Given the actions of quinolinic acid as an NMDA receptor agonist and kynurenic acid as an antagonist, and that their concentrations are altered by infection (via interferon induction of cellular indoleamine-2,3-dioxygenase, IDO) and stress (via the corticosteroid induction of hepatic tryptophan-2,3-dioxygenase, TDO), it is reasonable to consider the possibility that changes in kynurenine metabolism could be involved. The gene discussed is IDO1; the disease is infection.