Importantly, the HIS mouse model would also permit investigations of the CD4+T cell-independent mechanisms of disease due to HIV infection that are not reproduced through generalized immune suppression with aminoguanidine or glucocorticoids, in vivo CD4+T cell subset depletion, or use of mouse strains with immune defects (Scanga et al., 1999; Botha and Ryffel, 2002; Cheigh et al., 2010). This evidence concerns the gene CD4 and HIV infectious disease.