Why Long COVID Won't Resolve: A Mechanistic Reading of Viral Persistence, Mitochondrial Dysfunction, and the Gut–Brain Axis the Standard Model Is Missing — Part 4: How to Read Your Own Case Through This Lens

The clinical heterogeneity of long COVID is real. The convergent mechanism does not mean every patient looks the same. It means the same upstream lesion expresses differently in different patients based on which mechanisms in the convergent set are most active and which body systems are most affected. A careful read of your own case typically identifies one or two dominant subsystems through which the convergent lesion is expressing itself most strongly. Several patterns are common. The gut–vagal–cognitive pattern. Dominant brain fog, post-prandial cognitive crash, food reactivity, GI symptoms, and the characteristic relief of cognitive symptoms when GI symptoms are quiet. This pattern fits most cleanly the Penn group's serotonin–vagal mechanism (Finding Two), the microbiome signature (Finding Eight), and the persistent gut antigen burden (Finding One). The lesion in these patients is most accessible through gut-targeted intervention at the capacity layer. The post-exertional metabolic pattern. Dominant fatigue, exercise intolerance, post-exertional malaise lasting days to weeks, characteristic delay between exertion and symptom worsening. This pattern fits most cleanly the mitochondrial findings (Findings Three, Four), the microclot literature (Finding Five), and the skeletal muscle glycolytic shift. The lesion is most accessible through systemic mitochondrial intervention at