@markgurman To be clear, regardless of the color, the 17 Pro / Pro Max feels and looks far inferior in both design and build compared to the 16 Pro / Pro Max. In hand, it comes across as fragile and cheap. I might reconsider. First time in many years.
Long COVID Hitting Doctors and Nurses Hard.
David Putrino, PhD, at Mount Sinai, has treated about 3,500 people w/ long COVID & sees 500–700 new patients per year. He says 5–7% are healthcare workers, showing disproportionate LC impact in this group. https://t.co/NvXiR29clu
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Thank you @cstroeckw for your incredible message 💙 You are always in my thoughts and heart. With great colleagues, I will continue to investigate #MECFS with every fiber of my being so that one day we can meet in person. (Thank you Felda for all you do 🙏🏼)
Hi, it's Felda! 🙏💙
Christoph asked me to post this for him:
"I am deeply grateful to Prof. Akiko Iwasaki for dedicating her scientific talk at the Immunology Congress to me - and, in a sense, to all people living with ME/CFS. It was a profoundly moving gesture. At the same time, I deeply regret and am deeply saddened that my health did not allow me to meet her while she was in Vienna. Only those with very severe ME/CFS will truly understand what this means and how crushing and sould-deadening such limitations are.
In a time of remarkable cynicism, I can tell you from my own experience with her that her work is guided by genuine compassion. From a rational perspective, there would be little reason for someone in her position to work on ME/CFS - let alone to stand up for us, and to say clearly when others are speaking nonsense about this disease. For me, shaped quite deeply by Christian and Buddhist thought, compassion is the highest human goal - and without ever having met her personally, I can say with certainty she comes remarkably close to embodying this ideal, and I am deeply humbled by it. Thank you."
Congratulations on securing the new grant to expand the Long‑COVID lymph‑node study—what an exciting and timely development! Your focus on the EBV–SARS‑CoV‑2 interface is particularly compelling given the accumulating evidence of viral co‑reactivation and immunological interplay in post‑COVID syndromes I think it is a key area of focus.
I wanted to share some reflections on our earlier in silico epitope analysis with @iximeno : we identified regions of high sequence similarity, or shared antigenic epitopes, between SARS‑CoV‑2’s S1 subunit and EBV nuclear antigens such as EBNA‑6, and observed analogous matches with other herpesvirus proteins. These overlaps raise the intriguing possibility that such molecular mimicry could skew the humoral response towards non‑neutralizing or cross‑reactive antibodies, potentially diverting protective immunity. Further, the involvement of IL‑10 in these scenarios may be especially relevant. An area of focus that our time and resources do not allow us to investigate further, but they could certainly be a hint or area to double check.
Again, congratulations on advancing this promising line of investigation. I’m very much looking forward to following to your progress.
Vaccines are developed under the assumption that the pathogen is absent from the host at the time of administration. However, current evidence indicates that, in certain cases, SARS-CoV-2 can evade the host immune response through mechanisms such as mutational escape and persistent intracellular infection. This raises an important question: does the vaccinated individual still harbor the S1 subunit of the spike protein prior to vaccination? The situation is more complex than it may initially appear, and the underlying issue may not lie solely with the vaccine itself. Notably, the S1 protein, by virtue of its pathogenic potential, can independently contribute to significant immunopathological effects.
Breakthrough COVID-19 Protease Inhibitors Outperform Current Drugs
A new class of SARS-CoV-2 protease inhibitors (AVI-4516 & AVI-4773) shows exceptional potency, pan-coronavirus activity, and rapid in vivo efficacy, surpassing existing drugs like Paxlovid.
In animal models, including mice, the drugs demonstrated excellent tissue distribution, including the brain, with concentrations significantly exceeding effective levels.
These findings promise stronger preparedness and broader therapeutic options for #Longcovid.
#longcovid #drugdevelopment
https://t.co/7AfvRvS3RL
Many people have stopped talking about Covid-19, but across the world, 100 million people across the world are still suffering from its aftermath. 🌎
We were told it’s just a respiratory virus, but the truth is that research is shown the SARS-CoV-2 virus can enter the brain. What if it’s still in there? 🧠
Persistent viral infection is emerging as the most likely hypothesis behind the many symptoms people with #longcovid expedience.
On top of that, a recent study showed that many of the same biomarkers signaling that the virus is still present in Long Covid patients have also been found in people who don’t feel any long-term symptoms at all.
This brings us to an even larger question- could the virus also be lingering in the bodies of people who DON’T (yet) have any LC symptoms?
👉While our immediate goal is to find treatments to help the 100 million LC patients globally, the frightening reality is that the number of people who will need treatments to clear persistent virus may in fact be much larger.
We don’t yet know what the long-term consequences of having this virus in our bodies could be.
It’s possible that it could silently be wreaking havoc inside of many people who don’t experience long covid symptoms yet.
As science progresses, we’re learning more and more about how certain virus can perished in the body and cause long-term health consequences.
For example, a potential casual link appears to be developing between EBV infection and multiple sclerosis. Persistent viral infection may also be the root cause of diseases such as Alzheimer’s and ME/CFS. 🦠
It’s highly possible that the same may turn out to be true for the SARS-CoV-2 virus.
Figuring out how to treat Long Covid will allow us to not only alleviate the suffering of the 100 million people in this specific patient population- it may be necessary to prevent disease and restore the health of millions more.
There is an unprecedented crisis here- and also a huge opportunity to flip the old way of doing things on its head, and create change for good. ❤️🩹 1/
New preprint: “Using the golden hamster as a model, we provide further evidence that #SARS-CoV-2 is neuroinvasive and can persist in the central nervous system, as we found viral RNA and replicative #virus in the brainstem after 80 days of infection.”
https://t.co/wtK1BqhMxJ
The #SARSCoV2 spike protein can persist in the brain—skull bone marrow and meninges—to induce neurologic damage https://t.co/FtsftML1m4 just published @cellhostmicrobe@erturklab open-access
Hi Manuel,
I regularly read your posts and truly appreciate the effort and determination you bring to researching and clarifying these conditions, especially given your personal experience and those around you.
I hope you don’t mind, but I would gently suggest that ME/CFS and Long Covid may not belong in the same category. While I understand the potential overlap—particularly in cases of immune suppression and the involvement of reactivate viruses.
Long Covid appears to be more specifically characterized by the persistence of the SARS-CoV-2 virus and/or autoimmunity triggered by it, which seems to set it apart from ME/CFS based on your own findings. That said, I agree there could be overlaps, especially given the state of debilitated immune systems and the frequent reactivation of EBV and other herpes-type viruses in Long Covid patients.
Consequently, it is possible that ME/CFS might present as the result of an unresolved SARS-CoV-2 infection. However, by now there is direct evidence of persistent viral presence in exosomes, PBMCs, endothelial cells, and ACE2-rich tissue, even many months after infection. This seems to be the primary issue for about 50% of Long Covid patients, who don’t yet have access to effective, long-term antiviral treatments, neither to affordable SARS-CoV-2 viral load tests.
As an example, a Long Covid patient may be treating EBV, for example, or CMV as a main target. However, a big majority of the mysterious symptoms may prevail, possibly associated with the inmune system persistent activation and, after a while, its exhaustion.
I obviously write about it with all due care and respect to the medical profession. My opinions are simply educated opinions based on self-study of scientific papers and my own experience.
Thank you again for all your valuable insights—I always look forward to reading your work.
Persistence of #SARSCoV2 antigens and link with symptoms of #LongCovid
21% of >700 participants infected had persistent antigens > 1-month
43% of symptomatic participants were antigen-positive
https://t.co/c8Gqua0LQ2
Important findings! 👉 “Compared to people who didn’t report long #COVID symptoms, those who reported persisting symptoms affecting heart and lung, brain, and musculoskeletal systems were twice as likely to have #virus proteins circulating in their blood”
https://t.co/9NcLOGuMLy