Since genital infections with both Cs and Ct induce an IFN-γ response [10,11,20], the observed lack of IFN-γ production despite a clear proliferative response can potentially be explained by the fact that all pre-exposed pigs were mainly infected in the GI tract; however, chlamydia infections of the GI tract have been shown to be rather homeostatic [45]. The gene discussed is IFNG; the disease is infection.