It has been shown that eukaryotic viruses in the GI tract are capable of (i) restoring gut architectural and immune status during gut bacterial dysbiosis and (ii) regulating host homeostasis, and (iii) it has been hypothesized that their latent infection might induce continuous and persistent immune stimulation via antiviral IFNγ and systemic macrophage activation at basal levels, protecting the host from infections. The gene discussed is IFNG; the disease is infection.