(1/4) Long Covid: Latest Evidence-based Pathophysiology Clues Infographic 🧩 On this day, exactly 5 years ago I tested positive for a Covid infection that triggered the onset of my Long Covid and its devastating symptoms, which still debilitate me to this day. To mark this unhappy anniversary, I have pieced together and summarised the latest research findings into the below one-page, accessible infographic in the hopes of raising awareness and sparking interest. Clickable PDF link in next post

1) An NIH study found that ME/CFS and Long Covid patients have reduced levels of norepinephrine and its metabolites in the cerebrospinal fluid. The norepinephrine reduction correlated with clinical measures such as fatigue, handgrip strength, and general health.

1) There's an interesting lead in the ME/CFS genetic data: the eccentric medium spiny neuron (eMSN), a cell type in the brain discovered only a couple of years ago. All based on preliminary findings, but the data looks rather interesting.

This may be one of the more important long COVID papers in a while. A new study in Frontiers in Immunology suggests that COVID can trigger new-onset insulin resistance - and that this may drive abnormal NETosis in neutrophils months after infection🧵

For #FluorescenceFriday, the work that motivated my move to Germany! I join the @erturklab to help develop novel approaches to neutralize and eliminate residual viral proteins commonly observed in #LongCovid patients, particularly in the brain. Keep an eye out for our work!🧠💪🔬

An antiviral pill has, for the first time, been shown to prevent COVID-19 in people exposed to the SARS-CoV-2 virus go.nature.com/4nAMi6g

“AIDS once was a mysterious, predominantly fatal disease of healthy individuals. Now, it is a treatable and preventable infection. The same could be true for Long Covid, if we aggressively invest in the research and the clinical system so urgently needed.” foxnews.com/opinion/innovati…

Pleased to share our latest COVID Mind Study @ Yale publication: "Vascular inflammation in neuropsychiatric long COVID" Elevated markers of endothelial adhesion in LC correlates with lower verbal fluency and learning. doi.org/10.1016/j.bbih.2026.…

Fascinating new research from @PlzSolveCFS: What is going on with T cells in Long COVID and ME/CFS? 🤔👇 In this talk, researchers Dr. Liisa Selin, Dr. Ayano Kohlgruber, and Dr. Roshan Kumar discuss their newest work, arguing that dysfunctional T-cells are driving MECFS and Long COVID. They examined the CD8 T cells of patients with these diseases, and found signs of clonal expansion - which only happens when the immune system is chronically exposed to an antigen. 🦠 Clonal expansion can happen in response to a foreign antigen (such as a virus or bacteria), however it can also happen in autoimmunity, where the immune system has accidentally recognized part of the person's own body as "foreign." They also identified signs of exhaustion in these T cells- meaning that they're becoming worn out trying to fight these antigens, whether they're foreign (as in the case of chronic infection) or self-antigens (as in autoimmunity). In MECFS and LC patients, they found their CD8 tells were able to produce much lower levels of Interferon-gamma and TNF-a compared to healthy controls.🧪 Previously, Dr. Selin and other researchers had studied an experimental, nebulized treatment called Inspiritol (unfortunately it is not available to patients at this time). In this new work, the team tested Inspiritol's effects on these exhausted T cells in-vitro, and found it was able to greatly improve the cells' function. **Other Chronic Pathogens** Dr. Selin explains that once you have the overactivation and subsequent exhaustion of the CD8 T cells, it impairs the immune system's ability to keep other chronic pathogens that may be in the person's body under control. This is why patients with these diseases may have a reactivation of herpesviruses such as EBV, CMV, HHV-6, enteroviruses, tick-borne illnesses, and more.🦠 **Identifying T cell Targets** In the future stage of the work, this team will use technology developed by Dr. Kumar and his company that seeks to identify exactly which pathogens these T-cells are targeting. Knowing the cause of this abnormal clonal exhaustion will help us to understand exactly why this process is occurring, shedding light on the underlying cause of LC and MECFS. ✨It's pretty exciting to see these advances occurring! Although it may not always seem like it, we get closer to the answers every day!✨ 1/

𝗖𝘂𝗿𝗲 𝗠𝗘/𝗖𝗙𝗦 💙🤍

Simmaron publication shows mechanisms of #PEM in #ME! Our new findings show a lack of ATG13 inside cells induces macrophages to take on an inflammatory role, impairing myelin in muscles, in processes aggravated by exercise. #Longcovid @UWM @SpringerNature link.springer.com/article/10…

Turn 36 today & I’ve spent my entire thirties with #LongCovid. When I turned 30 I was biking to work 10 miles a day, & since my mild covid infection — I struggle to walk more than a block or work more than a few hours a week. Here’s 4 things I wish everyone knew:

Great info here. Millions of people all over the world are waiting for treatments. 🌍 So much needs to be done- but we are also starting to see more and more pathways to the answer 🙏

You’re harming a patient with ME/CFS if you recommend exercise. Here are the highlights of the recent paper by @DrMaureenHanson , who has been studying this field for decades, and her colleagues: ✔️Plasma profiling of 7,288 proteins during post-exertional malaise in ME/CFS. ✔️ME/CFS participants show sustained immune, metabolic, and neuromuscular dysregulation during post-exercise recovery. ✔️Exertion disrupts T and B cell signaling, IL-17 pathways, and mitochondrial metabolism. ✔️Protein signatures correlate with symptom severity and impaired exercise performance in ME/CFS subjects. ✔️Sex-stratified analysis reveals distinct molecular responses, underscoring the importance of sex in ME/CFS pathophysiology. mcponline.org/article/S1535-…