The AuRx herpes therapy is thought to work via cell-mediated immunity (CMI). It is based on accumulating evidence that recurrent disease is associated with a preponderance of immune regulatory T cells [helper type 2 (Th2)] that function to downregulate the ability of the virus-specific CMI to control virus replication. The AuRx therapy shifts the balance of the virus-specific T cells to a preponderance of protective T cells [helper type 1 (Th1) T cells] and CD8+ killer (cytotoxic) T cells. These cells cause lysis of the virus-infected cells. Soluble mediators are released which produce a response cascade that includes elevated levels of interferon gamma, a stimulator of the Th1 response which also inhibits HSV reactivation from latently infected ganglia. The AuRx therapy also reduces the production of the soluble mediator IL-10 which stimulates the production of Th2 cells.