Proud to have worked with the brilliant @drmfreire on this new study looking into spike protein in #LongCOVID. The most important part of this study that doesn't just look for spike protein in folks with LC and healthy controls, but it also uses a technique called 1/
spatial transcriptomics to better understand how spike protein might be interacting with the tissue around it. Here's what is interesting about this trial: lots of gut tissue samples, in both healthy controls and #LongCOVID showed evidence of persistent spike protein. However,
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in the folks with #LongCOVID that persistent spike protein was causing problems in the tissue: pro-inflammatory, tissue-damaging trouble. So not only do folks with LC have more spike, but the spike is actively irritating and damaging the surrounding tissue compared to healthy
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controls who present with less, more inert spike. As we reflect on what this might mean, a couple of questions and calls to action quickly become evident: 1) in a % of folks with #LongCOVID, spike is persisting and causing tissue problems, making it essential that we develop
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and deploy medications that will comprehensively clear spike. 2) In many healthy controls, persistent antigen is present, but inert. Should we be concerned that these folks may be at risk of being one trigger away from that spike becoming "not inert"? 3) No matter how it gets
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in your system, it would seem that some folks cannot seem to easily clear spike and/or have it persist in the body without inflammation and other tissue problems emerging. These folks deserve timely and effective interventional options.
This is one more piece of hard
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evidence that antigen persistence is a legitimate driver of symptoms and organ system dysfunction for #LongCOVID and vaccine injury. We need to be studying targeted mitigation strategies for persistent SARS-CoV-2 antigen YESTERDAY.
@Invivyd let's make it happen 👀
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Excited to finally get this one out in @Nature_NPJ! In the largest study of its kind to date, we used data from the @visible_health platform to answer a simple question: can we predict symptom fluctuations and crashes from both the physiological and
patient-reported data? The answer to this question is yes. Not perfectly, but actually quite well. A few important takeaways: 1) Just as we have seen previously in people living with chronic pain, the ability to predict symptom flares and crashes in ppl with #LongCOVID,
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#MECFS and other complex chronic illnesses can represent a massive life upgrade. The ability to prepare for or expect a crash or a bad symptom day is preferable to many than these things just seemingly randomly appearing with no warning. 2) The fact that physiological signal
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I want to thank everyone for the interest in this work that we completed in a #LongCOVID cohort with this novel device. I always appreciate feedback and want to thank folks for holding me accountable to a high standard of communication. To that end, I want to re-clarify this 1/
thread: this was a safety/feasibility trial which means that our primary endpoints were related to safety and feasibility. In the paper, we state clearly that we hit those endpoints: no device-related adverse events and 100% adherence to the protocol in all participants. That
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is great for a safety/feasibility trial. I then went on to express excitement that some cognitive scores moved. I understand that folks have (rightly) pointed out that without a larger sample size and correcting for multiple comparisons we can’t make definitive statements
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Excited to get this out in preprint: triple-blind, placebo-controlled microtesla magnetic therapy (MMT) is safe, feasible and effective in reducing cognitive impairment in people with #LongCOVID. I get excited about interventions for cognitive symptoms
as they can be so disabling and frightening because you don't know if the symptoms are going to be permanent. This paper makes us feel hopeful that Long COVID cognitive impairment related to neuroinflammation is something that is treatable. This was a first-in-human safety-
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feasibility trial. Typically in trials like this, because they haven't been done in humans and only in animals, we're happy if we see safety and good adherence to the protocol, but we're not usually expecting to see efficacy because the dosage is a bit of a "best guess". 3/
Crucial paper published Friday that deserves much more attention in the #LongCOVID world: .
TLDR: 13/15 immunocompromised patients who had chronic COVID infections (>200 days) cleared the virus in under 2 weeks when given combo antivirals/monoclonals
The caveat: yes these were cancer patients who were severely immunocompromised, and the "haters" are going to say that it isn't appropriate to draw parallels between this patient group and folks with #LongCOVID.
That's incorrect.
It is perfectly acceptable to draw such
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parallels and here is why: we (and others) have shown over and over again that immune dysregulation is associated with #LongCOVID, and T Cell Exhaustion, specifically, is a key feature of this dysregulation (first paper here: ). Why is T Cell exhaustion
3/nature.com/articles/s4158…
Great win early in the year to receive notification that our case series looking into Dr Pridgen’s Valacyclovir, Celecoxib and Paxlovid protocol seems to really help some folks with #LongCOVID. This paper is a start, not the be-all and end-all:
It is a small, open-label case series, but there are some interesting things that are worth noting that give me hope that what we are seeing is real and will hold up in a larger trial 1) People got to choose between Val/Cel only (called ‘IMC-2’ in the paper) and Val/Cel + Pax
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The people who chose the latter reported greater benefit. 2) The subset of people who started with Val/Cel only but then chose to retry the protocol with Paxlovid added experienced more benefit with the three drugs together than they did with the two drugs 3) The follow-up
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Wishing everyone a happy new year and we will be forging ahead in 2026 with renewed energy to find answers for people living with #LongCOVID, #MECFS, chronic #lyme and other infection-associated chronic conditions and illnesses. Speaking for myself, here are some questions I
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hope we can answer this year. Since it isn’t my first time on the internet let me explicitly state: there are other questions that we will be chasing equally aggressively, but these are the ones that I most want to answer to up-level my own understanding of the scientific and
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clinical problems that we face. 1) Why do some people test positive on certain persistence assays and negative on others? How can we use all of the commercially and scientifically available assays to create a unifying test for persistence that helps us to understand when and
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