Immune Failure Without Immune Collapse: A Lymphoid-Niche Model of EBV Persistence and Neuro-Endocrine Dysregulation in ME/CFS
Introduction If one takes Eriksen’s 3-step model of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) at face value, the fundamental defect is not Epstein–Barr virus (EBV) entering an uncontrolled lytic state . Rather, the pathology emerges from a subtler but more durable failure: loss of normal immune containment combined with abnormal lymphoid organization , allowing latently EBV-infected B cells to accumulate in anatomically inappropriate locations , particularly ectopic lymphoid aggregates near or within nervous tissue. In this framework, EBV acts less as an acutely cytopathic pathogen and more as a persistent immune stressor , exploiting vulnerabilities in immune surveillance, B-cell regulation, tissue-level immune architecture, and downstream neuro-endocrine control . The result is a self-reinforcing inflammatory loop that does not require overt viral replication to remain pathogenic. The Core Mechanistic Defect: Two Coupled Failures 1. A tendency to form and maint...