While these are, of course, sobering findings, they also provide some very potentially important insights into why some people develop LC.
We’re really excited to see these new findings develop, and look forward to seeing the full paper be published! 🙏
t.co/B5eK5OE4hB
...may serve as potential triggers of immune system activation over an extended period, as observed in our study by the cytotoxic activation in several cell populations.”
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They write,
“Chronic cell activation may lead to exhaustion, as observed in multiple long-term chronic illnesses. A continuous reaction to the presence of a permanent virus reservoir or to circulating SARS-CoV-2 residues...
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In addition, in LC patients 1.5-2 years after infection, they found signs of immune exhaustion and markers of cytotoxicity- signaling that the immune system maybe trying to fight off a chronic SARS-CoV-2 infection, and wearing itself out in the process.
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Essentially, LC patients mounted a stronger Type II but weaker Type I interferon response during acute infection.
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Meanwhile, those who later developed LC had an elevated interferon gamma response during acute infection, particularly in T cells, natural killer cells, and monocytes.
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Specifically, they found that those who did NOT go on to develop LC had a robust interferon alpha and beta response during acute infection. (Interferons are a type of antiviral protein that our cells make to fight off infection).
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When comparing people who did and didn’t develop Long COVID, they found differences in the immune response that began on acute infection, and then remained dysregulated in those with LC.
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Screenshot of article title and abstract https://link.springer.com/article/10.1186/s12967-026-08081-6
New study examines the role of lymphocytes in Long COVID 🩸
Pretty exciting new preprint!
Here, researchers examined the activity and function of lymphocytes - white blood cells that are part of the immune system.
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The better we're able to stratify groups and understand whose smell loss is caused by a particular mechanism, we'll be better able to match patients with treatments.
Thank you to the authors for this important study!
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We're pretty excited to see this new pathway for explaining and treating Long COVID smell loss.
While some people seem to respond to treatments such as stellate ganglion block or smell retraining, others don't. It seems likely that those who respond vs. not have different underlying causes.
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They examined this hypothesis using a few different methods. One way was to eliminate the senescent cells using a drug called ABT263, which did reverse the mice's smell loss.
👉Senolytic drugs could be a potential treatment here
👉The TLDR in more simple terms is that senesecent fibroblasts release harmful chemical signals which attract other immune cell to the area, releasing substances which reduce our ability to smell.
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From there, they identified a chain reaction where the senescent cells were releasing harmful inflammatory signals, known as Senescence-Associated Secretory Phenotype factors (or SASP factors).
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In this study, Tsuji et al found that SARS-CoV-2 was able to induce senecence in fibroblasts in the olfactory muscosa of mice - even though these fibroblasts were not themselves infected.
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While this sounds pretty dysfunctional, senescence may be the body's attempt at building an off-ramp to future disease such as cancer. If a particular cell in the body becomes damaged, we actually don't want it to continue to divide and form new cells.
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They stop dividing into new cells like healthy cells do and can end up secreting inflammatory substances that interfere with chemical messaging in the body and impact the functioning of nearby cells.
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What is a senescent cell?
Senescence is the term for a particular state that cells can sometimes enter. It's sometimes described as a "zombie-like" state, where the cells are no longer fully functioning - but they also aren't dead.
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diagram from the paper showing how events in the acute infection lead to sustained olfactory abnormality in Long COVID
Can senescent cells be driving smell loss in Long COVID? 🧠
In a new paper, Tsuji et al. look at a new potential cause of LC smell loss - senescent cells in the olfactory mucosa.
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True.... all it takes is one! Maybe one of them will be it!
We're very much looking forward to seeing how things pan out. Thanks to @invivyd.bsky.social for creating these monoclonals, and to everyone who's studying them!
By generating data from real-world use (those who are prescribed the monoclonals either for prophylaxis or as an off-label Long COVID treatment), we hope to show the FDA that mAbs are safe and can improve Long COVID symptoms.
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We're very much looking forward to the outcome of the study!
Our Patient Registry is *also* designed to help boost the case to the FDA to approve these treatments.
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However, this data from the Columbia team is quite promising, and shows that so far, VYD2311 seems to be holding up. The team writes, "We found that VYD2311 potently neutralized all tested variants in vitro, dramatically more so than pemivibart."
(Pemivibart = Pemgarda, Invivyd's first mAb)
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Unfortunately, they don't always get it right. Just because a particular region has remained unchanged up until a given point, it's not a guarantee that it won't continue to change in the future.
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When researchers create antibodies against COVID-19, they try to design it to target a "conserved" region in the virus.
What this means is they try to pick a piece of the virus, usually the spike protein, that doesn't change across variants, so the monoclonal antibody will remain effective.
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Screenshot of title and abstract from this paper: https://www.biorxiv.org/content/10.64898/2026.03.31.715419v1
Invivyd's new monoclonal VYD2311 shown to be effective against emerging SARS-CoV-2 variants
VYD2311 is Invivyd's new monoclonal antibody. It was designed for pre-exposure prophylaxis in immunocompromised adults, however they're also studying it for Long COVID as well.
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In the long run, as we move towards combination trials, it may be the case that something like red light therapy can be used to improve outcomes when patients are receiving another antiviral treatment.
We are grateful to everyone studying LC, and look forward to learning more every day! 🙏
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Conclusion
While we know some may write off the idea of photobiomodulation as less serious than other interventions, such as antivirals or monoclonals, we do believe every little bit helps -- especially if it can help us to understand the mechanisms of Long COVID.
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By boosting our mitochondria's own healthy, human functioning, it may help to increase their own built-in antiviral mechanisms, and resist this virus takeover better.
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