this is not the end - will discuss Pillars 2 and 3 in a bit!!!!!
26.11.2025 00:33 β π 1 π 0 π¬ 0 π 0@sun-in-winter12.bsky.social
https://linktr.ee/christycollins123
this is not the end - will discuss Pillars 2 and 3 in a bit!!!!!
26.11.2025 00:33 β π 1 π 0 π¬ 0 π 0I also used things like:
coconut oil - powerful antiviral
Brazil nuts for selenium - glutathione precursor
miso + yogurt for probiotics - immunomodulatory properties
Some of this I'd started earlier - more info in my previous update here:
longcovidbegone.substack.com/p/a-positive...
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There's a lot you can do to make it more difficult for the virus to invade your cells.
For example, Omega-3 and alpha lipoic acid can help strengthen your cells' membranes so the virus has to work harder to break through.
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bit.ly/41x8Ue1
Screenshot of title and abstract from this paper: https://pubmed.ncbi.nlm.nih.gov/40184815/ highlighted text says: "Overall, our study identifies dysregulated GSH metabolism as a key driver of NK cell dysfunction in acute leukemia and suggests that GSH-based interventions may provide a promising strategy to enhance NK cell-mediated immunotherapies."
Glutathione specifically has been shown to improve the immune response.
It plays an important role in t-cell and natural killer cell function - two types of cells which we need to clear virally infected cells!
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screenshot of title and abstract of this paper: https://bit.ly/45ZD1ft highlighted text says: An imbalance in GSH is observed in a wide range of pathologies, such as cancer, neurodegenerative diseases, cystic fibrosis (CF), several viral infections including HIV-1, as well as in aging. Several reports have provided evidence for the use of GSH and molecules able to replenish intracellular GSH levels in antiviral therapy.
Glutathione, CoQ10, alpha lipoic acid can all help with this.
Glutathione in particular has been shown to have multiple antiviral properties.
It's often depleted in chronic infections such as HIV, and supplementing it can help restore immune function.
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1: Mitochondrial & Metabolic Support
Viruses take over our mitochondria to replicate. The more difficult we can make for it to do that, by keeping our own human chemical reactions going, the more we can slow the virus down.
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My goal was to do everything I could to both fight the virus directly, as well as optimize my immune response.
β¨My plan had 3 main pillars:β¨
1) Mitochondrial & Metabolic Support
2) Antivirals
3) Immune Stimulants
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I planned my treatment meticulously before I started. With a virus that was possibly actively replicating, I knew I had to hit it as hard as I could, all at once.
I didnβt want to treat it halfway, and give it the chance to mutate.
So I planned a siege.
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The viral persistence hypothesis had always terrified me.
In the back of my mind, I think I always knew it was my root cause - but I was scared to face it.
Once I read this preprint, I decided it was time.
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Screenshot of my lab results for anti-spike antibodies. The amount says >12,500 U/mL
My own anti-spike antibodies immediately following my Feb 2023 acute infection were off the charts - >12,500 U/mL.
Compare this to Oct 2021 when I'd only been vaccinated - they were 2000 U/mL.
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In this paper, Rodriguez et al studied biomarkers from a cohort of patients with severe Long COVID.
What they found suggested a possible relationship between high anti-spike antibodies, a restrained T cell response, and viral persistence in LC.
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bsky.app/profile/sun-...
In spring 2024, I put together a 3-part treatment plan based on the idea that I needed to clear the SARS-CoV-2 virus from my body.
While viral persistence may not be the root cause for everyone with Long Covid, I was strongly influenced by this 2024 preprint...
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β¨How I Recovered from Long Covid PEM:β¨
Hey everyone, I've waited a while to share this - I wanted to make sure my improvements stuck.
It's been almost a year now, in total - wow!
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longcovidbegone.substack.com/p/my-recover...
These updates are so hopeful!!
29.08.2025 17:06 β π 0 π 0 π¬ 0 π 0La Jolla researchers screened 56 small molecules and found a new class that binds ETF1, a host protein, to disrupt viral ribosomal frameshifting.
These compounds blocked SARS-CoV-2, HIV, and other viruses without harming cells.
www.biorxiv.org/content/10.1...
Thanks for sharing! (I was gonna put it on here too but hadnβt had a chance yet- appreciate your spreading the word! π)
25.08.2025 22:21 β π 1 π 0 π¬ 1 π 0Thx for highlighting @sun-in-winter12.bsky.social
25.08.2025 19:48 β π 8 π 2 π¬ 2 π 0Happy to! Thanks so much for everything you and your colleagues are doing! π
25.08.2025 20:13 β π 1 π 0 π¬ 0 π 0Wow... seems like pretty strong evidence for SARS-CoV-2 persistence in pediatric Long COVID....
25.08.2025 02:06 β π 5 π 1 π¬ 0 π 0UPDATE: I also created a Substack in case you want to read this post in long-form!
Check it out here: π
longcovidbegone.substack.com/p/high-anti-...
Moving forward @polybiorf.bsky.social will support @petterbrodin.bsky.social @casanovalab.bsky.social and colleagues in studying the genetic and hormonal links to these restrained t-cell responses
Grateful for their support in this crisis π
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polybio.org/projects/gen...
We know there is likely more than one root cause of LC, and some people donβt make antibodies at all.
However I think itβs AMAZING that a phenotype of viral persistence has been clearly defined π
Weβve moved past asking whether the virus is still present, to proving WHY
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Screenshot from the paper. Highlighted text says: "All in all, our results suggest that a persistent viral reservoir is likely contributing to Long COVID pathology and ongoing efforts (NCT05823896) to remove such persisting viruses with prolonged antiviral therapies are important and hold clinical promise for delivering a much-needed cure to the community of Long COVID sufferers worldwide."
Of course, the #1 thing to take away from this is that the authors are now hypothesizing about a cure.
Thatβs right, they wrote the word CURE β¨
Specifically, antivirals (+presumably other strategies) to remove the persistent virus that our t-cells could not.
/15
Basically, we may have evolved this restrained t-cell response for a reason.
The authors say it may be a way for women's bodies to conserve energy for reproduction, and children's bodies for growth.
Now, this trait that was helpful to us in the past is now harming us
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Senior author @petterbrodin.bsky.social explains that the answer may lie in our genetics, as well as the fact that the immune system operates differently at different stages of life.
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They started to ask the question:
Why does Long Covid more often affect people we'd expect to have STRONGER immune systems?
Why do children and women of child-bearing age disproportionately develop LC, compared to those at high risk of severe acute disease?
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Why does this happen?
When the researchers took steps to select the patients who were the sickest, following a mild infection, their patient population came out to a 87% female.
With an average age of 48.
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It also tracks with these findings from
UCSF LIINC & @gladstoneinst.bsky.social
Not only did this team find higher anti-spike IgG antibodies, but they also noted a breakdown in coordination between the T- and the B- cells
gladstone.org/news/patient...
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The authors note that higher IgG responses to the virus were also found in this study from @putrinolab.bsky.social, @virusesimmunity.bsky.social and many others!
www.nature.com/articles/s41...
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Screenshot of my SARS-CoV-2 spike antibody result showing a level of 9,825.00 U/mL
Personally, I totally believe this is what happened to me.
According to the authors, antibody responses normally wane in 6 months, in people who fully recover.
Meanwhile my anti-spike antibodies were just under 10K, 10 months following my acute infection
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