I felt it clearly, the damn virus never left my body. 2+ years later - why is #viralpersistence still not properly investigated in #LongCovid ?! UNFATHOMABLE.
Breaking: Funding from Vitalik Buterin’s Balvi Fund Expands Long COVID Rapamycin Trial
PolyBio today announced new funding that is supporting an open-label extension phase in a clinical trial investigating low-dose Rapamycin as a potential treatment for Long COVID. All participants—including those initially randomized to placebo—will receive low-dose rapamycin during a defined follow-up period. 1/
for every single other disease this would be enough to justify empirical IVIG.
For MIS-C we used IVIG without such a strong evidence. Even in kawasaki disease we have less evidence about what is really going on.
May be that this is not happening in all patients, but until we can’t test those antibodies in clinical practice, I’ve got no single doubt that this pathogenesus must be considered until proved wrong
@horizontalviews@surf4children@frausteinbock I did three rounds.
Feeling better?
I had the absolute most severe crash ever, that lasted for months, after that, back to baseline with perhaps a small improvement, but not significant.
A growing body of evidence suggests that the COVID-19 pandemic has had major long-term effects on cardiovascular health, contributing to increased heart disease and stroke mortality even after the acute pandemic period.
➡️ Researchers believe this rise reflects a combination of direct cardiovascular injury from SARS-CoV-2 infection, worsening of chronic risk factors such as hypertension, diabetes, and obesity, and major disruptions in preventive and routine cardiac care during the pandemic. 1/
'STORM' is a short documentary about Scott Hugo. A story of Long COVID's impact on his life and family - a reminder of what is at stake in research on Long COVID.
His resilience humbles me.
Please watch and share 🙏🏼
https://t.co/tN7B5wcq2I
We have known for a while that #LongCOVID pathobiology for many involves reactivation of various herpesviruses. As we continue to validate this it is great to see this work coming out in collaboration with @VirusesImmunity’s incredible team. Here we
https://t.co/mm7FkGqQh6
1/
People don’t realise how much you can lose and still have to live every hour.
I’ve lost walking, my brain, normal vision, friends, food, music, love, career, hobbies, sunlight, sleep…
I can’t even grieve it without getting sicker.
Disease takes more than you realise you had.
What ties all the Polybio presentations together is a strong emphasis on the persistence of SARS2 - often in a replication-competent form.
This persistence is primarily located in tissues, especially in the gastrointestinal tract (ileum, lamina propria, sigmoid colon).
Nicolas Huot
Found replication-competent SARS2 in the ileum of primates, localized near lymphoid structures.
Marcus Buggert
Detected persistent viral RNA in the gut along with increased interferon signaling.
Tim Henrich
Showed persistence in the lamina propria and associated changes in immune cells.
Eduardo Reategui
Presented the BARA platform (using extracellular vesicles) with very strong detection accuracy.
Van Brocklin
PET scanning to identify areas of T cell activation across patient’s whole bodies
These studies strongly suggest functional parallels with HIV -
Viral reservoirs in immune cells and GALT
Chronic T-cell activation and exhaustion
Long term immune dysregulation driven by persistent viral antigens.
PolyBio is approaching Long COVID as a chronic infectious disease with a viral reservoir, rather than merely a post-viral syndrome.
The transfer of knowledge and experience from HIV research is one of the strongest accelerators of progress in this field!
Is there an association between human herpesviruses (HHVs) reactivation and Long COVID? We analyzed HHV DNA shedding in saliva and found that HHV-6 correlates with Long COVID severity. Claire Laxton, @S_Tabachnikova, Lily Cooke, Kexin Wang et al.
https://t.co/jsZznyXiGq (1/)
@DarainChains@TheExtraFiles I already had ME for 9 years before getting LC on top (who else? 🙋🏻♀️)
Kept telling doctors LC is different from ME (hey, 1st hand experience right) No one would listen to me, just told me my ME ”got worse” 🙄 Anyhow, it’s a helluva combo….
”Neuroinflammation: In autoimmune conditions like Multiple Sclerosis, excess extracellular glutamate triggers neurotoxicity. Conversely, pro-inflammatory cytokines can disrupt glutamatergic signaling, a mechanism implicated in neurodevelopmental conditions like ASD.”
@Google says:
”The "glutamatergic immune system" describes the profound biochemical crosstalk between the nervous and immune systems. Once thought to be restricted to neurotransmission, glutamate acts as a major immunomodulator. Immune cells—….” 🧵
https://t.co/OdbK8ozAA5
”Pathological & Protective RolesProtective Autoimmunity: In moderation, the immune system utilizes targeted responses against self-antigens to protect neurons from glutamate excitotoxicity (overstimulation by glutamate).”
Millions of Americans live with infection-associated chronic conditions and illnesses, including long COVID, ME/CFS, and Lyme disease–associated chronic symptoms; conditions that are often debilitating, misunderstood, and under-recognized.
In a new Clinical Infectious Diseases viewpoint, CAPT Iskander and Dr. Haridopolos of the Office of the U.S. Surgeon General call for making these “invisible illnesses” visible through patient-centered care, stronger surveillance, multidisciplinary management, and continued research investment.
The article emphasizes the importance of validating patients’ lived experiences while advancing evidence-informed care to improve outcomes for people living with these complex chronic conditions.