Biology, Philosophy, Technology. Joined Twitter to help fight against #longcovid

United Kingdom
Joined February 2021
(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
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Sam McIntyre retweeted
Charité Berlin researchers studied 49 Long COVID patients receiving head and neck lymphatic drainage. Brain fog, concentration, headaches and fatigue improved, raising questions about the brain’s waste clearance system. Controlled trials are needed. researchsquare.com/article/r…
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This ORF7a finding is interesting! ORF7A upregulates PDK4, Fluge (2016) found this same enzyme to be upregulated in ME/CFS. This upregulation prevents pyruvate from entering the TCA cycle, meaning extra lactate and the cell switching to burning fat and ketones instead of glucose
SARS-CoV-2 ORF7a: a mitochondrial saboteur! ➡️ A striking study shows that the viral accessory protein ORF7a hijacks host metabolism, impairing mitochondrial respiration, increasing ROS and disrupting glucose/lipid metabolism. It boosts PDK4, suppresses pyruvate oxidation—and, remarkably, also damages complex I and respiratory supercomplex assembly. 👉 The virus isn’t just using the cell’s machinery—it appears to be rewiring and destabilizing the mitochondria themselves. cell.com/cell-reports/fullte…
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Long COVID capillary damage is real. Here are my damaged capillaries. For comparison these small and straight capillaries were photographed by me testing the capillaroscope on the healthy clinic staff.
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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.
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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.
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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🧵
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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!🧠💪🔬
Our new study shows that SARS-CoV-2 spike protein accumulates & persists in the body for years after infection, especially in the skull-meninges-brain axis, potentially driving long COVID. mRNA vaccines help but cannot stop it🔬🧠🦠🧵👇@cellhostmicrobe cell.com/cell-host-microbe/f…
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Sam McIntyre retweeted
“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…
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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.…
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Sam McIntyre retweeted
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/
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NIH are launching a phase 1 trial of Cancer drug Keytruda for Long Covid. It works by blocking the PD-1 receptor on T cells which releases the brake and reinvigorates them, boosting the immune systems ability to clear viral reservoirs clinicaltrials.gov/study/NCT…
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The study will look to see if one dose can: - normalise markers of immune exhaustion - lead to clinically relevant improvement (subjective and objective markers) - change measures of SARS-CoV-2 antigen - change measures of cytokines
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Sam McIntyre retweeted
𝗖𝘂𝗿𝗲 𝗠𝗘/𝗖𝗙𝗦 💙🤍
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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…
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Sam McIntyre retweeted
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:
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(1/3) A team from UCL (infographic citation 31) discovered a dramatic change in the way LC patients' mitochondria are using ATP synthase. Instead of using it exclusively for ATP (energy) production, the enzyme also ran in reverse. ATP was actually being consumed in order to maintain membrane potential. Why might this be happening? 👇
(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
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(2/3) The authors speculate that this switch may be an ancient antiviral response to heat up the cell and block energy, in order to prevent viral replication. Persistence of SARS-CoV-2, or the high rate of reactive oxygen species (ROS) production could be contributing to this metabolic reprogramming.
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(3/3) The authors suggest that 'in LC, this catabolic enhancement appears to continue long after viral infection, despite it no longer serving a useful purpose'. However, growing evidence (see viral persistence section) suggests replicating virus may still be present. Potentially explaining the purpose of this metabolic shift
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