How the sickness syndrome assembles with dose
Raise the inflammatory dose — the circulating load of cytokines or bacterial endotoxin reaching the brain — and watch the syndrome build up one component at a time. Each response has its own recruitment threshold, so fever and appetite loss appear at low doses while anhedonia emerges only once the signal is strong. There is no single sickness switch; the state is a graded, dose-dependent reorganization. Illustrative teaching model; computed locally and not stored.
Two routes from the immune system to the brain
A peripheral infection reaches the brain two ways. The neural route — cytokines exciting vagal afferents — is fast but modest. The humoral route — blood-borne signaling at the leaky circumventricular organs — is slow to start but larger and sustained. Toggle each route to see the central signal it produces and how, together, a fast onset is handed off to a durable plateau. Illustrative teaching model of the relative dynamics; computed locally and not stored.
Why inflammation makes effort feel not worth it
A simple choice model: the value of acting is the reward minus an effort cost, V = R − k(E/D), where D is dopaminergic drive. Inflammation lowers D, which steepens the cost of effort and pulls the break-even point — the effort at which acting stops being worthwhile — sharply inward. Set the reward and drag the drive down to watch an action that paid off at full drive turn net-negative. Illustrative teaching model (Treadway, Cooper & Miller, 2019); computed locally and not stored.