CIITA has been shown to upregulate expression of Rab4B, a small GTPase involved in endocytic recycling [44, 47] . Therefore, we hypothesized that CIITA via the action of Rab4B, could increase Gag recycling back to the PM, thereby alleviating HLA-DR-mediated Gag retention. Commercially available Rab4 antibodies cannot distinguish between Rab4A and 4B. However, Krawczyk et al. (2007) demonstrated by chromatin immunoprecipitation that CIITA specifically associates with the Rab4B and not the Rab4A promoter [44] . Immunoblotting demonstrated that there is an increase in Rab4 in CIITA-expressing cells ( Figure 3A ), therefore it is likely that this is in the form of Rab4B. However, when Rab4B and HLA-DR were co-expressed in producer cells with the HIV-1 NL4-3 plasmid, it did not rescue intracellular retention of Gag ( Figure 3B ). In fact, infectious virus release from cells transiently co-expressing Rab4B and HLA-DR was further reduced, suggesting that Rab4B does not alleviate HLA-DRmediated retention of Gag ( Figure 3C ).