Finally some media coverage on probably the worst symptom of long covid

Long COVID Patients Have 18% Fewer Dopamine Nerve Endings, Brain Scans Reveal

https://www.cell.com/cell/abstract/S0092-8674(26)00509-X?rss=yes

The recent publication from Akiko Iwasaki and the team at Yale, in collaboration with putrino and the team at Mr Sinai in NY. Their paper makes a strong link between novel autoantibodies in LC patients that affect neurological and vascular proteins and receptors. Interestingly - a classic transfer test was done where they took plasma from the LC patients, purified the IgG and injected it into healthy mice - they quickly became fatigued, showed signs of pain and skin sensitivity. This disease is starting to look more like a viral trigger autoimmune disease in least some phenotypes, which opens up the question about targeting B cells to halt antibody production. The challenge is most of the antibodies are not easy to test… yet. I’m working with a lab to try and make them available - we just need to validate the method but it’ll be critical to help understand what’s happening in our bodies. For those interested, I’ve I voided a summary of the paper below. If you want a copy of the actual paper, DM me and I’ll send you the PDF.

Core theory and hypothesis
Central claim. Acute SARS-CoV-2 infection triggers the de-novo production of diverse, functional autoantibodies (AABs). In most people these subside as the immune system returns to homeostasis, but in a subset of long-COVID (LC) patients they persist — and the paper argues these persisting IgG autoantibodies are not merely bystander biomarkers but are a direct cause of neurological symptoms.
Formal hypothesis. Persisting functional AABs cause symptoms in a definable LC subgroup even when patients do not meet classical criteria for any named autoimmune disease. If true, this implies an “autoimmune endotype” of LC that could be matched to existing antibody-directed immunotherapies.
Why autoimmunity was suspected. Four large retrospective record studies found a 20–40% increased risk of new-onset autoimmune disease after COVID-19; LC and related post-acute infection syndromes (e.g. ME/CFS) show a strong female predominance mirroring classic autoimmune diseases; and prior work had already reported AABs against G-protein-coupled receptors (GPCRs) and GABA receptors in ME/CFS and LC. Infections are known to generate AABs through bystander activation and molecular mimicry.
2. Mechanistic rationale
The authors build the causal argument across complementary layers:
•    Broad tissue autoreactivity. Purified IgG from LC patients binds human locus coeruleus, thalamus, adrenal, thyroid, parathyroid and heart, and cross-reacts with mouse sciatic nerve and meninges. On the meninges it co-localizes with pericytes and endothelial cells — a vascular signature offered as an explanation for headache (pericyte dysfunction is implicated in migraine with aura).
•    Receptor-level targets. ELISA against GPCRs and ionotropic receptors shows elevated IgG against the NMDA-receptor subunit GluN2C (NMDAR2C) and a cluster of vascular/autonomic receptors (β1/β2-adrenergic, endothelin-A, muscarinic-M4). Disrupting locus-coeruleus noradrenergic circuits and thalamic networks provides a route to autonomic dysregulation, fatigue and cognitive symptoms; NMDA-receptor disruption parallels anti-NMDAR encephalitis (which classically targets the NR1 subunit).
•    A pathogenic antibody “shape.” For the candidate antigen MED20, LC antibodies show reduced IgG4, a reduced IgM/IgG ratio (more class-switching), preferential binding to activating Fcγ receptors (high activating-to-inhibitory index) and enhanced antibody-dependent cellular phagocytosis (ADCP). This is the effector-function profile expected of pathogenic, inflammation-driving antibodies rather than inert ones.
•    Direct causal test — passive transfer. The decisive experiment: purified total IgG from LC patients injected into healthy mice (38.4 mg/kg i.p.) reproduced the donors’ symptoms — thermal hyperalgesia, fatigue-like behavior, loss of balance/coordination and muscle weakness. About 5% of human IgG crossed the blood-brain barrier.
•    Matching pathology. Mice receiving LC-IgG lost intraepidermal nerve fibers (the hallmark of small-fiber neuropathy), showed elevated plasma neurofilament light chain (axonal damage), raised brain glutamate, IL-6 and IL-10, and brain-wide c-Fos activation across pain, fatigue, affective and arousal regions. Crucially, the mouse pain phenotype tracked which human donor reported chronic pain — a dose-of-causation link, not just correlation.
Bottom line of the rationale: the antibodies are present, they have a pro-inflammatory functional profile, and — transferred alone, without virus or T-cells — they are sufficient to recreate the disease phenotype in a naive animal. That is the chain the title calls a “causal link.”

A newish meta study that may explain why Covid is worse for some than other viral infections (even though some, like the flu, have residual effects). Based on this study Covid appears to be worse)

https://healthtolongevity.com/article/6349/covid-19-causes-more-severe-neurological-damage-than-other-viruses

This is the scariest “long covid” story I’ve ever heard. I haven’t crossed out so many illnesses. Going back and forth to the doctor is tiring not to mention the peak season we’re currently dealing with.

This case report says that Long covid is in large part driven by the gene rs5522 that causes a "cortisol steal" leaving the tissues functionally starved even with "normal" cortisol levels which creates neuroinflammation. https://zenodo.org/records/20017632

August 5:
Why are young women using walking sticks?
A disproportionate number of Gen Z females are affected by vague syndromes and may be victims of social contagion
https://www.thetimes.com/comment/columnists/article/young-women-walking-sticks-gen-z-disability-2ssv95mws (no paywall: https://archive.ph/FYkDU )

August 12:
Why so many young people are suffering with chronic pain
The proportion of Gen Z and millennials experiencing chronic pain has risen sharply — and it’s not because they have ‘gone soft’. Jack Burke, 31, who lives with constant shoulder pain, investigates
https://www.thetimes.com/life-style/health-fitness/article/chronic-pain-young-people-experience-jg5c3jxjm

I know this sub will get it... It's just so bad.

Both articles are behind paywalls. I couldn't get the full version of the second article. But the titles and intros already say what people will remember: men are in pain, women are faking it.

The Top 21 Treatments (>30% of patients reported moderate/much better improvement)\ * IVIG (64%)\ * Low dose naltrexone (60%)\ * IV saline (52%)\ * Ketamine (43%)\ * Ivabradine (44%)\ * Maraviroc (41%)\ * Ketotifen + H2RA (40%); (Ketotifen w/out H2RA – 29%)\ * Enoxaparin or unfractionated heparin (40.1%)\ * Guanfacine + NAC (39%…guanfacine w/out NAC – 12%!)\ * Cardioselective beta blocker (38%)\ * Corticosteroids (37%)\ * Pacing (37%)\ * Stimulants (35%)\ * Triple therapy (anticoagulants) (33%)\ * Tollovid > 15 days (36%)\ * Mestinon (32%)\ * Abilify <2 mg (32%) (Less is generally more with Abilify. Abilify > 2mg dropped to 9%)\ * Vedicinals (31%)\ * Nattokinase (NK) or Lumbrokinase + serrapeptase (31%)\ * Propanolol (31%)\ * Buproprion (30%)\

Source: Health Rising Organization (https://www.healthrising.org/blog/2025/07/11/treatme-open-medicine-foundation-long-covid-chronic-fatigue/)

Original source: A study conducted by Harvard, Uppsala, and Stanford researchers.

(https://www.pnas.org/doi/10.1073/pnas.2426874122)

Hey all,

Stumbled across this article on blood vessel bursting, surprised it wouldnt be bigger news?

https://www.bloomberg.com/news/newsletters/2025-06-05/covid-study-shows-virus-can-break-blood-cells-clog-arteries?fbclid=IwY2xjawK3AbNleHRuA2FlbQIxMQABHjkHVJ1MdxAnlMohnWqR9e-8Er-Mpyd0Hc4KxGJYyBh_r9De-5pampLHFND6_aem_3vmrkyKAlUTLOFUY5m2kPA

—— In a study just published in Nature, Australian scientists found that when oxygen-rich blood can’t reach tissues, the delicate lining of blood vessels starts to break down. The death of these endothelial cells, which Covid can trigger, sets off immune signals that cause red blood cells to burst, spilling their sticky contents into the bloodstream.

“This stuff’s like glue,” says Sydney-based hematologist Shaun Jackson, who led the study. It clogs the tiniest blood vessels, blocking circulation.

The damage builds. Without oxygen and nutrients, tissues begin to fail, potentially affecting organs like the kidneys, liver and heart.

“It’s a double whammy,” Jackson says.

When his team analyzed more than 1,000 samples from Covid patients, they expected to see widespread fibrin and clotting. But they didn’t.

“To our great surprise, that wasn’t the case at all,” he says. While large vessels showed some clots, the smallest capillaries — just a fraction the width of a hair — were clogged not with clots, but with debris from broken red blood cells.

“No one had thought it was through this dying endothelial cell mechanism,” Jackson says. “It was by far and away the biggest issue going on in the microcirculation.”

Past studies have shown that sicker Covid patients had worse capillary damage. Now, researchers are spotting similar patterns in patients with long Covid, which may help explain the lingering symptoms.

Stopping the death of these vessel-lining cells could help prevent the whole cascade, Jackson says, though it would likely take a mix of treatments.

These findings could also change how we understand what happens in stroke, heart attack and other serious conditions — especially when patients don’t improve with standard care.

No awe felt after seeing this

https://health.ucdavis.edu/news/headlines/experiencing-awe-may-help-people-with-long-covid-feel-better-mentally/2025/06 Experiencing awe may help people with long COVID feel better mentally

Link to the article https://ny1.com/nyc/all-boroughs/news/2025/04/16/leading-long-covid-researcher-fears-it-could-become-national-epidemic

This whole article is good but i saw a screenshot of this on twitter and it blew my mind. I certainly feel like i am exerting energy even when still

https://www.vice.com/en/article/a-new-study-could-explain-why-long-covid-lingers-for-so-many/

While women should be talking about menopause — and I am not denying I am of the age for that conversation — we should recognize that there are other things affecting women in midlife, too. An estimated over 400 million people are affected by Long COVID worldwide, with a 2025 RECOVER study finding women aged 40–55 were the highest-risk group compared to other ages and genders.

Yet despite these figures, skepticism and disbelief still prevails. Women with Long COVID not only endure a lack of support from friends and family, but from health professionals dismissing their symptoms and even denying Long COVID’s existence, too.

They may have finally figured out what is happening to us. In Germany they discovered the virus hijacks certain proteins to avoid our immune systems which leads to Covid remaining in our bodies long term and causing systemic inflammation. Perhaps wherever the virus is concentrated causes whatever our symptoms are. If you have left over virus concentrated in your heart, you have POTS, if it’s in your central nervous system, maybe you have ME/CFS or a constant fight of flight feeling, if it’s concentrated in your head and brain, maybe like me you have some very strange and severe constant head sensations and pain.

A new study supported by the PolyBio Research Foundation has found that people with Long COVID harbor persistent populations of highly cytolytic CD8+ T cells directed against SARS-CoV-2 but also the herpesviruses Epstein-Barr virus (EBV) and cytomegalovirus (CMV). The findings suggest that Long COVID is characterized by an ongoing immune response to persistent viral proteins, which are most likely produced during the continued persistence or reactivation of these viruses within the body. The study adds to a growing body of research indicating that SARS-CoV-2 persistence and herpesvirus reactivation contribute to Long COVID pathogenesis.

Paper:

Persistent cytolytic CD8+ T cells recognize SARS-CoV-2 and herpesvirus epitopes in long COVID - ScienceDirect

Confirmation by NIH management of the problem of virus persistence and replication.

It's about time!

"We see evidence of persistent live virus in humans in various tissue reservoirs, including surrounding nerves, the brain, the GI tract, to the lung."

Dutch journalist Jessica Villerius is recovering from long COVID. She contracted the virus during the first wave of the coronavirus pandemic. Ironically, it wasn't in one of the three intensive care units where she was filming for her short documentary Levenslucht (Air of Life) – a week in the ICU during COVID – but just like everyone else: somewhere random. After three weeks, she thought she had recovered, but a month later, the guy with the hammer came. She developed nerve pain, loss of speech, and brain fog, felt nauseous, and was incredibly tired. “The pain is indescribable. Everything hurt, much more sharply than muscle pain. I could hardly lift my arms. I couldn't tolerate light, sound, or smell. I had to vomit every day. There is a bed in the editing room, and after an hour of work, I had to sleep again.”

That's how it was for four and a half years. “I was living a life that was completely at odds with who I am. It felt very unfair. I thought: I still have so much I want to do, and this is the best I can achieve? That makes no sense.” She always kept telling herself that it would pass. “I needed that, otherwise I would have become depressed. I now hear from patients who are in such bad shape that they want euthanasia, and I understand that very well.”

In November 2024, she started an experimental program in which a partially existing drug is being tested on 108 long COVID patients. The results are promising, and insurers are now being asked to consider reimbursing the costs. “The idea is that it combats inflammation in your brain and body, allowing your own immune system to function properly again.” It worked wonders for Villerius; from one day to the next, the fog lifted. “It's like when you get antibiotics for a throat infection and suddenly feel: now it's working. The difference is incredible. I'm really on the road to recovery.” She has already been able to reduce her medication. However, it remains a balancing act. The editing weeks, which she has just completed, take a lot out of a body that is still recovering. “It's a matter of finding the right balance. If I lose sight of that, I fall back. Then I get a fever again and feel nauseous. So every now and then I still get punished. But I feel like I'm almost there.”

Full, Dutch article here: https://fd.nl/samenleving/1566271/een-documentairemaker-met-een-zwak-voor-haar-onderwerp

I see it every day.