inhibited by impaired glycolysis -> pentose phosphate pathway -> PRPP (and other) metabolism and the purine nucleotide cycle in muscles, post-exertion. These are known issues in ME/CFS, LC, PVS, etc In this manner, with the “dampening signal” inhibited, various accumulated “insults” could potentially lead to a form of dysautonomia, where the nervous system’s pattern recognition systems identify and amplify existing metabolic alarm signals, manifesting biochemically as a wide range of effectors - including hyperactive innate immune response and mast cell activation (see figure 19). Naviaux and others have been exploring suramin as an intervention to help shut down the P2X7 relay / loop with early success. I’m currently researching a different approach - restoring the problematic “dampening signal” metabolism, as part of a more comprehensive process. [Watch this space.]

📉 The person with ME we tested had a significant drop in blood flow to the head during PEM: 17% while supine and 23% while standing. The healthy person did not have a decline. 4/n

@exceedhergrasp1's presentation at #ICanCME2025 was so good! 💙 I learned so much about #MECFS and neurodivergence.

I made it to...and basically most of the way through...today's @ICanCMEResearch Conference! Yay! But my brain is fried, and I can't remember much of what I watched. However, I can tell you it was AWESOME again!! One more day tomorrow. Maybe you could follow @mecfsskeptic. :)

In #MECFS, there’s evidence that microglia are activated more often than in healthy people, which contributes to #neuroinflammation. OMF’s CRC at Uppsala is analyzing microglia activity via MRI as a way of detecting neuroinflammation. 👉 Learn more: omf.ngo/microglia/

Sudden onset myalgic encephalomyelitis is a medical emergency. Hospitalization IV antivirals, in lieu of so-far absent targeted therapy, may be opportunity to avoid life-long disability. Doctors need training to identify this disease when they see it. Do something, don't wait