🔴 “Long COVID came out of nowhere.” No, it did not. Before SARS-CoV-2.
Before COVID vaccines.
Before today’s debates about Spike, mRNA, or vaccine injury. Another coronavirus had already been followed by persistent long-term symptoms. It was called SARS-CoV-1. And almost everyone forgot what happened next. (1/33) 🧵

🔴 I think it is time to start taking seriously the disease model we have been proposing for Long COVID and ME/CFS. For years, we have argued that persistent viral reservoirs may be the initiating event connecting many of the mechanisms observed in these diseases: -Chronic antigenic stimulation. -Immune hyperactivation. -T-cell exhaustion. -Reactivation of latent herpesviruses. -Chronic inflammation. -Loss of immune tolerance. -Autoimmunity in genetically susceptible individuals. A new study has now identified the kind of cellular response that this model predicts: Persistent, virus-specific, cytolytic and exhausted CD8⁺ T cells directed not only against SARS-CoV-2, but also against EBV and CMV. This is not simply “an immune system that forgot to switch itself off.” These lymphocytes recognize viral antigens. The more important question is: What continues stimulating them? (1/13)🧵

🔴⚠️‼️Have you heard a flood of news stories about Epstein-Barr virus and multiple sclerosis over the last few days? Pay attention, because many headlines are telling the story incorrectly. Or, at the very least, they are telling you only part of it. The news is not simply that “the mononucleosis virus activates certain lymphocytes.” Nor have we only just discovered that Epstein-Barr virus is associated with multiple sclerosis. This had been suspected for decades and became extraordinarily well supported in 2022. The real news is that we are beginning to understand how a virus that remains inside our B cells for life could keep the immune circuit that eventually attacks the nervous system switched on. And that completely changes the therapeutic question: Why do we continue limiting ourselves to suppressing the immune system without also trying to control the virus that is probably fueling the process? (1/14)🧵👇🏻

‼️⚠️Please read this until the end. A widely shared article has presented a deeply misleading view of Long COVID, suggesting once again that cognitive behavioral therapy, exercise, and “mind-body” approaches may be the uncomfortable truth patients refuse to accept. This needs to be challenged. Not because the nervous system does not matter. Not because psychological support cannot help. But because confusing support with cure, physiology with psychology, and heterogeneity with “it might be in your head” is exactly how medicine has harmed post-infectious patients for decades. There are articles about Long COVID that look like science journalism, but in reality they repackage, in modern language, a very old idea: if we do not fully understand a disease, maybe the problem is in the patient’s mind. And that is not science. That is repeating history. The article begins with a striking sentence: “There isn’t a single approved pharmaceutical treatment, not even a test to verify the presence of the illness.” This may sound forceful, but it is a very misleading way of presenting the problem. The fact that there is still no drug specifically approved for Long COVID, or a single diagnostic test, does not mean that “nothing has been found.” It means that we are dealing with a heterogeneous disease, probably with several biological subgroups, and that medicine has not yet converted those findings into validated clinical tools. “No single diagnostic biomarker” is not the same as “no biology.” In just a few years, immunological, vascular, neurological, endocrine, and metabolic abnormalities have been described in subgroups of Long COVID patients: autonomic dysfunction, herpesvirus reactivations such as EBV/HHV-6, alterations in the cortisol axis, autoantibodies against GPCR receptors — including adrenergic and muscarinic receptors — persistent viral antigens, endothelial damage, muscle abnormalities after exertion, mitochondrial dysfunction, persistent inflammation, and differential immune changes. Is everything settled? No. Does that mean it is psychological? Also no. Science does not work like that. Multiple sclerosis did not stop existing before we had MRI. Many autoimmune diseases do not show up in routine blood tests. If a complete blood count, a basic biochemistry panel, or an X-ray comes back “normal, normal, normal,” that does not prove the absence of disease. It only proves that you are looking with inadequate tools. One of the article’s most serious mistakes is this: it confuses the absence of a simple clinical test with the absence of organic disease. And that mistake has caused harm for decades. The article also says: “Almost $2 billion and half a decade of international effort have yielded little more than hypotheses about micro blood clots and spike proteins and mitochondrial dysfunction.” No. That is not correct. A hypothesis is a provisional explanation. But when you compare patients and controls and find significant differences in muscle tissue, metabolism, response to exertion, immune biomarkers, viral antigens, autoantibodies, or vascular dysfunction, you are no longer talking about “little more than hypotheses.” You are talking about lines of biomedical evidence that still need to be organized, replicated, stratified, and translated into treatments. That is not scientific failure. That is research into a complex and new disease. 🔵Continued in the next post.👇🏻 (1/6)

⚠️‼️ I came across this news in Spain, and this discourse keeps doing enormous harm. The post literally says: “A study from Hospital del Mar reveals a worrying connection between childhood trauma and physical diseases in adult life. From headaches to diabetes, adverse childhood experiences could leave marks on our health. Early prevention has never been so crucial.” “A study from Hospital del Mar details numerous physical diseases linked to childhood trauma.” Not because they literally said that most organic diseases are caused by childhood trauma, but because in practice, many of the diseases they attribute to or reduce to trauma end up being organic diseases whose biomarkers have not yet been discovered, or whose proper medical workup was never even done. And that is the real problem. For years, many patients are first filtered through the lens of trauma, psychosomatic illness, or somatization, when in reality what they have is an organic disease that has simply not yet been diagnosed. I would even go further and say that this also happens with diseases we now understand well: before reaching the right specialist and before the appropriate tests are performed, many patients are treated as if the origin of their symptoms were psychological or trauma-related, simply because nobody has investigated their case properly. That is not precision medicine. That is a way of covering diagnostic ignorance with a psychological narrative. The history of medicine shows this again and again: many diseases that in their early stages were treated as “nervous,” “hysterical,” or “psychosomatic” later turned out to be well-defined organic diseases. This happened with multiple autoimmune, neurological, and inflammatory diseases. And it is still happening today. That is why this discourse is so dangerous. Because it not only delays the real diagnosis, but also blames the patient, isolates them, sends them into the wrong clinical pathways, and steals years of serious medical investigation from them. Most of these patients do not need their illness to be explained through trauma. They need the right tests, the right specialist, and serious investigation of their real biology instead of convenient theories being projected onto them. Enough of turning the absence of known biomarkers into a psychological explanation. What some people today call trauma or somatization too often ends up tomorrow having a name, a mechanism, and a biological marker.