In this model we observed that the infection is bi-phasic with innate and Th1- mediated immune responses (TLR activation and IFN-γ, IL-6 and TNF-α production) during the acute phase of infection and an increasing systemic regulatory immune response (rising frequency of regulatory T cells as well as increased levels of IL-10 and TGF-β) in the chronic phase. The gene discussed is IFNG; the disease is infection.