T-cell responses are needed though, as shown by how susceptible those with HIV infection are to M. tuberculosis infection, or the rapidly progressive infections seen in SCID mice, as well as the increased mycobacterial growth in mice lacking the ability to produce or respond to IFNγ; in mice and in man there are similar examples of genetic mutations in the IFNγ-IL-12 axis resulting in susceptibility to mycobacterial disease [29]. This evidence concerns the gene IFNG and HIV infectious disease.