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 2: The Convergence — Why These Mechanisms Are Not Independent

The standard practitioner reading of the long COVID literature treats these findings as parallel mechanisms, each addressable in isolation. The patient is offered antivirals for viral persistence, anticoagulants for microclots, NAD precursors and CoQ10 for mitochondrial dysfunction, antihistamines and mast cell stabilizers for MCAS overlap, SSRIs for serotonin depletion, midodrine and ivabradine for autonomic dysfunction, low-dose naltrexone for inflammation. The result is a polypharmacy of single-mechanism interventions, each one producing partial benefit at best, none of them resolving the illness. The mechanisms are not parallel. They intersect. And the layer at which they intersect is the layer the standard treatment approach is not addressing. The Gut Epithelium as Convergence Node The intestinal epithelium is the anatomical site where several of the major mechanisms converge. SARS-CoV-2 antigen persistence is documented preferentially in this tissue. ACE2 expression is highest here. The B0AT1 transporter that drives tryptophan absorption sits here. The enterochromaffin cells that produce ninety percent of the body's serotonin sit embedded in this epithelium. The vagal afferents that integrate gut signaling to the brain terminate here. The mucin layer that separates microbes from epithelium is produced here. The IgA that regulates the microbial community is secreted here.