The signal transducing molecule STAT-1 is required for signaling via receptors to IFN-γ-receptor-mediated signaling involves the dimerization of phosphorylated STAT-1 molecules. Signaling via IFN-α and IFN-β receptors involves the formation of a complex between STAT-1, STAT-2, and a third protein called interferon-stimulated gene factor 3-γ. Complete (homozygous) defects of the signal-transducing molecules STAT-1 results in defective responses to IFN-γ, IFN-α and IFN-β eater leading to the susceptibility to disseminated mycobacterial infections as well as fatal Herpes simplex infection. Partial STAT-1 deficiency, which interferes with STAT-1 dimerization required for signal transduction via IFN-γ receptors, leads to increased susceptibility to mycobacterial infections. In these patients, the cellular responses to IFN-α and IFN-β is intact, thus preserving antiviral immunity.