Closing the CNS Access Gap in EBV-Associated Multiple Sclerosis

EBV infection is a near-universal antecedent of MS and is supported by unusually strong temporal and mechanistic evidence: seroconversion precedes neuroaxonal injury in a cohort of more than 10 million military recruits [2], and clonally expanded cerebrospinal-fluid B cells cross-react with EBNA1 and the glial protein GlialCAM at crystallographic resolution [3]. Yet EBV’s own dossier under the Access–Recognition–Amplification (ARA) framework [1] documents Recognition to this standard while leaving Access — how a peripherally primed autoreactive population physically reaches the CNS compartment — unspecified. We propose a composite, falsifiable hypothesis that pairs EBV’s Recognition mechanism with a candidate second Access event drawn from an existing ARA dossier: Bartonella henselae, whose endothelial activation and monocyte chemotaxis are documented in vitro. We additionally define a nested, optional carrier-cell modifier: Bartonella-associated endothelial CCL2 signalling and CCL2-dependent transport of injected biopersistent particles in an experimental model suggest a shared chemotactic axis, but its operation in humans and its relevance to MS remain untested. The composite is not offered as established; it specifies, in advance, the co-detection pattern that would support it and the negative finding that would refute it. We outline the evidentiary basis, the falsifiable prediction, and the explicit boundaries of what this composite does and does not claim.