Long Covid - Attempted System Reboot - Update 1

In August of 2025 I decided to try and take everything we know (or don't know) about long COVID-19 and my own particular lab results and try to see if I can nudge myself back to health. My action plan, which I'll link to below, involves rougly 90 days of anti-inflammatories, JAK stat inhibitors, anti-virals, and several immune modulators. The goal is to try and address whatever it is that's causing my system to still be on high alert.

Pre-Trial Labs

Here is a list of my labs before starting this experiment. For a detailed overview of all of them, visit my main page.

Foundational metrics: eGFR >100 mL/min/1.73m²; HbA1c 4.7%; TSH 1.8 mIU/L (fT4/fT3 upper half per report).

Cytokine Panel

Th Subsets

Lymphocyte Panel

Immune Checkpoints (Exhaustion Markers)

Monocytes & hsCRP

Covid 19 Spike IgG

Here is a list of my Covid19 spike IgG levels over time, along with computed half-life (how fast they are declining) whenever there are serial values. What's noticable is that over time they are declining more and more slowly, especially after my December 2023 infection. While I am only showing the spike IgG here, the decay rate is similar for the IgG for the nucleocapsid as well, which seems to go against what the literature tells us.

Current Systemic State

I asked ChatGPT to summarize the overall state of my immune system during the snapshot above, taken roughly in July and August of 2025 (nearly 16 months after my December 2023 infection):

• This immune profile reflects a system in a sustained state of high-grade activation, coupled with signs of functional exhaustion in multiple immune compartments. The cytokine landscape is dominated by strong pro-inflammatory mediators: IL-1β, IL-6, IL-12p70, TNF-α, and IFN-γ are all several-fold above reference ranges. This constellation indicates persistent engagement of both the innate and adaptive arms of immunity, most often driven by ongoing exposure to a viral or other antigenic reservoir. IL-10, an anti-inflammatory cytokine, is also elevated, suggesting the immune system is actively trying to dampen inflammation but cannot bring it under control.

• T helper subset data show partial improvements since the prior testing. Th2 levels, which tend to drive allergic-type inflammation, have dropped by about 20%, and Th17 cells — important mediators of neutrophil recruitment and tissue inflammation — have decreased toward normal. The Th1/Th2 ratio has moved upward, indicating a relative strengthening of antiviral-type responses, though it remains low. T regulatory cells have declined into the reference range, meaning less inappropriate suppression. Th9 cells, however, remain borderline high, pointing to ongoing mast cell–linked inflammation.

• The lymphocyte compartment reveals depletion. Total T cells have dropped by nearly one-third, with both CD4 and CD8 subsets significantly reduced. CD8 effector memory cells, the critical tissue-patrolling cytotoxic cells, are now below reference, weakening the system’s capacity to clear infected cells. Activated CD8 cells have fallen by over 40%, deepening the concern about antiviral effectiveness. NK cell counts are stable within the normal range, while NKT cells have risen into the normal range — possibly compensatory. B cells are reduced by almost 40% but remain technically normal.

• Checkpoint analysis confirms that much of this cytotoxic potential is being throttled. Both NK and CD8 T cells show markedly elevated expression of exhaustion markers, including CTLA-4, PD-1, and TIGIT — all of which are inhibitory “brakes” that suppress killing capacity. NK–CTLA-4 is over fourfold above the upper limit, and CD8–PD-1 is more than triple the reference maximum. Tregs also show elevated PD-1 and CTLA-4, which can amplify suppression of antiviral responses. This checkpoint profile indicates that even when cytotoxic cells are present, they are likely to be functionally impaired.

• The myeloid compartment is heavily skewed toward classical inflammatory monocytes, with almost no non-classical (patrolling and repair) monocytes — a pattern associated with ongoing inflammation and poor tissue repair. Neutrophils and eosinophils have normalized since prior testing, but high-sensitivity CRP remains elevated, confirming systemic inflammatory activity.

• Conclusion: This pattern represents a chronically activated, antigen-engaged immune system that is simultaneously overproducing inflammatory signals and losing its functional capacity to eliminate the underlying trigger. The cytokine elevations are too pronounced to be explained by mild dysbiosis or bacterial translocation alone; they are more consistent with persistent viral antigen exposure, such as a long-term SARS-CoV-2 reservoir or other reactivating virus. The checkpoint overexpression compounds the problem by keeping cytotoxic cells in a suppressed state, preventing clearance. The combined goals in this context are: (1) reduce excessive inflammatory signaling, (2) restore functional cytotoxic capacity by addressing checkpoint-mediated exhaustion, and (3) eliminate or suppress the persistent antigen source driving the loop. Without all three addressed, the immune system is likely to remain locked in this high-output yet ineffective state.

Week 1: August 8 - August 15, 2025

This week I started with a dexamethasone taper over 3 days, the main goal of which was to dampen my inflammatory cytokines and give me some symptom relief. Day to day I still feel frequent crashes, difficulty sleeping, a general feeling of being unwell, tinnitus, vertigo, and brain fog.

Because I've had indication that my VZV (Shingles) has re-activated a few times over the last few years, I decided to get the Shingrix vaccine before starting. The steroid taper will likely blunt the effect of it, but I'll deal with that later with another booster. Not long after I did the vaccine I took my first dexa pill. I also concurrently started the paxlovid anti-virals, and SOFOSBUVIR/DACLATASVIR, which is another anti-viral with some affinity towards covid19. Because Paxlovid and SOFOSBUVIR/DACLATASVIR have some interaction, I halved the dose of SOFOSBUVIR/DACLATASVIR for the first week. Once the paxlovid leaves my system, I'll go back to a full dose of that.

I also paired this with maraviroc, also known as part of the Patterson protocol, starting a few weeks ago along with truvada. I take a statin anyways, pitavastatin 2mg per day, but I stopped that during the Paxlovid as well to reduce liver burden temporarily.

At the one week mark, I went and took a series of labs to track what's happening inside, something I'll continue with every week as this moves forward. I expected my inflammation to drop on the labs, but probably not much of anything else. That should change next week as I start the Jak Stat inhibitor along with colchicone, and thymosin alpha 1.

The vaccine kicked my ass for a few days, ramping my HR up to 120bpm for a few days, and tanked my HRV, but outside of that I actually felt pretty well the rest of the week. It's still too early to tell, but my post vaccine (or post steroid, post anti-viral) HRV seems to have notched up 10-15 points, which is impressive.

Journal Entries

Here are my day to day journal entries with how I was feeling.

Updated Labs

What's Next