These data show that latent Cryptococcus infection in C3HeB/FeJ mice does not induce IFN1 production, that SP140 deficiency does not enhance IFN1 production during latent infection, and that SP140 deficiency in C57Bl/6J mice does not replicate the latent Cryptococcus infection immune response seen in C3HeB/FeJ mice. The gene discussed is SP140; the disease is disease arising from reactivation of latent virus.