Microbial Valence Is Not Fixed: A Compartmental Framework for Divergent Autoimmune and Oncogenic Outcomes

Background. Certain microorganisms are associated, in different patients or tissue contexts, with both immune-mediated disease and malignancy. These pairings are usually treated as unrelated associations, as if the microorganism itself carried a fixed pathological sign. Hypothesis. We propose that microbial valence is not intrinsic to the agent. We define microbial valence operationally as the direction of pathological consequence generated by a microbial exposure within a specified host–compartment context. The sign emerges from the interaction among microbial effector repertoire, Access, compartment, host Recognition/Discrimination, and the Amplification loop that follows. Framework. We formalize two sister compartmental grammars: ARA (Access–Recognition–Amplification) for autoimmune trajectories and ADA (Access–Discrimination–Amplification; not adenosine deaminase) for oncogenic trajectories. Six microorganisms are used as a structured case bank: Campylobacter jejuni, Epstein–Barr virus (EBV), Helicobacter pylori, Porphyromonas gingivalis, hepatitis C virus (HCV), and HTLV-1. Results of the conceptual synthesis. The cases resolve into four recurrent mechanisms—effector switch, same-effector contextual switch, discrimination switch, and temporal valence transition—and support five falsifiable predictions. The evidence is intentionally graded rather than homogenized: C. jejuni, EBV, and H. pylori serve as primary anchors; P. gingivalis as a strong supporting case; HCV as a temporal bridge; and HTLV-1 as a boundary stress-test. Conclusion. The microorganism does not carry the disease class. It carries a repertoire of potential perturbations; disease class emerges from the compartmental trajectory those perturbations enter.