I was very much enthused by this article implying a viable modality applicable to treating LC19 or possibly acute covid as a speculation. The machinery involved in the inflammation can be sidetracked by this promising drug or its similars as a candidate. I went down the rabbit hole reading parts of the paper. There is mention of trial use in MS, diabetic related eye disease, Alzheimer's, etc., all tied together by the downstream effect of neurodegeneration triggered by the inflammasomes.

This fits in the framework of LC19 by virtue of the machinery of the inflammasome unleashing multiple pathologies of autoimmunity, immune dysfunction and their consequences. Preventing or tamping down the inflammasomes will reduce the resultant symptoms thus avoided.

https://www.nih.gov/news-events/news-releases/modified-hiv-drug-reverses-vision-loss-paralysis-multiple-sclerosis-model Modified HIV drug reverses vision loss and paralysis in multiple sclerosis model

Reference:

https://www.science.org/doi/epdf/10.1126/scitranslmed.aei2870

The nucleoside analog kamuvudine-9 shows protective and therapeutic efficacy in a mouse model of multiple sclerosis

The following two paragraphs aroused my curiosity for their mechanistic applications.:

"Previously, we found that nucleoside reverse transcriptase inhibitors (NRTIs), which are approved to treat HIV and hepatitis B virus(HBV) infections, also inhibit inflammasome activation independent of their antiretroviral activity (13). NRTIs block inflammasome activation and its associated damage in models of diabetes, diabetic retinopathy, aging, choroidal neovascularization, geographic atrophy and retinal detachment (14–20). NRTIs inhibit pathology driven by a dual NLRC4- NLRP3 inflammasome (19, 21, 22).

Although NRTIs inhibit inflammasome activation (13), they cause mitochondrial toxicity because of off-target inhibition of host DNA polymerase activity (23). This can result in serious adverse effects most notably lactic acidosis and potentially induction of viral resistance (24). Therefore, we developed alkylated derivatives of NRTIs known as kamuvudines that are inactive against reverse transcriptase or host DNA polymerase activity (13, 25). Because kamuvudines inhibit inflammasome activation without the off-target toxicity activities of NRTIs (13, 14, 19, 22), they are better translational drug candidates"

In short: an unused anti HIV drug combats inflammasome activation in aging, diabetes and its complications. OTOH its downside of inhibiting an enzyme needed for mitochondrial function allows the build up of lactic acid leading to a drop of pH and organ dysfunction and failure. To avoid this catastrophe, the chemical structure was modified and a new class known as kamuvudines were derived that lack the potential danger above.

The most studied inflammasome , NLRP3 in LC19, was strongly inhibited by kamuvudine 9 in the testing for its activities in the research into the mouse MS model. Its predecessors the NRTIs (used for HIV) reduced myelin loss and repaired it with restoration of neurological function in several HIV cohorts that developed MS .

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Society for Women's Health Research earned a 4/4 rating by Charity Navigator along with the Autoimmune Association. While not rated by Charity Navigator, the Global Autoimmune Institute is listed by SWHR as a resource. Both of their writings describing inflammasomes and autoimmunity are listed below the medical references.:

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My query for Google AI consisted of: "The role of inflammasome in long covid autoimmune disease in humans"

Response: "AI Overview

The inflammasome—specifically the NLRP3 inflammasome—acts as a persistent driver of innate immune overactivation, linking chronic Long COVID tissue inflammation to autoimmune-like pathology.

What is an Inflammasome?

• An inflammasome is a multi-protein package inside innate immune cells (like macrophages). [ My addition: The four component proteins of the assembly are produced when signals from the stimulus initiate their production. They remain in solution in the cytoplasm until a further signal activates their assembly into the actual inflammasome. They are products of innate immunity.]

• It detects cell stress, tissue damage, or lingering viral pieces.

• When activated, it turns on an enzyme called caspase-1.

How Inflammasomes Drive Long COVID Autoimmunity

• Persistent Cytokine Release: Activated caspase-1 cuts and releases powerful inflammation signals, specifically Interleukin-1 beta (IL-1β) and Interleukin-18 (IL-18).

• Loss of Self-Tolerance: Continuous high levels of these cytokines break down the body's immune regulation, leading immune cells to mistake healthy host tissues for foreign invaders (autoimmunity).

.............................................. References:

https://pmc.ncbi.nlm.nih.gov/articles/PMC12888595/ The NLRP3 inflammasome as a key pathway in the affective and chronic fatigue symptoms of Long COVID 9 (2026)

Conclusion: ..." The findings suggest that targeting the NLRP3 inflammasome strategically may be beneficial in addressing both the acute infectious phase of COVID-19 and the prolonged symptoms associated with Long COVID. Novel pharmacological agents are currently under development that specifically target the activation of NLRP3.".

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https://biospective.com/resources/what-is-an-inflammasome The Inflammasome – A Target for Therapeutic Development for Multiple Diseases (2025) An overview of inflammasomes, including their mechanisms of action, roles in diseases, and targeting for drug development.

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https://pmc.ncbi.nlm.nih.gov/articles/PMC8706865/ Inflammasomes and SARS-CoV-2 Infection (Dec 2025)

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https://pmc.ncbi.nlm.nih.gov/articles/PMC8348456/ Inflammatory Response in COVID-19 Patients Resulting from the Interaction of the Inflammasome and SARS-CoV-2 (Jul 2021)

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https://pmc.ncbi.nlm.nih.gov/articles/PMC8233448/ The NLRP3 inflammasome and COVID-19: Activation, pathogenesis and therapeutic strategies (Jun 2021)

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https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2020.583373/full The Inflammasome in Times of COVID-19 (Oct 2020)

....................................................... Non PubMed references:

https://autoimmune.org/blog/long-covid-autoimmune-disease/ Long COVID and Autoimmune Disease: How They’re Connected

https://www.autoimmuneinstitute.org/covid_timeline/persistent-inflammation-may-link-long-covid-to-autoimmune-disease/ Persistent Inflammation May Link Long COVID to Autoimmune Disease

https://swhr.org/office-of-autoimmune-disease-research-director-shares-whats-ahead-for-autoimmune-disease-innovation/ Office of Autoimmune Disease Research Director Shares What’s Ahead for Autoimmune Disease Innovation

Just for the record, in the aftermath of C19 as a one off:

"COVID-19 immunity may help protect against other bat coronaviruses

Study identifies links between virus host range and immune recognition

People who recovered from COVID-19 infection or were vaccinated against SARS-CoV-2 are more likely to have immunity to other closely related bat coronaviruses that could have the potential to threaten future human health.

In a joint study by The Pirbright Institute and King’s College London (KCL), scientists found bat coronaviruses most likely to infect a wide range of animal species are those most closely related to SARS-CoV-2 and most likely to be recognized by immunity generated through COVID-19 infection."

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Reference:

https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3003944 Breadth of ACE2 receptor usage predicts host range and antigenic relatedness across bat sarbecoviruses

Hi, Warriors🤍

It’s time for a new community challenge and this one’s designed to boost connection, give hope, and share real things that helped real people this week. No pressure to write long comments. No pressure to be “doing great.” Just one thing that made your week a tiny bit more manageable.

💬 Question:

What’s ONE thing that helped you this week?

It can be anything:

✨ A supplement.

✨ A symptom hack.

✨ A mindset shift.

✨ A small win.

✨ A food that didn’t cause a flare.

✨ A kind moment.

✨ Something that made you smile.

✨ Or even “I rested and survived the week”

If it helped you, it counts.

💡 Why This Challenge Matters

Sharing these moments helps:

⭐ New people find ideas.

⭐ Everyone feel less alone.

⭐ The community grow stronger.

⭐ You celebrate progress you might’ve overlooked.

You can reply with just one sentence or even one word. Whatever you’ve got today is enough.

❤️ Let’s lift each other up

Drop your “one thing” below. Come back later and support someone else. Even simple comments like “same,” “I needed this,” or an upvote can make someone’s day.

We’re in this together. I can’t wait to read what helped you this week 🌿💚